Central administration of ghrelin preferentially enhances fat ingestion

Shimbara, Takuya; Mondal, Muhtashan S.; Kawagoe, Takashi; Koji, Takehiko; Koda, Shuichi; Yamaguchi, Hideki; Date, Yukari; Nakazato, Masamitsu

doi:10.1016/j.neulet.2004.07.060

Cited by 111 publications

(77 citation statements)

References 27 publications

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“…These findings suggest an obligatory role for ghrelin in caloric restrictionassociated food-reward behaviors. Supporting these findings, ghrelin injection preferentially enhances fat intake over carbohydrate intake in rats (22). Ghrelin administration increases consumption of palatable saccharin solution and increases preference for saccharin-flavored foods in wild-type mice but not GHSR-deficient mice (19).…”

Section: Introductionmentioning

confidence: 66%

“…We also have assessed the relationship of stress-induced food-reward behavior to elevations in circulating levels of the peptide hormone ghrelin, because of the aforementioned studies demonstrating rises in ghrelin after various forms of stress, including CSDS (26,31), and ghrelin-enhanced preference for, place preference for, and operant responding for pleasurable, energy-dense foods (19)(20)(21)(22). We demonstrate that CSDS in mice increases both CPP for and intake of HFD.…”

Section: Introductionmentioning

confidence: 92%

“…Ghrelin's roles in promoting food intake and positive energy balance in response to caloric restriction have been documented in numerous studies (16)(17)(18). The mechanisms by which ghrelin promotes food intake are multifaceted and include enhancing the rewarding properties of certain foods (19)(20)(21)(22)(23)(24). For instance, conditioned place preference (CPP) for HFD, in which an animal will gravitate toward a chamber with environmental cues it has associated with a HFD reward, and operant nose poking for HFD, in which a motivated animal will exert increased effort (by poking a button with its nose) to receive a HFD reward, are induced in mice by peripheral ghrelin injection and prolonged caloric restriction, both of which increase plasma ghrelin (21,23).…”

Section: Introductionmentioning

confidence: 99%

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Ghrelin mediates stress-induced food-reward behavior in mice

Chuang¹,

Perelló²,

Sakata³

et al. 2011

J. Clin. Invest.

313

344

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The popular media and personal anecdotes are rich with examples of stress-induced eating of calorically dense "comfort foods." Such behavioral reactions likely contribute to the increased prevalence of obesity in humans experiencing chronic stress or atypical depression. However, the molecular substrates and neurocircuits controlling the complex behaviors responsible for stress-based eating remain mostly unknown, and few animal models have been described for probing the mechanisms orchestrating this response. Here, we describe a system in which food-reward behavior, assessed using a conditioned place preference (CPP) task, is monitored in mice after exposure to chronic social defeat stress (CSDS), a model of prolonged psychosocial stress, featuring aspects of major depression and posttraumatic stress disorder. Under this regime, CSDS increased both CPP for and intake of high-fat diet, and stress-induced food-reward behavior was dependent on signaling by the peptide hormone ghrelin. Also, signaling specifically in catecholaminergic neurons mediated not only ghrelin's orexigenic, antidepressant-like, and food-reward behavioral effects, but also was sufficient to mediate stress-induced food-reward behavior. Thus, this mouse model has allowed us to ascribe a role for ghrelin-engaged catecholaminergic neurons in stress-induced eating. IntroductionMost humans experience altered feeding behaviors upon stress, with approximately 40% eating more and 40% eating less than usual (1). Furthermore, upon stress, most people report an increase in the intake of highly palatable foods, independent of hyperphagia or hypophagia (2, 3). Altered eating is also a frequent finding in individuals with major depressive disorder, with the "atypical" subtype even containing hyperphagia as a possible distinguishing characteristic (4). In one study, 46% of study subjects who met DSM-IV criteria for major depressive disorder with atypical features reported increased appetite (5). Of the remaining depressed patients without atypical features, 18% reported increased appetite, while 50% reported decreased appetite (5). The complex eating behaviors that are associated with and/or stimulated by stress and major depression undoubtedly contribute to the increased number of overweight and obese individuals who experience or have experienced stress and depression. For example, a longitudinal study from New Zealand showed that major depression in late-adolescent girls was associated with a 2.3-fold increased risk of obesity in adulthood and, furthermore, that the prevalence of obesity in adulthood was positively correlated with the number of major depressive episodes during adolescence in these girls (6). In another study, 47% of a large cohort of subjects with atypical depression reported increased body weight (5). Also, the combined overweight and obesity prevalence in a sample of US veterans with posttraumatic stress disorder was found in a chart review study to exceed that within the US general population by 20% (7).

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Section: Introductionmentioning

confidence: 66%

Section: Introductionmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Ghrelin mediates stress-induced food-reward behavior in mice

Chuang¹,

Perelló²,

Sakata³

et al. 2011

J. Clin. Invest.

313

344

View full text Add to dashboard Cite

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“…Long-term ghrelin administration promotes weight gain, not only by stimulating food intake, but also by regulating other aspects of energy homeostasis. Indeed, ghrelin increases the preference for dietary fat [129] and directly promotes adipogenesis [144]. It can also decrease lipolysis [104], adipocyte apoptosis [76], energy expenditure and sympathetic nervous system activity [159], body temperature [148], proinflammatory cytokine production [41] and locomotor activity [141].…”

Section: Appetite and Body Weightmentioning

confidence: 99%

Ghrelin, des-acyl ghrelin and obestatin: Three pieces of the same puzzle

2008

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a b s t r a c tThe major active product of ghrelin gene is a 28-amino acid peptide acylated at the serine 3 position with an octanoyl group, called simply ghrelin. Ghrelin has a multiplicity of physiological functions, affecting GH release, food intake, energy and glucose homeostasis, This suggests the existence of a novel endocrine system with multiple effector elements which not only may have opposite actions but may regulate the action of each other. In this review, we summarize the steps which lead to the production of the different ghrelin gene products and examine the most significant differences between them in terms of structure and actions.

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“…Exogenous infusions of ghrelin or GHSR agonists similarly increase eating and, in addition, lower energy expenditure and upregulate the expression of lipogenic and fat storage-promoting enzymes (5,(14)(15)(16)(17). Ghrelin also shifts food preference toward high-fat diets (HFDs), shifts fuel preference away from metabolic utilization of fat, and engages several food reward behaviors (5,13,18,19). Collectively, these actions are likely contributors to the ability of administered ghrelin to increase BW in normal subjects and maintain BW or delay weight loss in cachectic subjects (5,15,17,20).…”

Section: Introductionmentioning

confidence: 99%