Abstract
Exercise and physical activity improve the glycemic control in people with type 2 diabetes (T2D). It is known that activity improves muscle utilization of glucose, and that exercise can spare islets if initiated prior to the onset of diabetes. However, any effect of exercise on pancreatic islet function after the diagnosis of overt diabetes is unknown. The aim of the study was to investigate the effects of exercise training on pancreatic islets in a rodent model of overt T2D. 12-week old male Zucker Diabetic Fatty (ZDF) rats and control lean rats were divided into 4 groups: sedentary control exercised control, sedentary diabetic and exercised diabetic. Exercised rats were trained with moderate intensity running on a treadmill for 7 weeks. Assessment of plasma insulin levels, islet cell composition (relative proportion of α, β and δ cells), islet density, insulin content and islet core diameter was conducted at the end of the study. Diabetes in ZDF rats lead to high HbA1c and BGLs, which was not reversed by exercise. Diabetes caused destruction of the islet structure and significant loss of β-cells, with an increased proportion of α- and δ-cells. Exercise improved islets morphology in the diabetic group, while islet density and islet cell composition were not affected by exercise. Increased insulin immunostaining of the pancreatic islets was identified in the diabetic animals after exercise. Although exercise did not affect the diabetes-induced decrease in the proportion of islet β cells, there appeared to be an improvement in the islet architecture and in β-cell insulin content.
Highlights
Diabetes affects more than 300 million people in the world [1]
The non-diabetic animals gained a greater percentage of their weight during the 7 week study, still the sedentary diabetic rats weighed more than the control animals at the termination of the study (p
Exercise maintained a higher level of intact islets in diabetic rats compared to the sedentary diabetic rats (p < 0.001).The results suggest that exercise helps the diabetic pancreatic islets maintain more of their normal morphology
Summary
Diabetes affects more than 300 million people in the world [1]. The recent staggering increase in the number of people with type 2 diabetes (T2D) can be attributed partially to changing lifestyle. Insulin is at the heart of metabolic control, and when the insulin secretion or utilization pathways are impaired, diabetes ensues. A loss of insulin production and secretion by the pancreatic β-cells is typically associated with type 1 diabetes, while ineffective action of insulin at the peripheral tissue, such as skeletal muscle is associated with T2D [3]. Research has confirmed that people with T2D have reduced islet numbers along with β-cell reductions, and inadequate insulin secretion [6,7]
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