Amylin reduces food intake more potently than calcitonin gene-related peptide (CGRP) when injected into the lateral brain ventricle in rats

Lutz, Thomas; Rossi, R.; Althaus, Janine; Prete, Eleonora Del; Scharrer, E.

doi:10.1016/s0196-9781(98)00114-4

Cited by 65 publications

(35 citation statements)

References 21 publications

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“…First, a lesion in the APaNTS region abolished amylin's anorectic effect after i.p. injection 3,11 while deafferentiation with the neurotoxin capsaicin did not affect the anorectic effect of amylin. 4,12 Second, anorectic doses of amylin have been shown to induce c-Fos expression in the APaNTS region.…”

Section: Discussionmentioning

confidence: 80%

“…Considering the pharmacokinetics of amylin, 14 we aimed at elevating the plasma amylin level for at least 2 h above fasting levels with this approach. Similar to recent experiments, 3,11 rats were food deprived for 24 h before injection. Amylin (50 mgakg i.p.)…”

Section: Data Recordingmentioning

confidence: 91%

“…injection. 3,11 Because amylin's anorectic effect was abolished in rats lesioned in the APaNTS region (AP-X rats 3,11 ) while chemical ablation of sensory afferent nerves with capsaicin left amylin's effect unaltered, 4,12 AP neurons seem to directly mediate amylin's satiety effect. Apart from the APaNTS region, amylin receptors have also been found in other brain areas involved in the control of food intake such as the lateral parabrachial nucleus, the central nucleus of the amygdala and the hypothalamus.…”

Section: Introductionmentioning

confidence: 99%

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The anorectic effect of a chronic peripheral infusion of amylin is abolished in area postrema/nucleus of the solitary tract (AP/NTS) lesioned rats

et al. 2001

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OBJECTIVE: Neurons in the area postremaanucleus of the solitary tract (APaNTS) region mediate amylin's anorectic effect elicited by a single intraperitoneal (i.p.) injection of a low dose (5 mgakg). Here, we tested if a sustained elevation in amylin levels which was achieved by chronic amylin infusion reduces food intake by acting in the APaNTS region or, possibly, at other brain sites. Further, we tested the role of the APaNTS region in mediating the anorectic effects of high doses of amylin and its receptor agonist salmon calcitonin (sCT) after an acute single injection. DESIGN: Amylin (2 mgakgah) was chronically infused i.p. by osmotic minipumps in APaNTS-lesioned (AP-X) or sham-lesioned (SHAM) rats. For the acute experiments, amylin or sCT was injected i.p. at doses of 0.5 (only sCT), 5 or 50 mgakg. Food intake was measured by a computerized system. Body weight was assessed by manually weighing the rats. RESULTS: Amylin signi®cantly reduced cumulative food intake for about 7 days in SHAM but not in AP-X rats. Amylin's effect in SHAM rats was mainly due to a reduction of the size of nocturnal meals (eg average meal size during the ®rst four dark phases; SHAM, NaCl 4.1 AE 0.6 vs amylin 2.6 AE 0.4 g; n 6, P`0.05; AP-X, 2.6 AE 0.3 vs 3.7 AE 0.3) while light phase food intake was unaffected. Body weight gain over the whole 14 day infusion period was reduced by amylin in SHAM (NaCl 61 AE 6 vs amylin 46 AE 4 g; P`0.05) but not in AP-X rats (54 AE 4 vs 62 AE 4). After single injection, the anorectic effect of high doses of amylin and sCT (50 mgakg) was attenuated, but not abolished, in AP-X rats. CONCLUSION: We conclude that, under our experimental conditions, neurons in the APaNTS region are necessary for chronically elevated peripheral amylin to reduce food intake in rats. High doses of amylin, however, may be able to overrun these receptors and reduce feeding by acting at other brain sites.

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Section: Discussionmentioning

confidence: 80%

Section: Data Recordingmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

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The anorectic effect of a chronic peripheral infusion of amylin is abolished in area postrema/nucleus of the solitary tract (AP/NTS) lesioned rats

et al. 2001

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“…Central amylin produces very potent effects on eating (e.g., Rushing et al, 2000;Osaka et al, 2008;Wielinga et al, 2010) that at least under certain conditions are independent of an intact AP (Lutz et al, 1998b), and most reports indicate that lower doses of amylin are required to reduce eating (and body weight) after infusion into the lateral or third than in the fourth cerebral ventricle (Lutz et al, 1997(Lutz et al, , 1998bRushing et al, 2000). Nonetheless, the physiologic relevance of the eatinginhibitory effect of central amylin is less clear, because for most of the potential sites of action, activation by peripheral amylin has not been demonstrated and it is also unclear which areas are primarily targeted by centrally infused amylin.…”

Section: E Amylin Action In Other Brain Areasmentioning

confidence: 99%

Amylin: Pharmacology, Physiology, and Clinical Potential

Hay¹,

Chen²,

Lutz³

et al. 2015

Pharmacol Rev

302

297

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“…Both amylin and cacitonin gene-related peptides reduce food intake, although amylin is more potent than cacitonin generelated peptide. 23 Other properties of amylin include maintenance of glucose homeostasis, decreasing gastric acid secretion, and decreasing gastric emptying. 24 …”

Section: Amylin Agonistsmentioning

confidence: 99%

β₃-Adrenergic Receptor Agonists and Other Potential Anti-obesity Agents

Vansal¹

2004

Am J Pharm Educ

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Obesity has been measured in several ways such as skin-fold thickness, waist-to-hip circumference ratio, percent of body fat, and weight adjusted for height. The most commonly used measure of weight adjusted to height is the body mass index (BMI), which is defined as weight in kilograms divided by height in meters squared (kg/m 2 ). The BMI is highly correlated to body fat, hence it is almost universally used among epidemiologists. The BMI can be quite accurately used to estimate the body fat percentage in adults using the following equation:Body fat % = 1.2 (BMI) + 0.23 (Age) -10.8 (Gender) -5.4where gender = 1 for men and 0 for women. 1 The National Institutes of Health, the American Health Foundation, and the World Health Organization (WHO) 2 have defined healthy weight as a BMI below 25 kg/m 2 , overweight as a BMI between 25 kg/m 2 and 30 kg/m 2 , and obesity as a BMI greater than 30 kg/m 2 .According to the National Health and Nutrition Examination Survey (NHANES) 1999-2000 data, 64% of Americans are overweight or obese, compared with 56% in NHANES III (1988) and 47% in NHANES II (1976-1980. 3 Increased adiposity occurs when food intake exceeds energy expenditure. Therefore, an increase in food intake or a decrease in energy expenditure, or a combination of both could cause one to gain weight. Evolutionarily, food scarcity has led to our genetic predisposition to effectively store energy in times of food abundance. Abundantly available highcalorie foods and an accompanying sedentary lifestyle are major contributing factors to the obesity epidemic. Examination of trends over the past 6 decades in England shows no relationship between either total food intake or fat consumption and the prevalence of clinical obesity, while proxy measures of physical inactivity (television viewing and car ownership) are closely related. 4 This by no means implies that the amount and type of food intake have no bearing upon obesity, but it does imply that over a large period of time, energy expenditure seems to be the more important variable in the food intake and energy expenditure balance. There is now extensive evidence that links excessive body weight with overall mortality. The relationship between BMI and mortality is a J-shaped curve with an acceleration of mortality risk above a BMI of 30 kg/m 2 . 5 Recent evidence shows that a loss of more than 9 kg in women is associated with a 25% reduction in all causes (diabetes, cardiovascular, and cancer) of mortality and this is most marked for cancer (40%-50% reduction) and diabetes (30%-40% reduction). 6 Obesity is reaching epidemic proportions in America and rising at an alarming rate throughout the world. The morbidity of cardiovascular disease, diabetes, osteoarthritis, and some cancers increases in proportion with increased obesity. Numerous anti-obesity agents are being developed that produce effects through diverse mechanisms. This paper discusses various targets for the pharmacotherapy of obesity with special attention to ß 3 -adrenergic receptors (ß 3 -AR) in obesit...

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Amylin reduces food intake more potently than calcitonin gene-related peptide (CGRP) when injected into the lateral brain ventricle in rats

Cited by 65 publications

References 21 publications

The anorectic effect of a chronic peripheral infusion of amylin is abolished in area postrema/nucleus of the solitary tract (AP/NTS) lesioned rats

The anorectic effect of a chronic peripheral infusion of amylin is abolished in area postrema/nucleus of the solitary tract (AP/NTS) lesioned rats

Amylin: Pharmacology, Physiology, and Clinical Potential

β₃-Adrenergic Receptor Agonists and Other Potential Anti-obesity Agents

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Amylin reduces food intake more potently than calcitonin gene-related peptide (CGRP) when injected into the lateral brain ventricle in rats

Cited by 65 publications

References 21 publications

The anorectic effect of a chronic peripheral infusion of amylin is abolished in area postrema/nucleus of the solitary tract (AP/NTS) lesioned rats

The anorectic effect of a chronic peripheral infusion of amylin is abolished in area postrema/nucleus of the solitary tract (AP/NTS) lesioned rats

Amylin: Pharmacology, Physiology, and Clinical Potential

β3-Adrenergic Receptor Agonists and Other Potential Anti-obesity Agents

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β₃-Adrenergic Receptor Agonists and Other Potential Anti-obesity Agents