Ghrelin is an appetite-stimulatory signal from stomach with structural resemblance to motilin

Asakawa, Akihiro; Inui, Akio; Kaga, Toshihiro; Yuzuriha, H; Nagata, Toshiaki; Ueno, Naohiko; Makino, Susumu; Fujimiya, Mineko; Niijima, Akira; Fujino, Masayuki; Kasuga, Masato

doi:10.1053/gast.2001.22158

Cited by 1,083 publications

(846 citation statements)

References 29 publications

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“…In rodents, acute injection of ghrelin, peripherally or centrally, induces a rapid orexigenic response (Asakawa et al 2001;Wren et al 2000). It was also found that chronic stimulation of this receptor by ghrelin (Tschöp et al 2000) or by synthetic growth hormone secretagogues (Lall et al 2001) increases fat mass in rodents, by a mechanism that is independent of the hypothalamo-pituituary growth axis and, unexpectedly, did not appear to involve a hyperphagic response.…”

Section: The Central Ghrelin Signalling Systemmentioning

confidence: 96%

The role of the central ghrelin system in reward from food and chemical drugs

Dickson

Egecioglu

Landgren

et al. 2011

Molecular and Cellular Endocrinology

217

168

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Here we review recent advances that identify a role for the central ghrelin signalling system in reward from both natural rewards (such as food) and artificial rewards (that include alcohol and drugs of abuse). Whereas ghrelin emerged as a stomach-derived hormone involved in energy balance, hunger and meal initiation via hypothalamic circuits, it now seems clear that it also has a role in motivated reward-driven behaviours via activation of the so-called "cholinergic-dopaminergic reward link". This reward link comprises a dopamine projection from the ventral tegmental area (VTA) to the nucleus accumbens together with a cholinergic input, arising primarily from the laterodorsal tegmental area. Ghrelin administration into the VTA or LDTg activates the "cholinergicdopaminergic" reward link, suggesting that ghrelin may increase the incentive value of motivated behaviours such as reward-seeking behaviour ("wanting" or "incentive motivation"). Further, direct injection of ghrelin into the brain ventricles or into the VTA

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Section: The Central Ghrelin Signalling Systemmentioning

confidence: 96%

The role of the central ghrelin system in reward from food and chemical drugs

Dickson

Egecioglu

Landgren

et al. 2011

Molecular and Cellular Endocrinology

217

168

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“…[1][2][3][4] Furthermore, ghrelin seems to decrease the metabolic rate and the catabolism of fat. 5,6 Therefore, biological effects of ghrelin appear to be the opposite of those of leptin, which has been suggested to be the key signal reflecting adipose stores. 2,7,8 Increasing ghrelin levels during weight reduction are considered to be responsible for compensatory mechanisms that make reduction of overweight unlikely to be sustained.…”

Section: Introductionmentioning

confidence: 99%

Ghrelin levels before and after reduction of overweight due to a low-fat high-carbohydrate diet in obese children and adolescents

et al. 2005

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BACKGROUND: There are conflicting results for ghrelin changes in reduction of overweight. Increasing ghrelin levels in weight reduction are considered to be responsible for compensatory mechanisms that make the reduction of overweight unlikely to be sustained. METHODS:We have analyzed fasting serum ghrelin levels, weighed dietary record and, as biochemical markers of clinically relevant reduction of overweight, leptin, adiponectin and insulin levels and insulin resistance measured by homeostasis model assessment (HOMA) at baseline and after a 1-y outpatient weight reduction program based on a high-carbohydrate and low-fat diet in 37 obese children (median age 10 y). We divided these children into two subgroups according to their degree of weight loss (substantial reduction of overweight: decrease in SDS-BMIZ0.5). Furthermore, we analyzed ghrelin levels in 16 normalweight children. RESULTS: Obese children demonstrated significant (Po0.001) lower ghrelin levels compared to normal-weight children. Daily caloric intake (P ¼ 0.004) and percentage fat content decreased significantly (Po0.001), while percentage carbohydrate content increased significantly (P ¼ 0.003) between baseline and 1-y follow-up in the obese children. The substantial reduction of overweight in 16 children (median SDS-BMI ¼ À0.7) was associated with significant changes in insulin resistance (median decrease of HOMA 27%; P ¼ 0.013), insulin (median decrease 25%, P ¼ 0.036), adiponectin (median increase 15%; P ¼ 0.003), and leptin levels (median decrease 19%; P ¼ 0.023), while there were no significant changes in ghrelin levels (median increase 4%; P ¼ 0.326). In the 21 children without substantial reduction of overweight (median SDS-BMI ¼ À0.3), there were no significant changes in insulin resistance and in insulin, adiponectin, leptin and ghrelin levels. CONCLUSIONS: We conclude that in obese children, low-fat high-carbohydrate diet-induced weight loss does not change ghrelin secretion, but significantly decreases leptin levels, increases adiponectin levels and improves insulin resistance determined by significantly decreased insulin resistance indices as well as lowered serum insulin levels.

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“…For example, the in vitro experiments used stomach preparations, whereas the experiments in vivo focused on the small intestine. In addition, studies in vivo suggest that ghrelin may affect gastric emptying and perhaps intestinal motility via an action within the gastric-vagal-brainstem pathway (e.g., Asakawa et al, 2001), whereas in vitro the prokinetic-like activities of ghrelin (Dass et al, 2003) and also prucalopride (Briejer et al, 2001) may be mediated predominantly via the enteric nervous system (ENS). Accordingly, it is possible that these differences in the models used and/or in the sites of action of ghrelin may explain the different effects of obestatin in vitro and in vivo.…”

mentioning

confidence: 99%

Little or no ability of obestatin to interact with ghrelin or modify motility in the rat gastrointestinal tract

Bassil

Häglund

Brown

et al. 2007

British J Pharmacology

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Background and purpose: Obestatin, encoded by the ghrelin gene may inhibit gastrointestinal (GI) motility. This activity was re-investigated. Experimental approach: Rat GI motility was studied in vitro (jejunum contractility and cholinergically-mediated contractions of forestomach evoked by electrical field stimulation; EFS) and in vivo (gastric emptying and intestinal myoelectrical activity). Ghrelin receptor function was studied using a GTPgS assay and transfected cells. Key results: Contractions of the jejunum or forestomach were unaffected by obestatin 100 nM or 0.01-1000 nM, respectively (P40.05 each; n ¼ 4-18). Obestatin (0.1-1 nM) reduced the ability of ghrelin 1 mM to facilitate EFS-evoked contractions of the stomach (increases were 42.777.8% and 21.275.0 % in the absence and presence of obestatin 1 nM; Po0.05; n ¼ 12); higher concentrations (10-1000 nM) tended to reduce the response to ghrelin but changes were not statistically significant. Similar concentrations of obestatin did not significantly reduce a facilitation of contractions caused by the 5-HT 4 receptor agonist prucalopride, although an inhibitory trend occurred at the higher concentrations (increases were 69.3714.0% and 42.678.7% in the absence and presence of 1000 nM obestatin; n ¼ 10). Obestatin (up to 10 mM) did not modulate recombinant ghrelin receptor function. Ghrelin increased gastric emptying and reduced MMC cycle time; obestatin (1000 and 30,000 pmol kg À1 min À1 ) had no effects. Obestatin (2500 pmol kg À1 min À1 , starting 10 min before ghrelin) did not prevent the ability of ghrelin (500 pmol kg À1 min À1 ) to shorten MMC cycle time. Conclusions and implications: Obestatin has little ability to modulate rat GI motility.

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Ghrelin is an appetite-stimulatory signal from stomach with structural resemblance to motilin

Cited by 1,083 publications

References 29 publications

The role of the central ghrelin system in reward from food and chemical drugs

The role of the central ghrelin system in reward from food and chemical drugs

Ghrelin levels before and after reduction of overweight due to a low-fat high-carbohydrate diet in obese children and adolescents

Little or no ability of obestatin to interact with ghrelin or modify motility in the rat gastrointestinal tract

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