Environmental stress modifies glycemic control and diabetes onset in type 2 diabetes prone Otsuka Long Evans Tokushima Fatty (OLETF) rats

Kai, Keiko; Morimoto, Isao; Morita, Emiko; Okada, Yosuke; Yamamoto, Setsu; Kanda, Kikuo; Uriu, Kohei; Eto, Sumiya

doi:10.1016/s0031-9384(99)00187-0

Cited by 30 publications

(22 citation statements)

References 38 publications

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“…In addition to beneficial adaptations, such as increased oxidative capacity and improved insulin sensitivity, forced treadmill running is associated with unwanted physiological adaptations indicative of chronic stress (29). Importantly, glucose homeostasis itself can be affected by nonexercise forms of stress (19). Hence, ZDF rats bathing in 5 cm of water and serving as a sham control group to a swimming group of rats had increased plasma corticosterone concentrations, which was associated with delayed onset of postprandial hyperglycemia (22).…”

Section: Discussionmentioning

confidence: 99%

Voluntary running exercise prevents β-cell failure in susceptible islets of the Zucker diabetic fatty rat

Delghingaro-Augusto

Décary²,

Peyot

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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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 shown in vivo and in vitro. Surprisingly, ZDF-A islets had persistent defects in fatty acid oxidation, GL/FA cycling, and β-cell gene expression. ZDF-A islets, however, had preserved islet insulin mRNA and insulin stores compared with ZDF-I rats. Physical activity did not prevent hyperphagia, dyslipidemia, or obesity in ZDF rats. In conclusion, islets of ZDF rats have a susceptibility to failure that is possibly due to altered β-cell fatty acid metabolism. Depletion of pancreatic islet insulin stores is a major contributor to islet failure in this T2D model, preventable by physical activity.

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Section: Discussionmentioning

confidence: 99%

Voluntary running exercise prevents β-cell failure in susceptible islets of the Zucker diabetic fatty rat

Delghingaro-Augusto

Décary²,

Peyot

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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“…However, this assumption does not consider the variability, complexity, or divergence between effects of chronic and intermittent stress and has resulted from the paucity of adequately controlled human studies examining these in the context of T2DM. We (4,5) and others (27) have demonstrated that intermittent stress delays development of hyperglycemia in genetic models of T2DM. This contrasts with common views that all stressors are deleterious for diabetes and illustrates that intermittent exposure to stressors and the ensuing adaptations may instead be important for normal physiological functioning by preparing the body to deal with threats to homeostasis.…”

mentioning

confidence: 83%

Adaptation to intermittent stress promotes maintenance of β-cell compensation: comparison with food restriction

Bates¹,

Sirek²,

Király³

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

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SG, Vranic M. Adaptation to intermittent stress promotes maintenance of ␤-cell compensation: comparison with food restriction. Am J Physiol Endocrinol Metab 295: E947-E958, 2008. First published August 19, 2008 doi:10.1152/ajpendo.90378.2008.-Intermittent restraint stress delays hyperglycemia in ZDF rats better than pair feeding. We hypothesized that intermittent stress would preserve ␤-cell mass through distinct mechanisms from food restriction. We studied temporal effects of intermittent stress on ␤-cell compensation during pre-, early, and late diabetes. Six-week-old obese male ZDF rats were restraint-stressed 1 h/day, 5 days/wk for 0, 3, 6, or 13 wk and compared with age-matched obese ZDF rats that had been food restricted for 13 wk, and 19-wk-old lean ZDF rats. Thirteen weeks of stress and food restriction lowered cumulative food intake 10 -15%. Obese islets were fibrotic and disorganized and not improved by stress or food restriction. Obese pancreata had islet hyperplasia and showed evidence of neogenesis, but by 19 wk old ␤-cell mass was not increased, and islets had fewer ␤-cells that were hypertrophic. Both stress and food restriction partially preserved ␤-cell mass at 19 wk old via islet hypertrophy, whereas stress additionally lowered ␣-cell mass. Concomitant with maintenance of insulin responses to glucose, stress delayed the sixfold decline in ␤-cell proliferation and reduced ␤-cell hypertrophy, translating into 30% more ␤-cells per islet after 13 wk. In contrast, food restriction did not improve insulin responses or ␤-cell hyperplasia, exacerbated ␤-cell hypertrophy, and resulted in fewer ␤-cells and greater ␣-cell mass than with stress. Thus, preservation of ␤-cell mass with adaptation to intermittent stress is related to ␤-cell hyperplasia, maintenance of insulin responses to glucose, and reductions in ␣-cell mass that do not occur with food restriction.

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“…On the contrary, adaptation to intermittent restraint stress (Bates et al, 2008a,b) and immobilization (Kai et al, 2000) delays development of hyperglycemia and hyperinsulinemia (Bazhan et al, 2007) in rodent genetic models of DM2. It is partially due to stress-induced anorexia that likely improves insulin sensitivity and maintains ␤-cell compensation (Bates et al, 2008a,b;Kelley et al, 1993).…”

Section: Stress and Glucose Metabolismmentioning

confidence: 99%

“…1) stimulate (Bartolomucci et al, 2009;Bjorntorp, 2001;King and Smith, 1985), while stress, as a whole, inhibits food intake (Bazhan et al, 2007;De Souza et al, 2000;Harris et al, 2001;Krahn et al, 1990;Rybkin et al, 1997). It is also not clear if stress is diabetogenic (Rosmond, 2003;Surwit et al, 1992) or an antidiabetogenic factor (Bates et al, 2008a,b;Kai et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Food-intake regulation during stress by the hypothalamo-pituitary-adrenal axis

Бажан¹,

Zelena²

2013

Brain Research Bulletin

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a b s t r a c tThe prevalence of obesity is increasing worldwide with serious consequences such as diabetes mellitus type 2 and cardiovascular diseases. Emotional stress is considered to be one of the main reasons of obesity development in humans. However, there are some contradictory results, which should be addressed. First of all stress induces anorexia, but not overeating in laboratory animals. Glucocorticoids, the effector molecules of the hypothalamo-pituitary-adrenocortical (HPA) axis stimulate and stress inhibits food intake. It is also not clear if stress is diabetogenic or an antidiabetogenic factor. The review will discusses these issues and the involvement of the whole HPA axis and its separate molecules (glucocorticoids, adrenocorticotropin, corticotropin-releasing hormone) in food intake regulation under stress.

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Environmental stress modifies glycemic control and diabetes onset in type 2 diabetes prone Otsuka Long Evans Tokushima Fatty (OLETF) rats

Cited by 30 publications

References 38 publications

Voluntary running exercise prevents β-cell failure in susceptible islets of the Zucker diabetic fatty rat

Voluntary running exercise prevents β-cell failure in susceptible islets of the Zucker diabetic fatty rat

Adaptation to intermittent stress promotes maintenance of β-cell compensation: comparison with food restriction

Food-intake regulation during stress by the hypothalamo-pituitary-adrenal axis

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