Central amylin acts as an adiposity signal to control body weight and energy expenditure

Wielinga, Peter Y.; Löwenstein, Christian; Muff, Sabine; Munz, M.; Woods, Stephen C.; Lutz, Thomas

doi:10.1016/j.physbeh.2010.04.012

Cited by 78 publications

(77 citation statements)

References 44 publications

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“…Though our elevated levels of amylin, which were still in the physiological range, did not produce dramatic changes in body weight and food intake, our results do provide further evidence that amylin may play a role in the long-term control of energy balance, similar to well known adiposity signals, like insulin and leptin [43].…”

Section: Hyperamylinemia Alone Does Not Cause Amylin Insensitivitysupporting

confidence: 52%

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: Hyperamylinemia Alone Does Not Cause Amylin Insensitivitysupporting

confidence: 52%

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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“…Furthermore, centrally administered amylin levels seem to directly influence the target body weight of rats (Wielinga et al, 2010). Together, these data suggest that central amylin, like leptin or insulin, may encode the regulated level of body weight and hence may contribute to the relative constancy of body weight throughout adult life.…”

Section: A Amylin As a Satiation Signalmentioning

confidence: 80%

“…This indicated that amylin infusions most likely reduced eating and increased energy expenditure (Mack et al, 2007;Wielinga et al, 2007Wielinga et al, , 2010. Hence, amylin shares another similarity with leptin because it influences energy balance by an eating and an energy expenditure effect (Isaksson et al, 2005;Roth et al, 2006;Mack et al, 2007;Osaka et al, 2008).…”

Section: Amylin and Energy Expenditurementioning

confidence: 93%

Amylin: Pharmacology, Physiology, and Clinical Potential

Hay¹,

Chen²,

Lutz³

et al. 2015

Pharmacological Reviews

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“…Amylin increases energy expenditure after peripheral and central administration in animals (Lutz et al, 2006(Lutz et al, , 2010. Chronic infusion of amylin into the brain reduces body weight gain and adiposity, while chronic infusion of an antagonist of amylin receptors into the brain increases body adiposity (Lutz et al, 2010;Wielinga et al, 2010). In vitro, amylin was found to inhibit both basal and insulin-stimulated glycogenesis in rat skeleton muscle (Leighton et al, 1988) and to impair glucose disposal in liver cells (Hoppener et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Correlations between endogen amylin hormone and some hormonal, biochemical and bone parameters in pullets

Guzel

Güneş

2014

Rev. Bras. Cienc. Avic.

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The objective of this study was to assess the correlations of amylin (a pancreatic polypeptide hormone) with some hormonal, biochemical and bone parameters in pullets. Forty 18-week-old pullets were used. Plasma amylin, CT (calcitonin), 1,25 (OH)2 vitamin D (1,25 dihydroxycholecalciferol ), serum osteocalcin, glucose, ALP (alkaline phosphatase), cholesterol, and triglycerides, as well as weight, length and total volume of tibiotarsi were measured. Plasma amylin concentration was negatively correlated with serum cholesterol (p<0.05) and triglycerides (p<0.05) concentrations. Plasma amylin concentration was significantly and positively correlated with plasma calcitonin concentrations (p<0.001). Serum ALP and plasma amylin concentrations were positively correlated (p<0.01). There were no correlations between amylin hormone and other parameters. Based on these results, it is possible to conclude that endogen amylin may effect cholesterol, triglycerides, calcitonin, and ALP levels in pullets without changing some other hormonal, biochemical and bone parameters related to calcium and lipid metabolism.

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Central amylin acts as an adiposity signal to control body weight and energy expenditure

Cited by 78 publications

References 44 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

Amylin: Pharmacology, Physiology, and Clinical Potential

Correlations between endogen amylin hormone and some hormonal, biochemical and bone parameters in pullets

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