| Objective: Type 2 diabetes (T2DM) is a major public health problem. Recently, with the improvement of living standard level, people suffered from T2DM are increasing. The pathogenesis of T2DM is not completely clear. Exploring the etiology of T2DM is fundamental for prevention and treatment of the disease. Both environmental and genetic factors play roles in development of T2DM, environmental factors (dietary regimen, aging) may play the major part. Epidemiological studies show glucose tolerance progressively declines with increasing of age, and there is a higher prevalence of T2DM in the older population. However, the mechanism for such a trend is not fully understood. In addition, enough evidence implicates insulin secretory defects in T2DM patients and nondiabetic elders. All these suggest the relationship between T2DM and organismic aging. Aging is a cellular as well as an organismic phenomenon. Hence, we propose a hypothesis that pancreatic beta cell senescence may be involved in development of T2DM. We observed the influence of aging or caloric restriction (CR) on pancreatic beta cell senescence and its insulin secretion.Methods: (1)18-month-old SD rats received caloric restriction (60% of regular intake) for 6months. (2)SD rats were divided into five groups (n=10×5):Neonatal, 1-month-old,6-month-old, 24-month-old, calorie-restricted group. They were killed andpancreas was examined. (3)The expression of insulin and cell senescence molecular marker p16 inpancreatic islets was examined by immunohistochemical stain. (4)The expression of senescence-associated-beta-galactosidase (SA- β -gal), a...
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