The Effects of Aging on Glucose Metabolism in Adipocytes from Fischer Rats*

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Abstract
We have studied glucose metabolism in adipocytes from younger (6 months) and older (24 months) Fischer rats. Insulin binding was similar in both groups, expressed per cell number (2.67 .+-. 0.41% vs. 2.96 .+-. 0.38%) or per cell surface area (4.59 .+-. 0.70% vs. 4.15 .+-. 0.53%) in the 6- and 24-month-old animals, respectively. Maximal insulin-stimulated 3-O-methylglucose transport was decreased by 40% in the older group (0.234 .+-. 0.032) compared with that in the younger group (0.411 .+-. 0.031 pmol/2 .times. 109 .mu.m2 .cntdot. sec (P < 0.01), with no change in basal rates of transport. The decrease in glucose transport was due to a 36% reduction in the maximum velocity (91 pmol/sec in the younger vs. 59 pmol/sec in the older group), with no change in the Km. Postglucose transport steps of glucose metabolism, including CO2 oxidation, triglyceride synthesis, and lactate production, were measured at a higher glucose concentration (2 mM), where glucose transport is not rate limiting. Overall maximal insulin-stimulated glucose metabolism was decreased by 45% in the older group (15.6 nmol) compared with that in the younger group (28.6 nmol/105 cells .cntdot. h; P < 0.05). Glucose oxidation was decreased by 42% (2.9 vs. 5.0 nmol/105 cells .cntdot. h; P < 0.05), triglyceride synthesis by 40% (5.9 vs. 9.8 nmol/105 cells .cntdot. h; P < 0.05), and lactate production by 47% (6.3 vs. 11.8 nmol/105 cells .cntdot. h; P < 0.05). We conclude that in adipocytes from aged Fischer rats, cellular insulin resistance is due to multiple post-binding defects involving the glucose transport system and more distal intracellular processes.