Rats maintained on high-fat diets exhibit reduced satiety in response to CCK and bombesin

Covașă, Mihai; Ritter, Robert C.

doi:10.1016/s0196-9781(98)00096-5

Cited by 152 publications

(117 citation statements)

References 33 publications

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“…This study demonstrates that 0.06 g/kg is subthreshold for inhibiting food intake under these conditions and that the smallest effective dose was 0.125 g/kg. These results are consistent with the findings of many others (3,28).…”

Section: Experiments 1 Effect Of Recombinant Apo Aiv On Food Intakesupporting

confidence: 94%

Interaction of apolipoprotein AIV with cholecystokinin on the control of food intake

Zhang

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Apolipoprotein AIV (apo AIV) and cholecystokinin (CCK) are peptides that act both peripherally and centrally to reduce food intake by decreasing meal size. The present study examined the effects of intraperitoneally administered bolus doses of recombinant apo AIV, CCK-8, and a combination of subthreshold doses of apo AIV and CCK on 4-h food intake in rats that were fasted overnight. Apo AIV at 100 μg/kg reduced food intake significantly relative to the saline control for 1 h, as did doses of CCK-8 at or above 0.125 μg/kg. Doses of apo AIV (50 μg/kg) or CCK (0.06 μg/kg) alone had no effect on food intake. However, when these subthreshold doses of apo AIV and CCK were administered together, the combination produced a significant inhibition of food intake relative to saline controls ( P < 0.001), and the duration of the effect was longer than that caused by the administration of either apo AIV or CCK alone. The satiation effect produced by CCK-8 + apo AIV was attenuated by lorglumide, a CCK1 receptor antagonist. We conclude that, whereas the intraperitoneal administration of doses of either recombinant apo AIV or CCK at or above threshold levels reduces food intake, the coadministration of subthreshold doses of the two peptides is highly satiating and works via CCK1 receptor.

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Section: Experiments 1 Effect Of Recombinant Apo Aiv On Food Intakesupporting

confidence: 94%

Interaction of apolipoprotein AIV with cholecystokinin on the control of food intake

Zhang

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…In a study of shorter duration, Covasa and Ritter had observed a similar effect of exogenous amylin in rats fed a HF (approx. 75% by energy) diet for three weeks; there was no difference in the acute anorectic effect of amylin between animals adapted to either a low or high fat diet [8]. Interestingly, using the same paradigm, there was a significant attenuation of the CCK effect in Sprague-Dawley rats after maintenance on the HF diet.…”

Section: Amylin-induced Suppression Of Energy Intake Is Decreased Aftmentioning

confidence: 84%

“…It was also shown recently that hyperleptinemia is required for the full development of leptin resistance [7]. Obesity can also affect the sensitivity to satiation hormones, which control meal size, such as glucagon-like peptide-1 (GLP- 1) and cholecystokinin (CCK) [8,9].…”

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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“…In fact, the magnitude and duration of the effects induced by similar doses of [Gly 2 ]GLP2 were less pronounced in obese than lean animals and the native GLP2 was less effective in DIO mice. These observations appear particularly interesting because it has already been described that maintenance of rats on HFD reduces sensitivity to some satiety peptide signals (Covasa & Ritter 1998, Covasa et al 2001, principally the sensitivity to cholecystokinin (Covasa & Ritter 1998, Covasa et al 2001, Nefti et al 2009). …”

Section: Lovshinmentioning

confidence: 88%

Food intake in lean and obese mice after peripheral administration of glucagon-like peptide 2

Baldassano¹,

Bellanca²,

Serio³

et al. 2012

Journal of Endocrinology

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We investigated the potential anorectic action of peripherally administered glucagon-like peptide 2 (GLP2) in lean and diet-induced obese (DIO) mice. Mice, fasted for 16 h, were injected i.p. with native GLP2 or [Gly 2 ]GLP2, stable analog of GLP2, before or after GLP2 (3-33), a GLP2 receptor (GLP2R) antagonist, or exendin (9-39), a GLP1R antagonist. Food intake was measured at intervals 1, 2, 4, 8, and 24 h postinjection. In addition, we tested in lean mice the influence of [Gly 2 ]GLP2 on gastric emptying and the effects of GLP1 alone or in combination with [Gly 2 ]GLP2 on food intake. [Gly 2 ]GLP2 dose dependently and significantly inhibited food intake in lean and DIO mice. The reduction of food intake occurred in the first hour postinjection and it was sustained until 4 h postinjection in lean mice while it was sustained until 2 h postinjection in DIO mice. GLP2 significantly inhibited food intake in both lean and DIO mice but only in the first hour postinjection. ]GLP2 decreased the gastric emptying rate. Results suggest that GLP2 can reduce food intake in mice in the short term, likely acting at a peripheral level. DIO mice are less sensitive to the anorectic effect of the peptide.

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Rats maintained on high-fat diets exhibit reduced satiety in response to CCK and bombesin

Cited by 152 publications

References 33 publications

Interaction of apolipoprotein AIV with cholecystokinin on the control of food intake

Interaction of apolipoprotein AIV with cholecystokinin on the control of food intake

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

Food intake in lean and obese mice after peripheral administration of glucagon-like peptide 2

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