Diet, not aging, causes skeletal muscle insulin resistance

The purpose of this study was to compare the effects of raising female Fischer rats on a low-fat, high-complex-carbohydrate diet (LFCC) versus a high-fat, sucrose diet (HFS) on serum glucose and insulin as well as skeletal muscle glucose transport. No significant differences were observed between 6- and 24-month-old rats raised on the LFCC diet for serum glucose (3.6 +/- 0.1 vs. 3.7 +/- 0.2 mM) and insulin (88 +/- 6 vs. 98 +/- 10 pM) or for basal (35 +/- 3 vs. 39 +/- 6 pmol/mg protein/15 s) or insulin-stimulated (74.2 +/- 7.6 vs. 69.4 +/- 3.8 pmol/mg protein/15 s) glucose transport. These data indicate that aging per se does not lead to insulin resistance. When the 24-month-old animals raised on the HFS diet were compared with those on the LFCC diet, major differences were observed. Fasting serum insulin was significantly higher in the HFS group (437 +/- 118 vs. 98 +/- 10 pM) and insulin-stimulated glucose transport was significantly reduced (52.5 +/- 3.7 vs. 69.4 +/- 3.8 pmol/mg protein/15 s). Fasting glucose (3.7 +/- 0.2 vs. 3.6 +/- 0.1 mM) and basal glucose transport (38 +/- 6 vs. 39 +/- 6 pmol/mg protein/15 s) were unchanged. These results indicate that diet and not aging per se caused insulin resistance.