Revistas
Autores:
Baquerizo-Sedano, L. (Autor de correspondencia); Chaquila, J. A.; Aguilar, L.; et al.
Revista:
CLINICAL NUTRITION
ISSN:
0261-5614
Año:
2022
Vol.:
41
N°:
12
Págs.:
2988 - 2995
Background & aims: Emergency measures in the face of the recent COVID-19 pandemic have been different among countries, although most have opted for confinement and restrictions on social contact. These measures have generated lifestyle changes with potential effects on individuals' health. The dis-turbances in daily routines due to confinement and remote work have impacted circadian rhythms and energy balance; however, the consequences of these disruptions have not been studied in depth. The objective was to evaluate the impact of 12-week confinement on body weight, considering changes in several external synchronizers of the biological clock.Methods: The participants, 521 university students (16-35 years), responded to 52 questions oriented to determine light exposure, sleep patterns, sedentary lifestyle, and eating times.Results: We found a reduction in sunlight exposure and sleep duration, an increment in sedentarism and screen exposure, and a delay in the timing of the main meals and sleep in the whole cohort. These behavioral changes were associated with a twofold increase in obesity. Subjects who increased their sedentary hours and shortened their sleep to a higher degree were those who gained more bodyweight. The most influential factors in body weight variation during confinement were sleep duration, physical activity (sedentarism), and light (timing of screen exposure). The mediation model explained 6% of the total body weight variation.Conclusions: Results support a significant impact of confinement on several external synchronizers of the biological clock and on body weight. Health-related recommendations during the pandemic must include behavioral recommendations to mitigate the adverse effects on the biological clock.(c) 2021 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.
Revista:
NUTRIENTS
ISSN:
2072-6643
Año:
2022
Vol.:
14
N°:
20
Págs.:
4240
Obesity and aging promote chronic low-grade systemic inflammation. The aim of the study was to analyze the effects of long-term physical exercise and/or omega-3 fatty acid Docosahexaenoic acid (DHA) supplementation on genes or proteins related to muscle metabolism, inflammation, muscle damage/regeneration and myokine expression in aged and obese mice. Two-month-old C57BL/6J female mice received a control or a high-fat diet for 4 months. Then, the diet-induced obese (DIO) mice were distributed into four groups: DIO, DIO + DHA, DIO + EX (treadmill training) and DIO + DHA + EX up to 18 months. Mice fed a control diet were sacrificed at 2, 6 and 18 months. Aging increased the mRNA expression of Tnf-alpha and decreased the expression of genes related to glucose uptake (Glut1, Glut4), muscle atrophy (Murf1, Atrogin-1, Cas-9) and myokines (Metrnl, Il-6). In aged DIO mice, exercise restored several of these changes. It increased the expression of genes related to glucose uptake (Glut1, Glut4), fatty acid oxidation (Cpt1b, Acox), myokine expression (Fndc5, Il-6) and protein turnover, decreased Tnf-alpha expression and increased p-AKT/AKT ratio. No additional effects were observed when combining exercise and DHA. These data suggest the effectiveness of long-term training to prevent the deleterious effects of aging and obesity on muscle dysfunction.
Autores:
Baquerizo-Sedano, L. (Autor de correspondencia); Chaquila, J. A.; Aguilar, L.; et al.
Revista:
CLINICAL NUTRITION
ISSN:
0261-5614
Año:
2022
Vol.:
41
N°:
12
Págs.:
3135 -3136
Revista:
NUTRIENTS
ISSN:
2072-6643
Año:
2021
Vol.:
13
N°:
7
Págs.:
2465
Resistance training (RT) and n-3 polyunsaturated fatty acids (n-3 PUFA) supplementation have emerged as strategies to improve muscle function in older adults. Overweight/obese postmenopausal women (55-70 years) were randomly allocated to one of four experimental groups, receiving placebo (olive oil) or docosahexaenoic acid (DHA)-rich n-3 PUFA supplementation alone or in combination with a supervised RT-program for 16 weeks. At baseline and at end of the trial, body composition, anthropometrical measures, blood pressure and serum glucose and lipid biomarkers were analyzed. Oral glucose tolerance tests (OGTT) and strength tests were also performed. All groups exhibit a similar moderate reduction in body weight and fat mass, but the RT-groups maintained bone mineral content, increased upper limbs lean mass, decreased lower limbs fat mass, and increased muscle strength and quality compared to untrained-groups. The RT-program also improved glucose tolerance (lowering the OGTT incremental area under the curve). The DHA-rich supplementation lowered diastolic blood pressure and circulating triglycerides and increased muscle quality in lower limbs. In conclusion, 16-week RT-program improved segmented body composition, bone mineral content, and glucose tolerance, while the DHA-rich supplement had beneficial effects on cardiovascular health markers in overweight/obese postmenopausal women. No synergistic effects were observed for DHA supplementation and RT-program combination.
Autores:
Graham, C. A. M. (Autor de correspondencia); Pilic, L.; King, A.; et al.
Revista:
FOOD QUALITY AND PREFERENCE
ISSN:
0950-3293
Año:
2021
Vol.:
92
Págs.:
104202
Over the past decade, a potential sixth taste, fat taste ("oleogustus"), has been identified. Studies in adults and children of various ethnicities have demonstrated that both lifestyle and genetic factors may contribute to fat taste sensitivity (FTS). Data on females in the UK is limited. The aim of this study was to determine, using an ethnically similar, healthy, female cohort, whether known genotypes related to fat taste and dietary intake lead to differences in FTS. A cross-sectional study was carried out on a UK cohort of Caucasian females (32.7 +/- 11.4 years, 23.7 +/- 3.6 kg/m2). We report that FTS differed in individuals with differing genotypes; genotypes that have previously been associated with differences in dietary intake. Specifically, FTS was lower in rs1514175 Troponin I-Interacting Protein Kinase (TNNI3K) gene AA/AG genotype and was higher in rs6265 Brain Derived Neurotrophic Factor (BDNF) gene TT/CT genotype (both p < 0.05). We also report that participants in the rs1514175 TNNI3K AA/AG genotype group had a higher energy intake, total fat intake, and subsequently, higher monounsaturated fat and saturated fat intake when compared to the GG genotype (all p < 0.05). To our knowledge, this is the first study showing associations between genotypes that have been previously associated to dietary intake are also associated to FTS. Due to the heterogeneity of previous research and the infancy of fat taste research, further research is required on a larger, ethnically similar cohort.
Revista:
JOURNAL OF PHYSIOLOGY AND BIOCHEMISTRY
ISSN:
1138-7548
Maresin 1 (MaR1) is a DHA-derived pro-resolving lipid mediator. The present study aimed to characterize the ability of MaR1 to prevent the alterations induced by TNF-alpha on insulin actions in glucose uptake and Akt phosphorylation in cultured human adipocytes from overweight/obese subjects, as well as to investigate the effects of MaR1 acute and chronic administration on Akt phosphorylation in absence/presence of insulin in white adipose tissue (WAT) and skeletal muscle from lean and diet-induced obese (DIO) mice. MaR1 (0.1 nM) prevented the inhibitory effect of TNF-alpha on insulin-stimulated 2-Deoxy-D-glucose uptake and Akt phosphorylation in human adipocytes. Acute treatment with MaR1 (50 mu g/kg, 3 h, i.p.) induced Akt phosphorylation in WAT and skeletal muscle of lean mice. However, MaR1 did not further increase the stimulatory effect of insulin on Akt activation. Interestingly, intragastric chronic treatment with MaR1 (50 mu g/kg, 10 days) in DIO mice reduced the hyperglycemia induced by the high fat diet (HFD) and improved systemic insulin sensitivity. In parallel, MaR1 partially restored the impaired insulin response in skeletal muscle of DIO mice and reversed HFD-induced lower Akt phosphorylation in WAT in non-insulin-stimulated DIO mice while did not restore the defective Akt activation in response to acute insulin observed in DIO mice. Our results suggest that MaR1 attenuates the impaired insulin signaling and glucose uptake induced by proinflammatory cytokines. Moreover, the current data support that MaR1 treatment could be useful to reduce the hyperglycemia and the insulin resistance associated to obesity, at least in part by improving Akt signaling.
Autores:
López-Pascual, A.; Trayhurn, P.; Martínez, JA; et al.
Revista:
ANTIOXIDANTS AND REDOX SIGNALING
ISSN:
1523-0864
Año:
2021
Vol.:
35
N°:
8
Págs.:
642 - 687
Significance: In recent years, a number of studies have shown altered oxygen partial pressure at a tissue level in metabolic disorders, and some researchers have considered oxygen to be a (macro) nutrient. Oxygen availability may be compromised in obesity and several other metabolism-related pathological conditions, including sleep apnea-hypopnea syndrome, the metabolic syndrome (which is a set of conditions), type 2 diabetes, cardiovascular disease, and cancer. Recent Advances: Strategies designed to reduce adiposity and its accompanying disorders have been mainly centered on nutritional interventions and physical activity programs. However, novel therapies are needed since these approaches have not been sufficient to counteract the worldwide increasing rates of metabolic disorders. In this regard, intermittent hypoxia training and hyperoxia could be potential treatments through oxygen-related adaptations. Moreover, living at a high altitude may have a protective effect against the development of abnormal metabolic conditions. In addition, oxygen delivery systems may be of therapeutic value for supplying the tissue-specific oxygen requirements. Critical Issues: Precise in vivo methods to measure oxygenation are vital to disentangle some of the controversies related to this research area. Further, it is evident that there is a growing need for novel in vitro models to study the potential pathways involved in metabolic dysfunction to find appropriate therapeutic targets. Future Directions: Based on the existing evidence, it is suggested that oxygen availability has a key role in obesity and its related comorbidities. Oxygen should be considered in relation to potential therapeutic strategies in the treatment and prevention of metabolic disorders.
Autores:
Banaszczak, M.; Maciejewska, D.; Drozd, A.; et al.
Revista:
MEDICINA-LITHUANIA
ISSN:
1010-660X
Año:
2020
Vol.:
56
N°:
2
Págs.:
58
Background: It was previously shown that a bodyweight reduction among patients with nonalcoholic fatty liver (NAFLD) was connected to the lower concentration of arachidonic and linoleic acid derivatives in their blood. We hypothesized that the concentration of these lipids was correlated with the extent of their body mass reduction and, thus, liver steatosis. Methods: We analyzed 68 individuals who completed the dietary intervention. Patients were divided into two groups depending on their body mass reduction (more or less than 7%). Before and after the dietary intervention, all patients had the following measurements recorded: body mass, waist circumference, stage of steatosis, fatty liver index, liver enzymes, lipid parameters, insulin and glucose. Concentrations of lipoxins A4 (LTX A4), hydroxyeicosatetraenoic fatty acids (5(S)-HETE, 12(S)-HETE and 16(S)-HETE), hydroxyoctadecaenoic acids (9(S)-HODE and 13(S)-HODE) and 5-oxo-eicosatetraenoic acid (5-oxo-ETE) were measured in serum samples collected before and after the dietetic intervention using high-performance liquid chromatography (HPLC). Results: Patients who reduced their body mass by more than 7% revealed a significant improvement in their steatosis stage, waist circumference, fatty liver index, triglycerides and cholesterol. Conclusion: A reduction in body mass by more than 7% but not by less than 7% revealed a significant improvement in steatosis stage; waist circumference; fatty liver index; and levels of triglycerides, cholesterol, 5-oxo-ETE and LTXA-4.
Autores:
Ovalle-Marin, A.; Reyes-Farias, M.; Vasquez, K. ; et al.
Revista:
JOURNAL OF BERRY RESEARCH
ISSN:
1878-5093
Año:
2020
Vol.:
10
N°:
3
Págs.:
531 - 545
BACKGROUND: Obesity occurs due to a positive energy imbalance, leading to the expansion of adipose tissue. This phenomenon triggers a chronic low-grade inflammatory state, which is associated with comorbidities development. It is, therefore, of great interest to investigate new counteracting nutritional strategies. In this regard, polyphenol-rich Chilean native fruits, Aristotelia chilensis (Maqui) and Berberis microphylla (Calafate), and also the non-Chilean Vaccinium corymbosum (Blueberry), have been associated with antioxidant and anti-inflammatory features. OBJECTIVE: To evaluate Maqui, Calafate, and Blueberry aqueous extracts treatments on the pathogenic response of human activated macrophages and visceral adipocytes. METHODS: THP-1 monocyte human cell line and differentiated human visceral preadipocytes were activated (with lipopolysaccharide and TNF-a, for 48 and 24 h, respectively), and treated with the aqueous extracts. Inflammation and oxidative stress markers were assessed. RESULTS: Lower NO and IL-6 secretion, and inhibited apoptosis in activated macrophages, were observed. Also, decreased gene expression of MCP-1 and secretion of IL-6, inhibited apoptosis, and increased levels of GSH in activated adipocytes were detected. CONCLUSIONS: Maqui, Calafate, and Blueberry extracts showed anti-inflammatory and antioxidant responses in human macrophages and adipocytes.
Autores:
Graham, C. A. M. (Autor de correspondencia); Pedlar, C. R.; Hearne, G.; et al.
Revista:
LIFESTYLE GENOMICS
ISSN:
2504-3161
Año:
2020
Vol.:
13
N°:
2
Págs.:
99 - 106
Introduction: In the UK, the number of comorbidities seen in children has increased along with the worsening obesity rate. These comorbidities worsen into adulthood. Genome-wide association studies have highlighted single nucleotide polymorphisms associated with the weight status of adults and offspring individually. To date, in the UK, parental genetic, lifestyle, and social determinants of health have not been investigated alongside one another as influencers of offspring weight status. A comprehensive obesity prevention scheme would commence prior to conception and involve parental intervention including all known risk factors. This current study aims to identify the proportion of overweight that can be explained by known parental risk factors, including genetic, lifestyle, and social determinants of health with offspring weight status in the UK. Methods: A cross-sectional study was carried out on 123 parents. Parental and offspring anthropometric data and parental lifestyle and social determinants of health data were self-reported. Parental genetic data were collected by use of GeneFiX saliva collection vials and genotype were assessed for brain-derived neurotrophic factor (BDNF) gene rs6265, melanocortin 4 receptor (MC4R) gene rs17782313, transmembrane protein 18 (TMEM18) gene rs2867125, and serine/threonine-protein kinase (TNN13K) gene rs1514175. Associations were assessed between parental data and the weight status of offspring. Results: Maternal body mass index modestly predicted child weight status (p < 0.015; R-2 = 0.15). More mothers of overweight children carried the MC4R rs17782313 risk allele (77.8%; p = 0.007) compared to mothers of normal-weight children. Additionally, fathers who were not Caucasian and parents who slept for <7 h/night had a larger percentage of overweight children when compared to their counterparts (p = 0.039; p = 0.014, respectively). Conclusion: Associations exist between the weight status of offspring based solely on parental genetic, lifestyle, and social determinants of health data. Further research is required to appropriately address future interventions based on genetic and lifestyle risk groups on a pre-parent cohort.
Autores:
Lopez-Pascual, A. ; Urrutia-Sarratea, A. ; Lorente, Silvia; et al.
Revista:
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
ISSN:
1942-0900
Año:
2019
Vol.:
2019
Págs.:
2695289
Insulin resistance is associated with oxidative stress, mitochondrial dysfunction, and a chronic low-grade inflammatory status. In this sense, cerium oxide nanoparticles (CeO2 NPs) are promising nanomaterials with antioxidant and anti-inflammatory properties. Thus, we aimed to evaluate the effect of CeO, NPs in mouse 3T3-L1 adipocytes, RAW 264.7 macrophages, and C2C12 myotubes under control or proinflammatory conditions. Macrophages were treated with LPS, and both adipocytes and myotubes with conditioned medium (25% LPS-activated macrophages medium) to promote inflammation. CeO2 NPs showed a mean size of <= 25.3 nm (96.7%) and a zeta potential of 30.57 +/- 0.58 mV, suitable for cell internalization. CeO, NPs reduced extracellular reactive oxygen species (ROS) in adipocytes with inflammation while increased in myotubes with control medium. The CeO2 NPs increased mitochondrial content was observed in adipocytes under proinflammatory conditions. Furthermore, the expression of Adipoq and Il10 increased in adipocytes treated with CeO, NPs. In myotubes, both Il1b and Adipoq were downregulated while Irs1 was upregulated. Overall, our results suggest that CeO2 NPs could potentially have an insulin-sensitizing effect specifically on adipose tissue and skeletal muscle. However, further research is needed to confirm these findings.
Autores:
Norouzirad, R. ; Gholami, H. ; Ghanbari, M.; et al.
Revista:
LIFE SCIENCES
ISSN:
0024-3205
Año:
2019
Vol.:
230
Págs.:
188 - 196
Aims: Hyperoxia has beneficial metabolic effects in type 2 diabetes. However, hyperoxia exacerbates already existing oxidative stress in type 2 diabetes. Nitrate, a nitric oxide donor, is an effective new treatment in type 2 diabetes and also has antioxidant properties. The aim of this study was to determine whether nitrate administration can attenuate hyperoxia-induced oxidative stress in obese type 2 diabetic rats. Main methods: Fifty-six male Wistar rats (190-210 g) were divided into 8 groups: Controls (non-treated, nitratetreated, O-2-treated, and nitrate + O-2-treated) and diabetes (non-treated, nitrate-treated, O-2-treated, and nitrate + O-2-treated). Diabetes was induced using high-fat diet and low-dose of streptozotocin (30 mg/kg). Rats in intervention groups, were exposed to 95% oxygen and consumed sodium nitrate (100 mg/L) in drinking water. Serum fasting glucose, oxidized (GSSG) and reduced (GSH) glutathiones, total oxidant status (TOS), catalase and superoxide dismutase (SOD) activities, and total antioxidant capacity (TAC) were measured after intervention. Oxidative stress index (OSI) was calculated as TOS/TAC ratio. Key findings: Diabetic rats had increased oxidative stress and hyperoxia exacerbated it. In 0 2 -diabetic rats, nitrate decreased GSSG (102.7 +/- 2.1 vs. 236.0 +/- 20.1 mu M, P < 0.001), TOS (67.7 +/- 7.3 vs. 104 +/- 3.8 mu M, P < 0.001), and OSI (0.44 +/- 0.04 vs. 0.91 +/- 0.07, P < 0.001) and increased catalase (2.8 +/- 0.13 vs. 1.8 +/- 0.21 KU/L, P = 0.014), SOD (53.4 +/- 1.5 vs. 38.4 +/- 1.2 U/mL, P < 0.001), GSH (43.7 +/- 1.4 vs. 17.8 +/- 0.5 mM, P = 0.003), TAC (152.5 +/- 1.9 vs. 116.7 +/- 5.0 mM, P < 0.001), and GSH/GSSG ratio (0.43 +/- 0.01 vs. 0.08 +/- 0.01, P = 0.005). Nitrate also potentiated effects of hyperoxia on decreasing fasting glucose. Significance: Our results showed that dietary nitrate attenuates hyperoxia-induced oxidative stress in type 2 diabetic rats.
Revista:
MOLECULAR NUTRITION & FOOD RESEARCH (ONLINE)
ISSN:
1613-4133
Año:
2019
Vol.:
63
N°:
24
Págs.:
1 - 9
SCOPE: To study the effects of Maresin 1 (MaR1), a docosahexaenoic-acid-derived lipid mediator, on fibroblast growth factor 21 (FGF21) production and to characterize the tissue-specific regulation of Fgf21 and its signaling pathway in liver, skeletal muscle, and white adipose tissue (WAT).
METHODS AND RESULTS: Diet-induced obese (DIO) mice are treated with MaR1 (50g kg-1 , 10 days, oral gavage) and serum FGF21 levels and liver, muscle and WAT Fgf21, beta-Klotho, Fgfr1, Egr1, and cFos mRNA expression are evaluated. Additionally, MaR1 effects are tested in mouse primary hepatocytes, HepG2 human hepatocytes, C2C12 myotubes, and 3T3-L1 adipocytes. In DIO mice, MaR1 decreases circulating FGF21 levels and HFD-induced hepatic Fgf21 mRNA expression. MaR1 increases hepatic beta-Klotho, Egr1, and cFos in DIO mice. In WAT, MaR1 counteracts the HFD-induced downregulation of Fgf21, Fgfr1, and beta-Klotho. In muscle, MaR1 does not modify Fgf21 but promoted Fgfr1 expression. In mouse primary hepatocytes, MaR1 decreases Fgf21 expression and downregulated Pparalpha mRNA levels. In HepG2 cells, MaR1 reverses the increased production of FGF21 and the downregulation of FGFR1, Beta-KLOTHO, EGR1, and cFOS induced by palmitate. Preincubation with a PPARalpha antagonist prevents MaR1 effects on FGF21 secretion.
CONCLUSION: The ability of MaR1 to modulate FGF21 can contribute to its beneficial metabolic effects.
Revista:
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
ISSN:
1942-0900
Revista:
NUTRIENTS
ISSN:
2072-6643
Año:
2019
Vol.:
11
N°:
10
Págs.:
2411
Revista:
JOURNAL OF CELLULAR PHYSIOLOGY
ISSN:
0021-9541
Año:
2018
Vol.:
234
N°:
1
Págs.:
550 - 560
Obesity is a multifactorial, chronic, inflammatory disease that involves different processes, such as adipose tissue hypoxia. The aim of the current study was to characterize the effects of conditioned medium (CM) from lipopolysaccharide (LPS)-activated macrophages on the regulation of hypoxia-inducible factor 1 alpha (HIF-1 alpha)-related genes in murine adipocytes. For the in vitro analyses, 3T3-L1 murine adipocytes (9 days postdifferentiation) were incubated either in CM (25% medium of RAW 264.7 murine macrophages with 24hr 500ng/ml LPS), LPS at 500ng/ml, or hypoxia (Hx; 1% O-2, 94% N-2, 5% CO2) for 24hr. For the in vivo experiments, mice were fed a high-fat diet. Both epididymal white adipose tissue (eWAT) and adipocytes in CM showed upregulation of Glut1, Mcp1, Il10, Tnf, and Il1b. The secretion of IL-6, TNF-alpha, and MCP-1 was also increased in CM-treated adipocytes. Moreover, increased levels of HIF-1 alpha subunit and nuclear factor kappa B p65 were found after CM treatment, linking Hx, and inflammation. HIF-1 alpha directly bound vascular endothelial growth factor A (Vegfa) and uncoupling protein 2 (Ucp2) genes, up- and downregulating its expression, respectively. Furthermore, the oxygen consumption rate was 30% lower in CM. The siRNA knockdown of mammalian target of rapamycin (Mtor) reversed the induction of HIF-1 alpha found in CM. The macrophage infiltration simulated through CM seems to be a similar environment to an abnormally enlarged eWAT. We have evidenced that HIF-1 alpha plays a regulatory role in the expression of Vegfa and Ucp2 in CM. Finally, the inhibition of the mTOR pathway prevented the HIF-1 alpha activation induced by CM. The involvement of HIF-1 alpha under proinflammatory conditions provides insight into the origins of Hx in obesity.
Autores:
Lopez-Pascual, A.; Arévalo, J.; Martínez, JA; et al.
Revista:
FRONTIERS IN ENDOCRINOLOGY
ISSN:
1664-2392
Background: Metabolic syndrome (MetS) is characterized by the clustering of hyperglycemia, hypertension, hypertriglyceridemia, low high-density lipoprotein cholesterol levels and central adiposity. Altitude has been proposed as a protective factor to prevent the development of MetS and its components. Aim: To determine whether living at geographical elevation is associated with MetS and its individual components after adjustment for potential confounders in an Ecuadoran population. Methods: The study included 260 Ecuadoran university graduates over 20 years of age, from the coastal or the Andean Altiplano region. The altitude of residence was imputed with the postal code of each participant residence according to the data of the Ecuadoran Geophysical Institute of the National Polytechnic School. MetS was defined according to the harmonizing definition. Logistic regression models were fitted to assess the relationship between altitude level and the prevalence of MetS and its individual components. To test the internal validity, re-sampling techniques were used (1,000 bootstrap samples). Results: Living at high altitude was associated with less hypercholesterolemia (OR = 0.24; p < 0.001), hyperglycemia (OR = 0.25; p < 0.05) and MetS (OR = 0.24; p < 0.05), after adjusting for potential confounders. At high altitude the bootstrapped logistic regressionmodels showed lower prevalence of hypercholesterolemia (OR = 0.30; p < 0.05), hyperglycemia (OR = 0.22; p < 0.001) and MetS (OR = 0.28; p < 0.05). The MetS score (0-5 points) showed a reduction in the number of MetS components at high altitude compared to sea level (B = -0.34; p = 0.002). A statistically significant lower self-reported energy intake was found in high altitude compared to sea level after adjustment for potential confounders (p < 0.001). Conclusion: In the present study concerning a small Ecuadoran population composed of highly educated adults living at the coast and the Andean Altiplano, living at high altitude (2,758-2,787m) was associated with a lower prevalence of MetS, hypercholesterolemia and hyperglycemia, compared to the participants at sea level (4-6m). In addition, an inverse association between altitude and self-reported energy intake was found after adjusting for covariates, suggesting a physiological role of appetite at high altitude even in acclimated subjects.
Revista:
FRONTIERS IN PHYSIOLOGY
ISSN:
1664-042X
Año:
2017
Vol.:
7
Págs.:
658
Living in a geographically higher altitude affects oxygen availability. The possible connection between environmental factors and the development of metabolic syndrome (MetS) feature is not fully understood, being the available epidemiological evidence still very limited. The aim of the present study was to evaluate the longitudinal association between altitude and incidence of MetS and each of its components in a prospective Spanish cohort, The Seguimiento Universidad de Navarra (SUN) project. Our study included 6860 highly educated subjects (university graduates) free from any MetS criteria at baseline. The altitude of residence was imputed with the postal code of each individual subject residence according to the data of the Spanish National Cartographic Institute and participants were categorized into tertiles. MetS was defined according to the harmonized definition. Cox proportional hazards models were used to assess the association between the altitude of residence and the risk of MetS during follow-up. After a median follow-up period of 10 years, 462 incident cases of MetS were identified. When adjusting for potential confounders, subjects in the highest category of altitude (>456 m) exhibited a significantly lower risk of developing MetS compared to those in the lowest tertile (<122 m) of altitude of residence [Model 2: Hazard ratio = 0.75 (95% Confidence interval: 0.580.97); p for trend = 0.029]. Living at geographically higher altitude was associated with a lower risk of developing MetS in the SUN project. Our findings suggest that geographical elevation may be an important factor linked to metabolic diseases.
Autores:
Lopez-Pascual, A.; Lasa, A.; Portillo, M. P.; et al.
Revista:
ANNALS OF NUTRITION AND METABOLISM
ISSN:
0250-6807
Año:
2017
Vol.:
71
N°:
1-2
Págs.:
16 - 25
BACKGROUND:
Deoxyribonucleic acid (DNA) methylation is an epigenetic modification involved in gene expression regulation, usually via gene silencing, which contributes to the risks of many multifactorial diseases. The aim of the present study was to analyze the influence of resting oxygen consumption on global and gene DNA methylation as well as protein secretion of inflammatory markers in blood cells from obese subjects with sleep apnea-hypopnea syndrome (SAHS).
METHODS:
A total of 44 obese participants with SAHS were categorized in 2 groups according to their resting oxygen consumption. DNA methylation levels were evaluated using a methylation-sensitive high resolution melting approach.
RESULTS:
The analyzed interleukin 6 (IL6) gene cytosine phosphate guanine (CpG) islands showed a hypomethylation, while serum IL-6 was higher in the low compared to the high oxygen consumption group (p < 0.05). Moreover, an age-related loss of DNA methylation of tumor necrosis factor (B = -0.82, 95% CI -1.33 to -0.30) and long interspersed nucleotide element 1 (B = -0.46; 95% CI -0.87 to -0.04) gene CpGs were found. Finally, studied CpG methylation levels of serpin peptidase inhibitor, clade E member 1 (r = 0.43; p = 0.01), and IL6 (r = 0.41; p = 0.02) were positively associated with fat-free mass.
CONCLUSIONS:
These findings suggest a potential role of oxygen in the regulation of inflammatory genes. Oxygen consumption measurement at rest could be proposed as a clinical biomarker of metabolic health.
Revista:
FASEB JOURNAL
ISSN:
0892-6638
Año:
2017
Vol.:
31
N°:
5
Págs.:
2135 - 2145
The beneficial actions of n-3 fatty acids on obesity-induced insulin resistance and inflammation have been related to the synthesis of specializedproresolving lipid mediators (SPMs) like resolvins.The aimof this study was to evaluate the ability of one of these SPMs, maresin 1 (MaR1), to reverse adipose tissue inflammation and/or insulin resistance in twomodels of obesity: diet-induced obese (DIO)mice and genetic (ob/ob) obesemice. In DIO mice, MaR1 (2 mg/kg; 10 d) reduced F4/80-positive cells and expression of the proinflammatory M1 macrophage
phenotype marker Cd11c in white adipose tissue (WAT). Moreover, MaR1 decreased Mcp-1, Tnf-a, and Il-1b expression, upregulated adiponectin and Glut-4, and increasedAkt phosphorylation inWAT.MaR1 administration (2 mg/kg; 20 d) to ob/ob mice did not modify macrophage recruitment but increased the M2 macrophage markers Cd163 and Il-10.MaR1 reduced Mcp-1, Tnf-a, Il-1b, andDpp-4 and increased adiponectin gene expression inWAT. MaR1treatment also improved the insulin tolerance test of ob/ob mice and increased Akt andAMPKphosphorylation in WAT. These data suggest that treatment with MaR1 can counteract the dysfunctional inflamed WAT and could be useful to improve insulin sensitivity in murine models of obesity.
Revista:
NATURE REVIEWS DISEASE PRIMERS
ISSN:
2056-676X
Año:
2017
Vol.:
3
Págs.:
17034
Excessive fat deposition in obesity has a multifactorial aetiology, but is widely considered the result of disequilibrium between energy intake and expenditure. Despite specific public health policies and individual treatment efforts to combat the obesity epidemic, >2 billion people worldwide are overweight or obese. The central nervous system circuitry, fuel turnover and metabolism as well as adipose tissue homeostasis are important to comprehend excessive weight gain and associated comorbidities. Obesity has a profound impact on quality of life, even in seemingly healthy individuals. Diet, physical activity or exercise and lifestyle changes are the cornerstones of obesity treatment, but medical treatment and bariatric surgery are becoming important. Family history, food environment, cultural preferences, adverse reactions to food, perinatal nutrition, previous or current diseases and physical activity patterns are relevant aspects for the health care professional to consider when treating the individual with obesity. Clinicians and other health care professionals are often ill-equipped to address the important environmental and socioeconomic drivers of the current obesity epidemic. Finally, understanding the epigenetic and genetic factors as well as metabolic pathways that take advantage of 'omics' technologies could play a very relevant part in combating obesity within a precision approach.
Revista:
JOURNAL OF ENDOCRINOLOGY AND METABOLIC DISORDERS
ISSN:
2380-548X
Año:
2016
Vol.:
2
N°:
1
Págs.:
1 - 4
Abstract Obesity is now considered to be a global epidemic, impacting a great number of women and leading to a higher risk of obstetrical and gestational complications. One of such possible adverse outcomes in gestating female is placental hypoxia, which has been related to vascular remodeling and hypertension, as well as adaptive phenomena to reduce levels of oxidative stress and damage. A pool of female Sprague Dawley rats (n=63) was first assigned into two dietary groups (Control and High Sugar). Following mating, the pregnant rats (n=39) were again distributed into two oxygen treatment groups (Normoxia and Hypoxia) for 3 weeks, and tissue sampling and biochemical analyses were carried out. The main results of this study are the following: 1) Hypoxia during gestation may lead to a reduction in the average number of pups per mother, 2) Hypoxia during gestation treatment may lead to a decrease in maternal serum TG levels, and consequentially 3) Hypoxia during gestation may lead to a reduction in TyG Index levels. These results suggest that hypoxia could generate a beneficial response in pregnant Sprague Dawley rats to salvage both maternal and fetal viability. Thus, reproducing mild hypoxic conditions could result being a viable therapeutic option in preventing gestational adversities. In conclusion, progress was made in recognizing the possible role of a mild hypoxic environment in stimulating a maternal protective response.
Revista:
PLOS ONE
ISSN:
1932-6203
Año:
2016
Vol.:
11
N°:
11
Págs.:
e0164483
BACKGROUND:
Residence at high altitude has been associated with lower obesity rates probably due to hypoxia conditions. However, there is no evidence of this association in a free-living population.
OBJECTIVES:
We assessed the association between the altitude where each participant of a Spanish cohort (the SUN Project) was living and the incidence of overweight/obesity.
METHODS:
The SUN Project is a dynamic, prospective, multipurpose cohort of Spanish university graduates with a retention rate of 89%. We included in the analysis 9 365 participants free of overweight/obesity at baseline. At the baseline questionnaire, participants reported their postal code and the time they had been living in their city/village. We imputed the altitude of each postal code according to the data of the Spanish National Cartographic Institute and categorized participants in tertiles. We used Cox regression models to adjust for potential confounding variables.
RESULTS:
During a median follow-up of 10 years, we identified 2 156 incident cases of overweight/obesity. After adjusting for sex, age, time of residence at current city, baseline body mass index, physical activity, sedentarism and years of education (¿ 3 years, ¿ 4 years, Master/PhD), those participants in the third tertile (>456 m) exhibited a statistically significant 14% reduction in the risk of developing overweight/obesity in comparison to those in the first tertile (<124 m) (adjusted HR = 0.86; 95% CI: 0.77, 0.96).
CONCLUSIONS:
Living in cities of higher altitude was inversely associated with the risk of developing overweight/obesity in a cohort of Spanish university graduates.
Revista:
CURRENT NEUROVASCULAR RESEARCH
ISSN:
1567-2026
Año:
2015
Vol.:
12
N°:
4
Págs.:
321 - 333
Ischemic stroke patients often show high concentrations of circulating inflammatory markers that are associated with increased risk of recurrence. Epigenetic mechanisms could be involved in obesity, inflammation and stroke. The objective of this research was to investigate, in obese patients suffering a previous stroke, the effects of a nutritional program on anthropometric and biochemical variables, and on the methylation patterns of two stroke-related genes (KCNQ1: potassium channel, voltage gated KQT-like subfamily Q, member 1; and WT1: Wilms tumor 1). Twenty-two ischemic stroke patients were compared with a control group composed of eighteen obese subjects with similar age and body mass index ranges. Both groups followed a 20-week nutritional program based on an energy-restricted balanced diet with high adherence to the Mediterranean dietary pattern. The intervention significantly improved anthropometric and metabolic variables, such as the Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) and C-reactive protein concentration, in ischemic stroke patients, and was accompanied by changes in the methylation patterns of both stroke-related genes, which correlated with anthropometric and biochemical variables.
Revista:
SLEEP AND BREATHING
ISSN:
1520-9512
Año:
2015
Vol.:
19
N°:
1
Págs.:
7 - 8
Revista:
JOURNAL OF PHYSIOLOGY AND BIOCHEMISTRY
ISSN:
1138-7548
Año:
2015
Vol.:
71
N°:
3
Págs.:
589 - 599
Strategies designed to reduce adiposity and cardiovascular-accompanying manifestations have been based on nutritional interventions conjointly with physical activity programs. The aim of this 13-week study was to investigate the putative benefits associated to hypoxia plus exercise on weight loss and relevant metabolic and cardiorespiratory variables, when prescribed to obese subjects with sleep apnea syndrome following dietary advice. The participants were randomly distributed in the following three groups: control, normoxia, and hypoxia. All the subjects received dietary advice while, additionally, normoxia group was trained under normal oxygen concentration and Hypoxia group under hypoxic conditions. There was a statistically significant decrease in fat-free mass (Kg) and water (%) on the control compared to normoxia group (p¿<¿0.05 and p¿<¿0.01, respectively). Body weight, body mass index, and waist circumference decreased in all the groups after the study. Moreover, leukocyte count was increased after the intervention in hypoxia compared to control group (p¿<¿0.05). There were no statistically significant variations within groups in other variables, although changes in appetite were found after the 13-week period. In addition, associations between the variations in the leukocyte count and fat mass have been found. The hypoxia group showed some specific benefits concerning appetite and cardiometabolic-related measurements as exertion time and diastolic blood pressure, with a therapeutical potential.
Revista:
JOURNAL OF ANIMAL PHYSIOLOGY AND ANIMAL NUTRITION
ISSN:
0931-2439
Año:
2015
Vol.:
99
N°:
5
Págs.:
834 - 840
Maternal nutrition during pregnancy and lactation influences offspring development and health. Novel studies have described the effects on next generation obesity-related features depending on maternal macro- and micro-nutrient perinatal feeding. We hypothesized that the maternal obesogenic diet during pregnancy and lactation programs an obese phenotype, while maternal micronutrient supplementation at these stages could partially prevent these features. Thus, the aim was to assess the influence of a perinatal maternal feeding with an obesogenic diet enriched in fat and sucrose and a micronutrient supplementation during pregnancy and lactation on offspring growth and obese phenotypical features during life course. Female Wistar rats were assigned to four dietary groups during pregnancy and lactation: control, control supplemented with micronutrients (choline, betaine, folic acid and vitamin B12 ), high-fat sucrose (HFS) and HFS supplemented. At weaning, the offspring were transferred to a chow diet, and weight and fat mass were measured at weeks 3, 12 and 20. At birth, both male and female offspring from mothers fed the obesogenic diet showed lower body weight (-5 and -6%, respectively), while only female offspring weight decreased by maternal micronutrient supplementation (-5%). During lactation, maternal HFS diet was associated with increased body weight, while micronutrient supplementation protected against body weight gain. Whole body fat mass content increased at weeks 3, 12 and 20 (from 16 to 65%) due to maternal HFS diet. Maternal micronutrient supplementation decreased offspring fat mass content at week 3 (-8%). Male offspring showed higher adiposity than females at weeks 12 and 20. In conclusion, maternal HFS feeding during pregnancy and lactation was associated with a low offspring weight at birth and obese phenotypical features during adult life in a sex- and time-dependent manner. Furthermore, maternal methyl donor supplementation protected against body weight gain in male offspring during lactation and in female offspring also during juvenile period.
Revista:
BRITISH JOURNAL OF NUTRITION
ISSN:
0007-1145
Año:
2015
Vol.:
113
N°:
2
Págs.:
331 - 342
The present study analyses the gene expression profile of peripheral blood mononuclear cells (PBMC) from obese boys. The aims of the present study were to identify baseline differences between low responders (LR) and high responders (HR) after 10 weeks of a moderate energy-restricted dietary intervention, and to compare the gene expression profile between the baseline and the endpoint of the nutritional intervention. Spanish obese boys (age 10-14 years) were advised to follow a 10-week moderate energy-restricted diet. Participants were classified into two groups based on the association between the response to the nutritional intervention and the changes in BMI standard deviation score (BMI-SDS): HR group (n 6), who had a more decreased BMI-SDS; LR group (n 6), who either maintained or had an even increased BMI-SDS. The expression of 28 869 genes was analysed in PBMC from both groups at baseline and after the nutritional intervention, using the Affymetrix Human Gene 1.1 ST 24-Array plate microarray. At baseline, the HR group showed a lower expression of inflammation and immune response-related pathways, which suggests that the LR group could have a more developed pro-inflammatory phenotype. Concomitantly, LEPR and SIRPB1 genes were highly expressed in the LR group, indicating a tendency towards an impaired immune response and leptin resistance. Moreover, the moderate energy-restricted diet was able to down-regulate the inflammatory 'mitogen-activated protein kinase signalling pathway' in the HR group, as well as some inflammatory genes (AREG and TNFAIP3). The present study confirms that changes in the gene expression profile of PBMC in obese boys may help to understand the weight-loss response. However, further research is required to confirm these findings.
Revista:
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
ISSN:
1422-0067
Año:
2013
Vol.:
14
N°:
9
Págs.:
17238 - 17255
The current nutritional habits and lifestyles of modern societies favor energy overloads and a diminished physical activity, which may produce serious clinical disturbances and excessive weight gain. In order to investigate the mechanisms by which the environmental factors interact with molecular mechanisms in obesity, a pathway analysis was performed to identify genes differentially expressed in subcutaneous abdominal adipose tissue (SCAAT) from obese compared to lean male (21-35 year-old) subjects living in similar obesogenic conditions: habitual high fat dietary intake and moderate physical activity. Genes involved in inflammation (ALCAM, CTSB, C1S, YKL-40, MIF, SAA2), extracellular matrix remodeling (MMP9, PALLD), angiogenesis (EGFL6, leptin) and oxidative stress (AKR1C3, UCHL1, HSPB7 and NQO1) were upregulated; whereas apoptosis, signal transcription (CITED 2 and NR3C1), cell control and cell cycle-related genes were downregulated. Interestingly, the expression of some of these genes (C1S, SAA2, ALCAM, CTSB, YKL-40 and tenomodulin) was found to be associated with some relevant metabolic syndrome features. The obese group showed a general upregulation in the expression of inflammatory, oxidative stress, extracellular remodeling and angiogenic genes compared to lean subjects, suggesting that a given genetic background in an obesogenic environment could underlie the resistance to gaining weight and obesity-associated manifestations.
Revista:
JOURNAL OF PHYSIOLOGY AND BIOCHEMISTRY
ISSN:
1138-7548
Año:
2012
Vol.:
68
N°:
4
Págs.:
663-669
Adipose tissue often becomes poorly oxygenated in obese subjects. This feature may provide cellular mechanisms involving chronic inflammation processes such as the release of pro-inflammatory cytokines and macrophage infiltration. In this context, the purpose of the present study was to determine whether a hyperoxia exposure on mature adipocytes may influence the expression of some adipokines and involve favorable changes in specific metabolic variables. Thus, 3T3-L1 adipocytes (14 days differentiated) were treated with 95 % oxygen for 24 h. Cell viability, intra and extracellular reactive oxygen species (ROS) content, glucose uptake, as well as lactate and glycerol concentrations were measured in the culture media. Also, mRNA levels of hypoxia-inducible factor (HIF)-1 alpha, leptin, interleukin (IL)-6, monocyte chemotactic protein (MCP)-1, peroxisome proliferator-activated receptor (PPAR)-gamma, adiponectin, and angiopoietin-related protein (ANGPTL)4 were analyzed. Hyperoxia treatment increased intra and extracellular ROS content, reduced glucose uptake and lactate release and increased glycerol release. Additionally, a higher oxygen tension led to an upregulation of the expression of IL-6, MCP-1, and PPAR-gamma, while ANGPTL4 was downregulated in the hyperoxia group with respect to control. The present data shows that hyperoxia treatment seems to produce an inflammatory response due to the release of ROS and the upregulation of pro-inflammatory adipokines, such as IL-6 and MCP-1. On the other hand, hyperoxia may have an indirect effect on insulin sensitivity due to the upregulation of PPAR-gamma signaling as well as a possible modulation of both glucose and lipid metabolic markers. To our knowledge, this is the first study analyzing the effect of hyperoxia in 3T3-L1 adipocytes.
Revista:
JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS
ISSN:
0393-974X
Año:
2012
Vol.:
26
N°:
3
Págs.:
379 - 388
Obese subjects often present a low-grade chronic inflammation in the white adipose tissue, which seems to play an important role in the initiation and development of obesity-related diseases. It has been reported that this inflammatory process may be due to a hypoxic state occuring within this tissue. Oxygen is used in current medicine as a treatment for several conditions. The aim of this study is to analyze the effects of 95% O-2 on specific metabolic variables and on the expression of some genes on murine adipocytes. 3T3-L1 adipocytes were exposed during 48 h to different treatments: 95% O-2 hyperoxia (HPx group), CoCl2 (CoCl2 group), hyperoxia with CoCl2 (HPx+CoCl2 group) and 1% O-2 hypoxia (Hx group). Cell viability, intracellular ROS content, glucose utilization, lactate and glycerol concentrations were measured. Also, mRNA expression of HIF-1 alpha, GLUT-1, ANGPTL4, PPAR-gamma, adiponectin, IL-6 and MCP-1 genes was analyzed. Importantly, 95% O-2 decreased cell viability and increased intracellular ROS production. Also, glycerol and lactate release were significantly increased and decreased, respectively, in HPx treated cells. This treatment also provoked a down-regulation of GLUT-1 and ANGPTL-4, while IL-6 and MCP-1 were up-regulated. Exposure to a hyperoxia of 95% 02 provoked an inflammatory response in adipocytes. The two hypoxia-inducing conditions (CoCl2 and 1% O-2) produced different outcomes in metabolic measurements as well as in the expression of some genes (GLUT-1, ANPGTL4, PPAR-gamma and adiponectin), while it remained similar in others (HIF-1 alpha, IL-6 and MCP-1). Indeed, hyperoxia increased significantly the ROS levels and the lipolytic activity, while it reduced lactate production. In addition to the effects on inflammation, the changes in GLUT-1, ANGPTL4 and PPAR-gamma genes lead to suppose that hyperoxia may be beneficial for the hypertrophied adipose tissues of obese subjects and for improving insulin sensitivity.
Revista:
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
ISSN:
0955-2863
Año:
2012
Vol.:
23
N°:
12
Págs.:
1676 - 1684
Revista:
OBESITY
ISSN:
1930-7381
Año:
2012
Vol.:
20
N°:
10
Págs.:
1974 - 1983
Nonalcoholic steatosis is an important hepatic complication of obesity linked to mitochondrial dysfunction and oxidative stress. Lipoic acid (LA) has been reported to have beneficial effects on mitochondrial function and to attenuate oxidative stress. The sirtuin (SIRT) family has been demonstrated to play an important role in the regulation of mitochondrial function and in the activation of antioxidant defenses. In this study, we analyzed the potential protective effect of LA supplementation, via the modulation of mitochondrial defenses through the SIRT pathway, against oxidative stress associated with high-fat feeding. Wistar rats were fed a standard diet (control group (C), n = 10), a high-fat diet (obese group (OB), n = 10) and a high-fat diet supplemented with LA (OLIP, n = 10). A group pair-fed to the latter group (pair-fed OLIP group (PFO), n = 6) was also included. LA prevented hepatic triglyceride (TG) accumulation (-68.2%) and liver oxidative damage (P < 0.01) through the inhibition of hydroperoxide (H2O2) production (P < 0.001) and the stimulation of mitochondrial antioxidant defenses. LA treatment upregulated manganese superoxide dismutase (SOD2) (60.6%) and glutathione peroxidase (GPx) (100.2%) activities, and increased the reduced glutathione (GSH): oxidized glutathione (GSSG) ratio and UCP2 mRNA levels (P < 0.001-P < 0.01). Moreover, this molecule reduced oxidative damage in mitochondrial DNA (mtDNA) and increased mitochondrial copy number (P < 0.001-P < 0.01). LA treatment decreased the acetylation levels of Forkhead transcription factor 3a (Foxo3a) and PGC1 beta (P < 0.001-P < 0.01) through the stimulation of SIRT3 and SIRT1 (P < 0.001). In summary, our results demonstrate that the beneficial effects of LA supplementation on hepatic steatosis could be mediated by its ability to restore the oxidative balance by increasing antioxidant defenses through the deacetylation of Foxo3a and PGC1 beta by SIRT1 and SIRT3.
Revista:
Current Nutrition & Food Science
ISSN:
1573-4013
Año:
2012
Vol.:
8
N°:
1
Págs.:
25 - 44
The metabolic syndrome is one of the most evident health concerns worldwide. It is characterized by several metabolic abnormalities, which include obesity, dyslipidemia, insulin resistance, increased oxidative stress, an increased pro-inflammatory state and hypertension. Nowadays, functional foods are used in the prevention and amelioration of several chronic diseases, such as the metabolic syndrome. The relation of the consumption of certain functional foods and the improvement in health status is regulated through health claims. This review focuses on the different features of the metabolic syndrome and the influence of functional foods on these aspects, involving weight management, improvement of insulin sensitivity, serum lipid profile, anti-oxidant status, inflammatory status and hypertension. The role of plant sterols, dietary fiber, soy protein, omega-3 fatty acids, coffee, vitamin E and C, isoflavones, lycopene, sodium-low foods, a high protein diet, mono-unsaturated fatty acids, minerals and thermogenic compounds is examined concerning their functional properties
Revista:
JOURNAL OF NUTRIGENETICS AND NUTRIGENOMICS
ISSN:
1661-6499
Año:
2011
Vol.:
4
N°:
3
Págs.:
146 - 153
Background/Aims: Hypoxia occurs in white adipose tissue in obesity, modulating the expression and release of specific inflammation-related adipokines. ANGPTL4 (angiopoietin-like protein 4/fasting-induced adipose factor), which is implicated in angiogenesis, lipid metabolism and glucose homeostasis, is a major hypoxia-sensitive gene; recent studies indicate that ANGPTL4 expression is also regulated by fatty acids. We have examined the effects of hypoxia and fatty acids, alone and together, on the expression and release of ANGPTL4 by human adipocytes. Methods: Human adipocytes were differentiated and incubated with fatty acids (250 mu M) in normoxia (21% O(2)) or hypoxia (1% O(2)). ANGPTL4 mRNA was measured by real-time PCR and the protein in the medium determined by ELISA. Results: In normoxia, ANGPTL4 gene expression was upregulated by palmitic, oleic, arachidonic and eicosapentaenoic acids, and ANGPTL4 release was increased. In contrast, there was no effect of lauric or myristic acids. Hypoxia alone increased the expression and secretion of ANGPTL4, and lauric, myristic, arachidonic and eicosapentaenoic acids each further increased expression and release in hypoxic adipocytes. Conclusion: The expression and secretion of ANGPTL4 by human adipocytes is upregulated by both hypoxia and fatty acids. The stimulatory effect of fatty acids on ANGPTL4 production is augmented under hypoxic conditions.
Revista:
JOURNAL OF PHYSIOLOGY AND BIOCHEMISTRY
ISSN:
1138-7548
Año:
2011
Vol.:
67
N°:
1
Págs.:
15 - 26
There are major variations in the susceptibility to weight gain among individuals under similar external influences (decreased physical activity and excessive calorie intake), depending on the genetic background. In the present study, we performed a microarray analysis and real-time PCR validations in order to find out differential gene expression in subcutaneous abdominal adipose tissue from two groups of subjects that despite living in similar environmental conditions such as a habitual high-fat dietary intake (energy as fat >40%) and similar moderate physical activity, some of them were successfully "resistant" (lean) to weight gain, while others were "susceptible" to fat deposition (obese). The classification of up- and downregulated genes into different categories, together with the analysis of the altered biochemical pathways, revealed a coordinated downregulation of catabolic pathways operating in the mitochondria: fatty acid ß oxidation (P¿=¿0.008), tricarboxylic acid cycle (P¿=¿0.001), and electron transport chain (P¿=¿0.012). At the same time, glucose metabolism (P¿=¿0.010) and fatty acid biosynthesis (P¿=¿0.011) pathways were also downregulated in obese compared to lean subjects. In conclusion, our data showed an orchestrated downregulation of nuclear-encoded mitochondrial gene expression. These genes are involved in cellular respiration and oxidative metabolic pathways and could play a role in the susceptibility to weight gain in some individuals.
Revista:
Physiology & Behavior
ISSN:
0031-9384
Año:
2011
Vol.:
103
N°:
2
Págs.:
173 - 180
Revista:
OBESITY FACTS
ISSN:
1662-4025
Año:
2010
Vol.:
3
N°:
5
Págs.:
312 - 318
Objective: The aim of the present study was to investigate the relationship between the differential expression of genes related to lipid metabolism in subcutaneous adipose tissue and metabolic syndrome features in lean and obese subjects with habitual high fat intake. Methods: Microarray and RT-PCR analysis were used to analyze and validate differential gene expression in subcutaneous abdominal adipose tissue samples from lean and obese phenotype subjects. Results: Several genes and transcripts involved in lipolysis were down-regulated, such as AKAP1, PRKAR2B, Gi and CIDEA, whereas NPY1R and CES1 were up-regulated, when comparing obese to lean subjects. Similarly, transcripts associated with cholesterol and lipoprotein metabolism showed a differential expression, with APOE and ABCA being decreased and VLDLR being increased in obese versus lean subjects. In addition, positive correlations were found between different markers of the metabolic syndrome and CES1 and NPY1R mRNA expressions, while APOE showed an inverse association with some of them. Conclusion: Different expression patterns in transcripts encoding for proteins involved in lipolysis and lipoprotein metabolism were found between lean and obese subjects. Moreover, the dysregulation of genes such as CES1 and APOE seems to be associated with some physiopathological markers of insulin resistance and cardiovascular risk factors in obesity.
Revista:
Nutricion Clinica-dietetica hospitalaria
ISSN:
0211-6057
Año:
2010
Vol.:
30
N°:
3
Págs.:
27 - 41
Revista:
HORMONE AND METABOLIC RESEARCH
ISSN:
0018-5043
Año:
2010
Vol.:
42
N°:
10
Págs.:
710 - 717
Inflammation in adipose tissue is a characteristic of obesity and the metabolic syndrome. It is suggested that the endocannabinoid system is involved in the regulation of inflammatory and angiogenic processes within the tissue. Human subcutaneous preadipocytes (Zen Bio) were used as the source of human preadipocytes or adipocytes. Gene expression was examined by RT-PCR and real-time PCR. The secretion of inflammation-related proteins was determined by an ELISA array. In experiments on adipocytes treated at day 14 post-differentiation, JTE-907, a synthetic cannabinoid, upregulated the expression of key inflammatory markers - IL-6, MCP-1 and IL-1 beta - and angiogenic factors - VEGF and ANGPTL4 - at 10 microM after 20 h of treatment, having also increased the expression of TRPV1 at 10 microM. JTE-907 showed no effect after 4 h. The ELISA array showed a 2.6-fold increase in IL-6 protein release. The effect of JTE-907 was inhibited by AM251 (CB1 antagonist), and partially by arachidonyl serotonin (TRPV1 and FAAH antagonist). The CB2 antagonist, AM630, partially upregulated the effect of JTE-907. Preadipocytes fed 14 days after 100% confluence exhibited downregulation of CB1, MCP-1, and IL-1 beta, 20 h after having been exposed to JTE-907. CB1 and TRPV1 receptors participate in the regulation of several inflammatory and angiogenic factors in human adipocytes, indicating their potential value as targets for the treatment of disorders related to obesity.
