Amylin in the Periphery

Wookey, Peter J.; xuereb, lori; Tikellis, Chris; Cooper, Mark E.

doi:10.1100/tsw.2003.17

Cited by 13 publications

(20 citation statements)

References 113 publications

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“…Amylin is cosecreted from pancreatic ␤-cells with insulin and has a role in signaling satiety, diminishing gastric emptying, inhibiting glucagon secretion, and stimulating growth of pancreatic ␤-cells (48,69). However, supraphysiological levels of amylin have inhibitory effects on insulin secretion and action (14,17,33,40,42,50,59) and aggregate to form amyloid plaques that result in pancreatic ␤-cell destruction (47).…”

Section: Discussionmentioning

confidence: 99%

Artificial selection for high-capacity endurance running is protective against high-fat diet-induced insulin resistance

Noland¹,

Thyfault²,

Henes³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

122

138

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Dohm GL, Cortright RN, Lust RM. Artificial selection for high-capacity endurance running is protective against high-fat diet-induced insulin resistance. Am J Physiol Endocrinol Metab 293: E31-E41, 2007. First published March 6, 2007; doi:10.1152/ajpendo.00500.2006.-Elevated oxidative capacity, such as occurs via endurance exercise training, is believed to protect against the development of obesity and diabetes. Rats bred both for low (LCR)-and high (HCR)-capacity endurance running provide a genetic model with inherent differences in aerobic capacity that allows for the testing of this supposition without the confounding effects of a training stimulus. The purpose of this investigation was to determine the effects of a high-fat diet (HFD) on weight gain patterns, insulin sensitivity, and fatty acid oxidative capacity in LCR and HCR male rats in the untrained state. Results indicate chow-fed LCR rats were heavier, hypertriglyceridemic, less insulin sensitive, and had lower skeletal muscle oxidative capacity compared with HCR rats. Upon exposure to an HFD, LCR rats gained more weight and fat mass, and their insulin resistant condition was exacerbated, despite consuming similar amounts of metabolizable energy as chow-fed controls. These metabolic variables remained unaltered in HCR rats. The HFD increased skeletal muscle oxidative capacity similarly in both strains, whereas hepatic oxidative capacity was diminished only in LCR rats. These results suggest that LCR rats are predisposed to obesity and that expansion of skeletal muscle oxidative capacity does not prevent excess weight gain or the exacerbation of insulin resistance on an HFD. Elevated basal skeletal muscle oxidative capacity and the ability to preserve liver oxidative capacity may protect HCR rats from HFD-induced obesity and insulin resistance. fatty acid; lipid metabolism; liver; heart; skeletal muscle THE INCIDENCE OF METABOLIC DISEASES such as obesity and type II diabetes is increasing dramatically and is strongly linked to the rise in cardiovascular disease. In 2002, ϳ64% of the population in the United States was classified as overweight or obese (22), and health care costs attributable to these conditions exceeded $78 billion dollars (13). Although type II diabetes afflicts a substantially lower percentage (ϳ6.3%) of the population (9), this disease accounts for $132 billion in annual health care costs (24). With the increase in the incidence of such metabolic diseases reaching epidemic proportions and the threat of health care costs spiraling out of control, much research has been focused toward elucidating the mechanisms involved in the etiology of these conditions in hopes of ultimately discovering better treatments. Several therapies are currently used to alleviate symptoms of these diseases, but other than dietary modifications, endurance exercise is the only universally prescribed treatment.Enhanced aerobic capacity has long been associated with diminished morbidity and improvements in functional living, yet all the physiological mechanisms ...

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Section: Discussionmentioning

confidence: 99%

Artificial selection for high-capacity endurance running is protective against high-fat diet-induced insulin resistance

Noland¹,

Thyfault²,

Henes³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

122

138

View full text Add to dashboard Cite

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“…Відомо, що останній синтезується в β-клітинах підшлун-кової залози та косекретується з інсуліном у відповідь на підвищення концентрації глюкози в крові [1,2]. Таким чином, амілін разом з інсуліном та глюкагоном бере участь в підтриманні гомеостазу глюкози [3,4].…”

Section: вступunclassified

The influence of amylin on the bile acid spectrum in rats

Ip¹,

Sp²,

Za³

et al. 2014

Fiziol Zh

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“…IAPP is believed to slow exogenous (meal-derived) glucose through inhibition of gastric emptying while reducing endogenous (liver-derived) glucose as a result of suppression of glucagon release from isolated islets. IAPP has been proposed to play a role in a number of other diverse effects, including inhibition of glucose-stimulated insulin secretion; the excretion of calcium, potassium, and sodium; vasodilatation; and the regulation of energy intake and fat storage [38][39][40][41]. Many of the early experiments on the putative physiological role(s) of IAPP were conducted at supraphysiological concentrations and thus may not provide an accurate view of its function.…”

Section: Normal Physiological Role Of Iappmentioning

confidence: 99%