Effect of Exercise on Pancreatic Islets in Zucker Diabetic Fatty Rats (original) (raw)
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Biochemical and Biophysical Research Communications, 2013
We evaluated the effect of chronic exercise on insulin secretion in response to high-glucose by using a perifusion method with isolated pancreatic islets from normal rats. Male Wistar rats were assigned to one of two groups: a sedentary group and a trained group. Running exercise was carried out on a treadmill for one hour per day, five days per week, for six, nine, or 12 weeks. The chronic exercise significantly enhanced the insulin secretion ability of pancreatic islets in response to the high-glucose stimulation upon nine and 12 weeks of exercise. The insulin content in the pancreas and the weight of the pancreas did not change upon nine weeks of exercise. Potassium-stimulated insulin secretion was also increased in the islets isolated from rats that trained for nine weeks compared with that in sedentary rats, suggesting that insulin secretion events downstream of membrane depolarization are involved in targets of the exercise effect. These findings suggest that chronic exercise could be a useful strategy not only for the maintenance of peripheral insulin sensitivity but also for the promotion of islet function to secrete insulin in non-diabetics.
American Journal of Physiology-Endocrinology and Metabolism, 2011
Physical activity improves glycemic control in type 2 diabetes (T2D), but its contribution to preserving β-cell function is uncertain. We evaluated the role of physical activity on β-cell secretory function and glycerolipid/fatty acid (GL/FA) cycling in male Zucker diabetic fatty (ZDF) rats. Six-week-old ZDF rats engaged in voluntary running for 6 wk (ZDF-A). Inactive Zucker lean and ZDF (ZDF-I) rats served as controls. ZDF-I rats displayed progressive hyperglycemia with β-cell failure evidenced by falling insulinemia and reduced insulin secretion to oral glucose. Isolated ZDF-I rat islets showed reduced glucose-stimulated insulin secretion expressed per islet and per islet protein. They were also characterized by loss of the glucose regulation of fatty acid oxidation and GL/FA cycling, reduced mRNA expression of key β-cell genes, and severe reduction of insulin stores. Physical activity prevented diabetes in ZDF rats through sustaining β-cell compensation to insulin resistance show...
Islets, 2016
The function and morphology of b-cells is largely dependent on insulin demand. As b-cells cover a bigger cell proportion in pancreas islets, changes of insulin producer cells affect the whole pancreatic islet morphology. Growth factors as the neurotrophins regulate the pancreas physiology, besides; physical exercise increases insulin sensitivity, and further modifies brain derived neurotrophic factor (BDNF) concentration in plasma. The aim of this study was to investigate the effects of chronic exercise (running in a treadmill for 8 weeks) intensity on pancreatic islet morphometry in healthy state. The BDNF receptor effect on the pancreatic islet morphometry was also evaluated. Adult male Wistar rats were divided in 6 groups: Control (C); moderate intensity training (MIT); high intensity training (HIT) did not treat with BDNF receptor inhibitor (K252a), and C, MIT and HIT treated with K252a. The results shown that chronic exercise induces b-cells hypertrophy without BDNF receptor participation. On the other hand, the moderate exercise increases the number of b cells per islet; the last effect does not require TrkB participation. In sedentary conditions, the K252a treatment reduced the b-cell density. Exercise intensity has differential effects on pancreas islet morphometry in healthy model; furthermore, BDNF receptor plays a role to maintain the amount of b-cells in sedentary state.
Islets
To evaluate the effect of acute exercise and exercise training at the anaerobic threshold (AT) intensity on aerobic conditioning and insulin secretion by pancreatic islets, adult male Wistar rats were submitted to the lactate minimum test (LMT) for AT determination. Half of the animals were submitted to swimming exercise training (trained), 1 h/day, 5 days/week during 8 weeks, with an overload equivalent to the AT. The other half was kept sedentary (sedentary). At the end of the experimental period, the rats were submitted to an oral glucose tolerance test and to another LMT. Then, the animals were sacrificed at rest or immediately after 20 minutes of swimming exercise at the AT intensity for pancreatic islets isolation. At the end of the experiment mean workload (% bw) at AT was higher and blood lactate concentration (mmol/L) was lower in the trained than in the control group. Rats trained at the AT intensity showed no alteration in the areas under blood glucose and insulin during ...
Diabetologia, 2018
Aims/hypothesis Pancreatic fat accumulation may contribute to the development of beta cell dysfunction. Exercise training improves whole-body insulin sensitivity, but its effects on pancreatic fat content and beta cell dysfunction are unclear. The aim of this parallel-group randomised controlled trial was to evaluate the effects of exercise training on pancreatic fat and beta cell function in healthy and prediabetic or type 2 diabetic participants and to test whether the responses were similar regardless of baseline glucose tolerance. Methods Using newspaper announcements, a total of 97 sedentary 40-55-year-old individuals were assessed for eligibility. Prediabetes (impaired fasting glucose and/or impaired glucose tolerance) and type 2 diabetes were defined by ADA criteria. Of the screened candidates, 28 healthy men and 26 prediabetic or type 2 diabetic men and women met the inclusion criteria and were randomised into 2-week-long sprint interval or moderate-intensity continuous training programmes in a 1:1 allocation ratio using random permuted blocks. The primary outcome was pancreatic fat, which was measured by magnetic resonance spectroscopy. As secondary outcomes, beta cell function was studied using variables derived from OGTT, and whole-body insulin sensitivity and pancreatic fatty acid and glucose uptake were measured using positron emission tomography. The measurements were carried out at the Turku PET Centre, Finland. The analyses were based on an intention-to-treat principle. Given the nature of the intervention, blinding was not applicable. Results At baseline, the group of prediabetic or type 2 diabetic men had a higher pancreatic fat content and impaired beta cell function compared with the healthy men, while glucose and fatty acid uptake into the pancreas was similar. Exercise training decreased pancreatic fat similarly in healthy (from 4.4% [3.0%, 6.1%] to 3.6% [2.4%, 5.2%] [mean, 95% CI]) and prediabetic or type 2 diabetic men (from 8.7% [6.0%, 11.9%] to 6.7% [4.4%, 9.6%]; p = 0.036 for time effect) without any changes in pancreatic substrate uptake (p ≥ 0.31 for time effect in both insulin-stimulated glucose and fasting state fatty acid uptake). In prediabetic or type 2 diabetic men and women, both exercise modes similarly improved variables describing beta cell function. Conclusions/interpretation Two weeks of exercise training improves beta cell function in prediabetic or type 2 diabetic individuals and decreases pancreatic fat regardless of baseline glucose tolerance. This study shows that short-term training efficiently reduces ectopic fat within the pancreas, and exercise training may therefore reduce the risk of type 2 diabetes. Marja A. Heiskanen and Kumail K. Motiani contributed equally to this study.
Physiology & Behavior, 1992
Metabolic mechanisms involved in the impaired insulin secretion in pancreatic islets isolated from exercised and fasted rats. PHYSIOL BEHAV 52(4) 723-726, 1992.-This study examined the metabolic mechanisms involved in the impaired insulin secretion by pancreatic islets isolated from fasted and exercised rats. Insulin secretion to glucose (8.3 to 16.7 mM) stimulus was lower in fasted (F), exercised (E), and fasted plus exercised (EF) rats as compared with the control group. The rate of glucose oxidation by isolated islets was reduced in F and EF rats, but it was not modified in the E group. In response to a-KIC (5, 10, 15, and 20 mM), insulin secretion was not different in EF and F rats, in comparison to controls, except in the E group, which showed values slightly higher. These findings suggest that changes in insulin secretion in fasted rats, associated or not to exercise training, might be a consequence of a reduced activity of the fight-hand side of the Krebs cycle (from pyruvate to oxoglutarate), leading to decreased glucose oxidation. However, the exercise itself caused a significant decrease of insulin secretion without altering glycolysis and Krebs cycle activities.
International Journal of Applied Pharmaceutics, 2019
Objective: This study is conducted to determine the protective effects of physical exercise and ascorbic acid on increasing blood glucose (BG) levels and islet pancreatic area in high-carbohydrate (HC) diet rats. Methods: A total of 20 rats were divided into four groups: Control group which was a HC and treatment groups which were HC plus exercise (HCEx), HC plus ascorbic acid (HCAs), and HCEx and ascorbic acid (HCExAs). The duration of treatment was 9 weeks. Swimming to exercise held 6 times a week and ascorbic acid dose was 9 mg. Results: It showed that the smallest body weight was HCEx group. BG difference (before and after treatment = BG diff) had a significant difference (p=0.021) among groups, and the lowest level of BG diff was HCEx group. HCAs had the biggest BG diff. However, there was no significantly difference among groups on islet pancreatic area, but HC group had the largest area. Conclusion: This study suggests that a combination of exercise and ascorbic acid on HC di...