Salmon calcitonin – a potent inhibitor of food intake in states of impaired leptin signalling in laboratory rodents

Eiden, Sandra; Daniel, Carolin; Steinbrueck, Alexandra; Schmidt, Ingrid; Simón, E.

doi:10.1113/jphysiol.2002.018671

Cited by 49 publications

(42 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…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: 56%

Activation of amylin receptors attenuates alcohol‐mediated behaviours in rodents

2018

View full text Add to dashboard Cite

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.

show abstract

Section: Discussioncontrasting

confidence: 56%

Activation of amylin receptors attenuates alcohol‐mediated behaviours in rodents

2018

View full text Add to dashboard Cite

show abstract

“…This was corroborated by the finding that rats treated with antibodies against IL-6 or mice deficient for IL-6 did not show the same enhancing effect of amylin on leptin signaling compared with their respective controls. 98 Finally, and consistent with earlier studies that leptin-deficient ob/ob mice are less sensitive to sCT, 75 we recently showed that leptin-receptor-deficient db/db mice or Zucker ZDF rats respond less to acute amylin injections than respective wild-type controls; further, the reduction of body weight and adiposity by leptin was lower in amylin-deficient mice than in wild-type controls, 85 and amylin-deficient mice had less leptin-induced pSTAT3 formation in the ventromedial hypothalamus. 85 In other words, endogenous leptin action may be required for a full action of amylin and the presence of amylin signaling may mutually be necessary for the full effect of leptin.…”

Section: Interactions Of Amylin With Other Factors Involved In the Cosupporting

confidence: 76%

“…One of the first studies in respect to amylin reported that rodent models with a defective leptin signaling system have a reduced response to anorectic doses of the amylin agonist sCT. 75 Subsequently, we reported that acute administration of leptin to the third ventricle increased the eating-inhibitory effect of peripheral amylin. 76 Interest in this type of interaction was fueled by the finding that amylin may be able to reduce the leptin resistance that is commonly associated with obesity.…”

Section: Interactions Of Amylin With Other Factors Involved In the Comentioning

confidence: 99%

Gut hormones such as amylin and GLP-1 in the control of eating and energy expenditure

Lutz

2016

Int J Obes Supp

View full text Add to dashboard Cite

“…ob/ob and MC4Rko mice, fa/fa rats) require higher doses of the amylin receptor agonist, salmon calcitonin (sCT) to reduce eating [17], suggesting that obesity may attenuate amylin sensitivity. Previous pilot work has also indicated that high circulating amylin levels may reduce the ability of amylin to slow gastric emptying [18].…”

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

View full text Add to dashboard Cite

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...

show abstract

Salmon calcitonin – a potent inhibitor of food intake in states of impaired leptin signalling in laboratory rodents

Cited by 49 publications

References 36 publications

Activation of amylin receptors attenuates alcohol‐mediated behaviours in rodents

Activation of amylin receptors attenuates alcohol‐mediated behaviours in rodents

Gut hormones such as amylin and GLP-1 in the control of eating and energy expenditure

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

Contact Info

Product

Resources

About