Amylin and Food Intake in Mice: Effects on Motivation to Eat and Mechanism of Action

Morley, John E.; Suarez, Michael; Mattamal, Michael; Flood, James F.

doi:10.1016/s0091-3057(96)00168-2

Cited by 50 publications

(27 citation statements)

References 24 publications

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“…Our results are contradicting to previous studies showing that sCT decreases lever pressing for palatable reward (Morley et al 1997) and palatable food intake in mice (Eiden et al 2002). However, either these studies used high doses of amylin in the range of 100 to 200 μg/kg in an operant paradigm (Morley et al 1997), or they were conducted in mice resistant to leptin after being scheduled on chocolate as a highly caloric substitute to chow for more than 40 days (Eiden et al 2002). Another difference is that our experiments were conducted in novel cages; thus, novelty could be considered as a factor potentially influencing our data.…”

Section: Discussioncontrasting

confidence: 99%

Activation of amylin receptors attenuates alcohol‐mediated behaviours in rodents

2018

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Alcohol expresses its reinforcing properties by activating areas of the mesolimbic dopamine system, which consists of dopaminergic neurons projecting from the ventral tegmental area to the nucleus accumbens. The findings that reward induced by food and addictive drugs involve common mechanisms raise the possibility that gut-brain hormones, which control appetite, such as amylin, could be involved in reward regulation. Amylin decreases food intake, and despite its implication in the regulation of natural rewards, tenuous evidence support amylinergic mediation of artificial rewards, such as alcohol. Therefore, the present experiments were designed to investigate the effect of salmon calcitonin (sCT), an amylin receptor agonist and analogue of endogenous amylin, on various alcohol-related behaviours in rodents. We showed that acute sCT administration attenuated the established effects of alcohol on the mesolimbic dopamine system, particularly alcohol-induced locomotor stimulation and accumbal dopamine release. Using the conditioned place preference model, we demonstrated that repeated sCT administration prevented the expression of alcohol's rewarding properties and that acute sCT administration blocked the reward-dependent memory consolidation. In addition, sCT pre-treatment attenuated alcohol intake in low alcohol-consuming rats, with a more evident decrease in high alcohol consumers in the intermittent alcohol access model. Lastly, sCT did not alter peanut butter intake, blood alcohol concentration and plasma corticosterone levels in mice. Taken together, the present data support that amylin signalling is involved in the expression of alcohol reinforcement and that amylin receptor agonists could be considered for the treatment of alcohol use disorder in humans.

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Section: Discussioncontrasting

confidence: 99%

Activation of amylin receptors attenuates alcohol‐mediated behaviours in rodents

2018

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“…The effect of amylin in reducing meal size is dose dependent and the effect is effectively and specifically blocked by amylin antagonism; on the other hand, amylin antagonists alone increase eating by a meal size effect (Mollet et al, 2004). Importantly, amylin and its analogs reduce meal size without producing signs of conditioned taste aversion or visceral illness (Lutz et al, 1995b;Morley et al, 1997;Mack et al, 2007Mack et al, , 2010. Overall, the data indicate that amylin acts as a physiologic short-term satiating hormone in rats.…”

Section: A Amylin As a Satiation Signalmentioning

confidence: 85%

Amylin: Pharmacology, Physiology, and Clinical Potential

Hay¹,

Chen²,

Lutz³

et al. 2015

Pharmacol Rev

302

297

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“…Peripheral administration decreases food intake, 8 and among systemically administered anorexigenic molecules (amylin, salmon calcitonin, peptide YY 3-36, cholecystokinin-8, glucagon-like peptide-1, CGRP, adrenomedullin, leptin, the melanocortin agonist MTII, the cannabinoid receptor antagonist AM251 and naloxone), amylin receptor agonism demonstrates the greatest potency to inhibit consumption. 9 Amylin suppresses food intake by reducing meal size, 10,11 while having no effect on conditioned taste aversion, 12,13 kaolin consumption (a preclinical marker of emesis), 11 or locomotor activity, 11 suggesting a direct effect of the hormone on metabolic pathways. Amylin's action is mediated by activation of amylin-binding sites in the area postrema (AP) as lesioning this site abolishes its ability to reduce food intake.…”

Section: Introductionmentioning

confidence: 99%

Davalintide (AC2307), a novel amylin-mimetic peptide: enhanced pharmacological properties over native amylin to reduce food intake and body weight

Mack¹,

Soares²,

Wilson³

et al. 2009

Int J Obes

105

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Objective: The current set of studies describe the in vivo metabolic actions of the novel amylin-mimetic peptide davalintide (AC2307) in rodents and compares these effects with those of the native peptide. Research design and methods: The anti-obesity effects of davalintide were examined after intraperitoneal injection or sustained peripheral infusion through subcutaneously implanted osmotic pumps. The effect of davalintide on food intake after lesioning of the area postrema (AP) and neuronal activation as measured by c-Fos, were also investigated. Results: Similar to amylin, davalintide bound with high affinity to amylin, calcitonin and calcitonin gene-related peptide receptors. Acutely, davalintide displayed greater suppression of dark-cycle feeding and an extended duration of action compared with amylin (23 versus 6 h). Davalintide had no effect on locomotor activity or kaolin consumption at doses that decreased food intake. Davalintide-induced weight loss through infusion was dose dependent, durable up to 8 weeks, fat-specific and lean-sparing, and was associated with a shift in food preference away from high-fat (palatable) chow. Metabolic rate was maintained during active weight loss. Both davalintide and amylin failed to suppress food intake after lesioning of the AP and activated similar brain nuclei, with davalintide displaying an extended duration of c-Fos expression compared with amylin (8 versus 2 h). Conclusion: Davalintide displayed enhanced in vivo metabolic activity over amylin while retaining the beneficial properties possessed by the native molecule. In vitro receptor binding, c-Fos expression and AP lesion studies suggest that the metabolic actions of davalintide and amylin occur through activation of similar neuronal pathways.

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Amylin and Food Intake in Mice: Effects on Motivation to Eat and Mechanism of Action

Cited by 50 publications

References 24 publications

Activation of amylin receptors attenuates alcohol‐mediated behaviours in rodents

Activation of amylin receptors attenuates alcohol‐mediated behaviours in rodents

Amylin: Pharmacology, Physiology, and Clinical Potential

Davalintide (AC2307), a novel amylin-mimetic peptide: enhanced pharmacological properties over native amylin to reduce food intake and body weight

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