Glucose tolerance in the elderly: the role of insulin and its receptor

McConnell, J. G.; Buchanan, K. D.; Ardill, Joy; Stout, R. W.

doi:10.1111/j.1365-2362.1982.tb00939.x

Cited by 12 publications

(4 citation statements)

References 27 publications

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“…96 For nondiabetic individuals, progressive impairment of glucose tolerance occurs with advancing age, independent of obesity and sex. 83 A previous investigation 97 comparing the response of older (those in their 80s) with that of younger (those in their 20s) individuals to oral glucose tolerance tests reported a 45% rate of impaired tolerance in older individuals. The pathogenesis of this age-related decline in glucose handling seems to result from increased insulin resistance rather than an impairment of insulin secretion.…”

Section: Alterations In Endocrine Immune and Stress Responsesmentioning

confidence: 99%

Physiological Features of Aging Persons

Aalami

Fang²,

Song³

et al. 2003

Arch Surg

108

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Section: Alterations In Endocrine Immune and Stress Responsesmentioning

confidence: 99%

Physiological Features of Aging Persons

Aalami

Fang²,

Song³

et al. 2003

Arch Surg

108

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“…Glucose transport, insulin action, and insulin metabolism. Most workers have found that insulin-receptor binding is unchanged with age (4,8,11,(83)(84)(85), although in some studies, insulin binding decreased (9,69) or even increased (86) with age. These data suggest that the defect in age-related glucose metabolism is postreceptor, but there is not complete agreement regarding the site(s) of this defect, which may differ in different target tissues.…”

Section: Insulin Antagonismmentioning

confidence: 99%

Mechanisms of Age-Related Glucose Intolerance

Jackson

1990

Diabetes Care

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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, insulininduced 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 Glucagon 1 ng/L = 1 pg/ml Glucose 1 mM = 18 mg/dl Insulin 1 pM = 0.167 jiU/ml From the

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“…For instance, a reduction in glucose tolerance when one gets older has been demonstrated in several studies 3–4 . Similarly, the effect of aging on plasma insulin response to loads of glucose has been studied with somewhat conflicting reports 5–10 . In addition, during hyperinsulinemic euglycemic clamps, with glycemia maintained at basal level during a constant insulin infusion by adapting the rate of the glucose infusion, 9 it has been shown that the amount of glucose metabolized was significantly decreased in elderly individuals.…”

mentioning

confidence: 99%

Decreased Thermogenic Response to an Oral Glucose Load in Older Subjects

Golay

Schütz

Broquet

et al. 1983

J American Geriatrics Society

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The thermogenic response to a 100 g oral glucose load was studied by indirect calorimetry in 13 older persons (age range, 38-68 years) and compared with that of 16 young matched controls of similar body weight (age range, 19-30 years). The glucose-induced thermogenesis measured over 180 min and expressed as a per cent of the energy content of the glucose load was found to be reduced in the older subjects, i.e., 5.8 +/- 0.3 per cent vs 8.6 +/- 0.7 per cent, P less than 0.002). This was also accompanied by a significant decrease in the glucose oxidation rate when averaged over the same three-hour period following the glucose load, i.e., 153 mg/min vs 213 mg/min in the control subjects (P less than 0.001) despite a similar time course of glycemia. This study suggests that the thermogenic response to an oral glucose load is blunted in older people, and this may represent an additional factor that contributes to the decreased energy requirement with age and therefore to the increased propensity to obesity if energy intake is not adjusted.

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Glucose tolerance in the elderly: the role of insulin and its receptor

Cited by 12 publications

References 27 publications

Physiological Features of Aging Persons

Physiological Features of Aging Persons

Mechanisms of Age-Related Glucose Intolerance

Decreased Thermogenic Response to an Oral Glucose Load in Older Subjects

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