The influence of aging on the kinetic response to glucose ingestion and the mechanisms underlying age-related glucose intolerance are described. Despite delayed absorption of the ingested glucose load, impaired glucose tolerance develops with age. This impairment is multifactorial, being characterized by delays in glucose-induced insulin secretion, insulin-induced suppression of hepatic glucose output, and a rise in insulin-mediated glucose uptake. The major disturbance appears to be impaired insulin-mediated glucose uptake, with skeletal muscle the principal site of this defect. Because insulin receptors are unchanged with age, the impairment in insulin action is primarily due to a postreceptor defect. Possible mechanisms associated with the age-related impairment in glucose uptake by muscle include 1) decreased muscle mass, 2) increasing obesity, 3) decreased physical activity, 4) poor diet, and 5) increased plasma free-fatty acid levels. However, evidence from recent research suggests that none of these factors plays a significant role in this regard. The principal postreceptor defect in insulin action may comprise a decreased maximum velocity of glucose transport due to a decreased number of glucose transporters, although each transporter functions normally. Conceivably, the transport defect may be due to a depletion of the intracellular pool of transporters, which may ultimately reflect insulin resistance at the level of glucose-transporter mRNA and/or defective insulin internalization and intracellular metabolism. However, an age-related impairment in intracellular glucose metabolism may be present in addition to any changes in the glucose-transport system. The phenomenon of age-related glucose intolerance is the result of defects specific for the aging process and distinct and separate from those characterizing obesity and non-insulin-dependent diabetes; their distinguishing features are discussed.
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