RETRACTED: Obestatin reduces food intake and suppresses body weight gain in rodents

Lagaud, Guy; Young, Andy; Acena, Auzon; Morton, Magda F.; Barrett, Terrance D.; Shankley, Nigel P.

doi:10.1016/j.bbrc.2007.03.138

Cited by 103 publications

(61 citation statements)

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“…All in all, data concerning obestatin's influence on feeding behavior when injected peripherally are conflicting. There are four studies describing a significant inhibitory effect on food intake [7,18,27,51], three investigations showing a non-significant trend towards a reduction [21,40,42], and seven reports of no effect on feeding behavior after obestatin administration [11,14,15,32,41,54, and present study]. The results of these studies seem to be independent from the investigated species (mice or rats), the metabolic status (fasted or fed ad libitum) and the route of delivery (ip, intravenous, intracerebroventricular and intracisternal) [16 and present study].…”

Section: Discussionmentioning

confidence: 99%

“…However, several recent studies performed in rats and mice under various experimental conditions showed that obestatin injected intraperitoneally (ip) has no inhibitory effect on short-term food intake [11,[14][15][16][17]21,32,41,54] and body weight gain [32,42]. The responsiveness to exogenous obestatin could be influenced by circadian rhythm and might account for the varying effects of peripheral obestatin on food intake found in recent studies [7,15,18,21,27,32,[40][41][42]51,54].…”

Section: Introductionmentioning

confidence: 99%

“…Ghrelin, a 28-amino acid peptide [10,26] is a well-characterized hormone that stimulates food intake in rodents [1,30,43,47,49,50] and humans [48]. In contrast to ghrelin, obestatin has been initially reported to elicit anorexigenic effects in mice and rats after peripheral or intracerebroventricular injection [7,18,27,51]. Furthermore, chronic administration of obestatin reduces body weight gain in mice [27,51].…”

Section: Introductionmentioning

confidence: 99%

“…In contrast to ghrelin, obestatin has been initially reported to elicit anorexigenic effects in mice and rats after peripheral or intracerebroventricular injection [7,18,27,51]. Furthermore, chronic administration of obestatin reduces body weight gain in mice [27,51]. These findings suggest that obestatin may be involved in the regulation of energy homeostasis in rodents.…”

Section: Introductionmentioning

confidence: 99%

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Peripheral obestatin has no effect on feeding behavior and brain Fos expression in rodents

et al. 2008

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Obestatin is produced in the stomach from proghrelin by post-translational cleavage. The initial report claimed anorexigenic effects of obestatin in mice. Contrasting studies indicated no effect of obestatin on food intake (FI). We investigated influences of metabolic state (fed/fasted), environmental factors (dark/light phase) and brain Fos response to intraperitoneal (ip) obestatin in rats, and used the protocol from the original study assessing obestatin effects in mice. FI was determined in male rats injected ip before onset of dark or light phase, with obestatin (1 or 5 μmol/kg), CCK8S (3.5 nmol/kg) or 0.15 M NaCl, after fasting (16 h, n = 8/group) or ad libitum (n = 10-14/group) food intake. Fos expression in hypothalamic and brainstem nuclei was examined in freely fed rats 90 min after obestatin (5 μmol/kg), CCK8S (1.75 nmol/kg) or 0.15 M NaCl (n = 4/group). Additionally, fasted mice were injected ip with obestatin (1 μmol/kg) or urocortin 1 (2 nmol/kg) 15 min before food presentation. No effect on FI was observed after obestatin administration during the light and dark phase under both metabolic conditions while CCK8S reduced FI irrespectively of the conditions. The number of Fos positive neurons was not modified by obestatin while CCK8S increased Fos expression in selective brain nuclei. Obestatin did not influence the refeeding response to a fast in mice, while urocortin was effective. Therefore, peripheral obestatin has no effect on FI under various experimental conditions and did not induce Fos in relevant central neuronal circuitries modulating feeding in rodents.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Peripheral obestatin has no effect on feeding behavior and brain Fos expression in rodents

et al. 2008

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“…Obestatin derived from the same polypeptide precursor as ghrelin, but which rather suppresses food intake [11], also appears to enhance learning and memory and, in addition, produces an anxiolytic effect as indicated by increased percentage of open arm entries in the elevated plus maze [12]. There is also a considerable literature showing that leptin can modulate excitability of hippocampal neurons (as reviewed by [13].…”

Section: Mnemonic Representations Of Experience With Foodmentioning

confidence: 99%

Eating for pleasure or calories

Zheng

Berthoud

2007

Current Opinion in Pharmacology

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A changing environment and lifestyle on the background of evolutionary engraved or perinatally imprinted physiological response patterns is the foremost explanation for the current obesity epidemic. However, it is not clear what the mechanisms are by which the modern environment overrides the physiological controls of appetite and homeostatic body weight regulation. Major advances have been made regarding cross talk between metabolic signals and the cognitive/emotional brain that primarily deals with the environment. On one hand, metabolic signals such as leptin and ghrelin have previously unexpected direct effects on learning and memory, as well as liking and wanting. On the other hand, brain areas involved in reward, cognition, and executive control, can override metabolic regulation by talking to the hypothalamus.

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Obestatin in human neuroendocrine tissues and tumours: expression and effect on tumour growth

Volante

Rosas

Ceppi

et al. 2009

The Journal of Pathology

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The hormone obestatin, which is derived from the same precursor as ghrelin and whose receptor(s) is still unrecognized, possesses a variety of metabolic/modulatory functions mostly related to food intake suppression and reduction of gastrointestinal motility. The distribution of obestatin in normal and neoplastic human tissues is poorly understood. We report that in fetal tissue samples, obestatin peptide was detected in the thyroid, pituitary, lung, pancreas and gastrointestinal tract, usually being co-localized with chromogranin A. In adult tissues, obestatin protein expression was restricted to pituitary, lung, pancreas and gastrointestinal tract and was co-localized strictly with ghrelin. By contrast, in endocrine tumours obestatin was expressed in a small fraction of thyroid, parathyroid, gastrointestinal and pancreatic neoplasms, in most cases with a focal immunoreactivity and co-localized with ghrelin. Messenger RNA levels of the specific fragments of ghrelin and obestatin were comparable in both normal and tumour samples, confirming that post-translational mechanisms rather than alternative splicing events lead to ghrelin/obestatin production. Finally, in TT and BON-1 cell lines obestatin induced antiproliferative effects at pharmacological doses, opposite to those observed with ghrelin. In summary, our data demonstrate that obestatin is produced by the same endocrine cells that express ghrelin in normal tissues from fetal to adult life, whereas, as compared to ghrelin, in neoplastic conditions it is down-regulated by post-translational modulation and shows potential antiproliferative properties in vitro.

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RETRACTED: Obestatin reduces food intake and suppresses body weight gain in rodents

Cited by 103 publications

References 0 publications

Peripheral obestatin has no effect on feeding behavior and brain Fos expression in rodents

Peripheral obestatin has no effect on feeding behavior and brain Fos expression in rodents

Eating for pleasure or calories

Obestatin in human neuroendocrine tissues and tumours: expression and effect on tumour growth

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