Amylin concentrations and glucose control

Koda, J.E.; Fineman, Mark; Rink, TimothyJ.; Dailey, G.; Muchmore, DouglasB.; Linarelli, L.G.

doi:10.1016/0140-6736(92)90785-2

Cited by 141 publications

(96 citation statements)

References 9 publications

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“…Thus, in response to nutrient ingestion, circulating amylin concentrations rise rapidly within minutes after meal onset ("phasic" increase), peak within 60 min, and return to baseline by 120 min [13]. When administered exogenously (peripherally or centrally), acute amylin dose-dependently decreases food intake, causing a decrease in meal size though having no effect on the intermeal interval [14,15].…”

Section: Introductionmentioning

confidence: 99%

Influence of high-fat feeding, diet-induced obesity, and hyperamylinemia on the sensitivity to acute amylin

Boyle¹,

Rossier²,

Lutz³

2011

Physiology & Behavior

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Obesity results in the increased secretion of various hormones controlling food intake and body weight, such as leptin, and insulin; increased circulating levels of pancreatic amylin have also been described in obese humans and rodents. Because leptin-resistance is present in diet-induced obese (DIO) rats, and because hyperleptinemia seems necessary for the full development of leptin resistance, we tested whether amylin sensitivity is inversely correlated with adiposity, such that DIO reduces the anorectic action of acute amylin. We also determined if hyperamylinemia leads to a change in amylin sensitivity. In the first experiment, rats were chronically exposed to a high fat (HF; 60% fat) diet or fed standard chow for control. The anorectic response to amylin was tested on several occasions over a 14 week observation period. HF feeding led to the expected increase in body adiposity; the response to an acute amylin injection (5-50 g/kg s.c.) was unaltered for 10 weeks of HF feeding. Even after 12 weeks on a HF diet, which clearly caused obesity, acute administration of amylin (5 g/kg, s.c.) was still able to suppress food intake, although the suppression was not statistically significant. Further experiments using additional doses of amylin will be necessary to demonstrate possible amylin resistance after HF feeding or in DIO rats. In the second experiment, we tested more specifically whether hyperamylinemia that may result from HF feeding and subsequent obesity, reduces the sensitivity of the amylin signaling system. To avoid confounding factors, we chronically infused lean chow fed rats with amylin (5 or 10 g/kg/day s.c.) to elevate their plasma amylin concentration to levels observed in obese rats (30-40 pM). In the absence of obesity, hyperamylinemia did not lead to a reduced sensitivity to acute amylin (5-20 g/kg s.c.) injections; acute amylin reduced eating similarly in all groups of rats. Overall, we concluded that direct diet effects by short term exposure to HF appear to be of little importance for amylin sensitivity; further, long-term maintenance on a HF diet and the resulting obesity only slightly attenuated the anorectic response to acute amylin. Because we observed no marked changes in amylin sensitivity in lean, chow fed rats with induced hyperamylinemia, amylin receptor downregulation in chronic hyperamylinemia does not seem to occur. 1 Long-term maintenance on a HF diet only slightly attenuates acute amylin action.2 Attenuation of amylin action seems more related to obesity than HF exposure.3 Acute amylin sensitivity is not reduced by chronic hyperamylinemia.3 ABSTRACTObesity results in the increased secretion of various hormones controlling food intake and body weight, such as leptin, and insulin; increased circulating levels of pancreatic amylin have also been described in obese humans and rodents. Because leptinresistance is e.g. present in diet-induced obese (DIO) rats, and because hyperleptinemia seems necessary for the full development of leptin resistance, we tested whether amyl...

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Section: Introductionmentioning

confidence: 99%

Influence of high-fat feeding, diet-induced obesity, and hyperamylinemia on the sensitivity to acute amylin

Boyle¹,

Rossier²,

Lutz³

2011

Physiology & Behavior

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“…Similar to meal-related insulin, amylin levels are low prior to a meal and are elevated following a glucose load or a mixed meal (9,19). Postprandial amylin levels have been shown to be higher following a high carbohydrate meal than following an isocaloric high-fat meal, and plasma amylin levels are positively related to subjective satiety ratings (15).…”

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Salmon calcitonin reduces food intake through changes in meal sizes in male rhesus monkeys

Bello

Kemm

Moran³

2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Amylin is a ␤-cell hormone that is normally co-secreted with insulin in response to meals and, therefore, is deficient in patients with type 1 diabetes (2). Preclinical studies indicate that amylin acts as a neuroendocrine hormone with several glucoregulatory effects that collectively complement the actions of insulin in postprandial glucose control by modulating the rate of glucose influx into the circulation (9,10).…”

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confidence: 99%

A Randomized Study and Open-Label Extension Evaluating the Long-Term Efficacy of Pramlintide as an Adjunct to Insulin Therapy in Type 1 Diabetes

Whitehouse

Kruger²,

Fineman³

et al. 2002

Diabetes Care

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248

253

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OBJECTIVE -To assess the effect of mealtime amylin replacement with pramlintide on long-term glycemic and weight control in patients with type 1 diabetes. RESEARCH DESIGN AND METHODS-In a 52-week, double-blind, placebocontrolled, multicenter study, 480 patients with type 1 diabetes were randomized to receive preprandial injections of placebo or 30 g pramlintide q.i.d., in addition to existing insulin regimens. At week 20, pramlintide-treated patients were re-randomized to 30 or 60 g pramlintide q.i.d. if decreases from baseline in HbA 1c were Ͻ1% at week 13. Of the 342 patients who completed the 52-week study, 236 individuals (ϳ70%) elected to participate in a 1-year openlabel extension in which all patients received 30 or 60 g pramlintide q.i.d..RESULTS -Treatment with pramlintide led to a mean reduction in HbA 1c of 0.67% from baseline to week 13 that was significantly (P Ͻ 0.0001) greater than the placebo reduction (0.16%), and a significant placebo-corrected treatment difference was sustained through week 52 (P ϭ 0.0071). The greater HbA 1c reduction was associated with an average weight loss, rather than weight gain, and was not accompanied by an increased overall event rate of severe hypoglycemia. In the open-label extension, mean HbA 1c levels decreased rapidly in patients receiving pramlintide for the first time and remained at reduced levels in patients who continued pramlintide treatment. The most common adverse events reported by the pramlintide group were mild nausea and anorexia, which both occurred during the initial weeks of treatment and dissipated over time.CONCLUSIONS -Mealtime pramlintide treatment as an adjunct to insulin improved longterm glycemic control without inducing weight gain or increasing the overall risk of severe hypoglycemia in patients with type 1 diabetes. Diabetes Care 25:724 -730, 2002

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Amylin concentrations and glucose control

Cited by 141 publications

References 9 publications

Influence of high-fat feeding, diet-induced obesity, and hyperamylinemia on the sensitivity to acute amylin

Influence of high-fat feeding, diet-induced obesity, and hyperamylinemia on the sensitivity to acute amylin

Salmon calcitonin reduces food intake through changes in meal sizes in male rhesus monkeys

A Randomized Study and Open-Label Extension Evaluating the Long-Term Efficacy of Pramlintide as an Adjunct to Insulin Therapy in Type 1 Diabetes

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