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[Aging and endocrine pancreas (author's transl)].
Nihon Naibunpi Gakkai Zasshi
|December 20, 1977
Summary
Diabetes is not accelerated aging. Elderly individuals show abnormal glucose tolerance due to factors other than diabetes mellitus, as insulin secretion and other markers remain normal.
Area of Science:
- Gerontology
- Endocrinology
- Metabolic Diseases
Background:
- Diabetes mellitus is a common metabolic disease.
- Aging is associated with various physiological changes and increased disease risk.
- The relationship between aging and diabetes mellitus, specifically whether diabetes represents accelerated aging, requires further investigation.
Purpose of the Study:
- To investigate the hypothesis that diabetes mellitus is a form of accelerated aging.
- To compare the incidence and characteristics of diabetes in elderly populations with aging-related changes.
- To elucidate the underlying mechanisms of impaired glucose tolerance in the elderly.
Main Methods:
- Analysis of diabetes mellitus incidence rates across different age groups.
- Oral glucose tolerance tests (OGTT) in elderly subjects (60-89 years).
- Assessment of insulin and glucagon secretion in response to glucose load.
- Measurement of serum beta-N-acetylhexosaminidase activity.
- Evaluation of liver enzyme activities in aged rats.
- Examination of insulin secretion in Werner's syndrome patients.
Main Results:
- Diabetes mellitus incidence peaks around age 50 and declines thereafter, unlike age-dependent diseases like arteriosclerosis.
- Elderly subjects exhibited high rates of abnormal glucose tolerance (21% diabetic, 53% borderline) during OGTT.
- Insulin and glucagon secretory capacities in the elderly were comparable to younger age groups, indicating impaired glucose tolerance is not due to deficient insulin secretion.
- Serum beta-N-acetylhexosaminidase activity was not elevated in the elderly, contrasting with diabetics.
- Liver glycolytic and gluconeogenic enzyme activities were reduced in aged rats.
- Werner's syndrome, a model for aging, showed no specific abnormalities in insulin secretion.
Conclusions:
- The findings do not support the hypothesis that diabetes mellitus is a form of accelerated aging.
- Impaired glucose tolerance in the elderly likely stems from pathogenesis distinct from typical diabetes mellitus.
- Further research is needed to identify the specific mechanisms driving glucose intolerance in aging populations.