Changes Induced by Aging and Long-Term Exercise and/or DHA Supplementation in Muscle of Obese Female Mice

Nutrients. 2022 Oct 12;14(20):4240. doi: 10.3390/nu14204240.

Abstract

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-α 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-α 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.

Keywords: DHA; aging; exercise; inflammaging; inflammation; muscle; myokines.

MeSH terms

  • Aging
  • Animals
  • Diet, High-Fat
  • Dietary Supplements
  • Docosahexaenoic Acids* / pharmacology
  • Fatty Acids, Omega-3* / pharmacology
  • Female
  • Glucose / metabolism
  • Glucose Transporter Type 1
  • Inflammation
  • Interleukin-6 / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Mice, Obese
  • Muscles / metabolism
  • Obesity / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Docosahexaenoic Acids
  • Glucose Transporter Type 1
  • Tumor Necrosis Factor-alpha
  • Interleukin-6
  • Proto-Oncogene Proteins c-akt
  • Fatty Acids, Omega-3
  • Glucose
  • RNA, Messenger
  • FNDC5 protein, mouse