Article

Lack of interaction between peripheral injection of CCK and obestatin in the regulation of gastric satiety signaling in rodents.

CURE/Digestive Diseases Research Center, Department of Medicine, Division of Digestive Diseases, University of California Los Angeles, VA Greater Los Angeles Healthcare System, Los Angeles, CA, USA.
Peptides (impact factor: 2.43). 12/2006; 27(11):2811-9. DOI:10.1016/j.peptides.2006.07.012 pp.2811-9
Source: PubMed

ABSTRACT Obestatin is a new peptide for which anorexigenic effects were recently reported in mice. We investigate whether peripheral injection of obestatin or co-injection with cholecystokinin (CCK) can modulate food intake, gastric motor function (intragastric pressure and emptying) and gastric vagal afferent activity in rodents. Obestatin (30, 100 and 300 microg/kg, i.p.) did not influence cumulative food intake for the 2h post-injection in rats or mice nor gastric emptying in rats. In rats, obestatin (300 microg/kg) did not modify CCK (1 microg/kg, i.p.)-induced significant decrease in food intake (36.6%) and gastric emptying (31.0%). Furthermore, while rats injected with CCK (0.3 microg/kg, i.v.) displayed gastric relaxation, no change in gastric intraluminal pressure was elicited by obestatin (300 microg/kg, i.v.) pre- or post-CCK administration. In in vitro rat gastric vagal afferent preparations, 20 units that had non-significant changes in basal activity after obestatin at 30 microg responded to CCK at 10 ng by a 182% increase. These data show that obestatin neither influences cumulative food intake, gastric motility or vagal afferent activity nor CCK-induced satiety signaling.

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    Article: Direct and indirect effects of obestatin peptides on food intake and the regulation of glucose homeostasis and insulin secretion in mice.
    B D Green, N Irwin, P R Flatt
    [show abstract] [hide abstract]
    ABSTRACT: Obestatin is a recently discovered peptide hormone that appears to be involved in reducing food intake, gut motility and body weight. Obestatin is a product of the preproghrelin gene and appears to oppose several physiological actions of ghrelin. This study investigated the acute effects of obestatin (1-23) and the truncated form, obestatin (11-23), on feeding activity, glucose homeostasis or insulin secretion. Mice received either intraperitoneal obestatin (1-23) or (11-23) (1 micromol/kg) 4h prior to an allowed 15 min period of feeding. Glucose excursions and insulin responses were lowered by 64-77% and 39-41%, respectively, compared with saline controls. However this was accompanied by 43% and 53% reductions in food intake, respectively. The effects of obestatin peptides were examined under either basal or glucose (18 mmol/kg) challenge conditions to establish whether effects were independent of changes in feeding. No alterations in plasma glucose or insulin responses were observed. In addition, obestatin peptides had no effect on insulin sensitivity as revealed by hypoglycaemic response when co-administered with insulin. Our observations support a role for obestatin in regulating metabolism through changes of appetite, but indicate no direct actions on glucose homeostasis or insulin secretion.
    Peptides 06/2007; 28(5):981-7. · 2.43 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.

Keywords

1 microg/kg
 
2h post-injection
 
30 microg
 
anorexigenic effects
 
basal activity
 
CCK-induced satiety signaling
 
cholecystokinin
 
food intake
 
gastric intraluminal pressure
 
gastric motor function
 
gastric relaxation
 
gastric vagal afferent activity
 
i.p.)-induced significant decrease
 
influences cumulative food intake
 
intragastric pressure
 
non-significant changes
 
obestatin
 
peripheral injection
 
post-CCK administration
 
vagal afferent activity