ARTÍCULO

Effect of aging and obesity on GLUT12 expression in small intestine, adipose tissue, muscle, and kidney and its regulation by docosahexaenoic acid and exercise in mice

Autores: Gil Iturbe, Eva; Félix Soriano, Elisa; Sáinz Amillo, Neira; Idoate Bayón, Adrián; Castilla Madrigal, Rosa María; Moreno Aliaga, María Jesús; Lostao Crespo, María del Pilar (Autor de correspondencia)
Título de la revista: APPLIED PHYSIOLOGY NUTRITION AND METABOLISM- PHYSIOLOGIE APPLIQUEE NUTRITION ET METABOLISME
ISSN: 1715-5312
Volumen: 45
Número: 9
Páginas: 957 - 967
Fecha de publicación: 2020
Resumen:
Obesity is characterized by excessive fat accumulation and inflammation. Aging has also been characterized as an inflammatory condition, frequently accompanied by accumulation of visceral fat. Beneficial effects of exercise and 11-3 long-chain polyunsaturated fatty acids in metabolic disorders have been described. Glucose transporter 12 (GLUT12) is one of the less investigated members of the GLUT family. Glucose, insulin, and tumor necrosis factor alpha (TNF-alpha) induce GLUT12 translocation to the membrane in muscle, adipose tissue, and intestine. We aimed to investigate GLUT12 expression in obesity and aging, and under diet supplementation with docosahexaenoic acid (DHA) alone or in combination with physical exercise in mice. Aging increased GLUT12 expression in intestine, kidney, and adipose tissue, whereas obesity reduced it. No changes on the transporter occurred in skeletal muscle. In obese 18-month-old mice, DHA further decreased GLUT12 in the 4 organs. Aerobic exercise alone did not modify GLUT12, but the changes triggered by exercise were able to prevent the DHA-diminishing effect, and almost restored GLUT12 basal levels. In conclusion, the downregulation of metabolism in aging would be a stimulus to upregulate GLUT12 expression. Contrary, obesity, an excessive energy condition, would induce GLUT12 downregulation. The combination of exercise and DHA would contribute to restore basal function of GLUT12.