Effect of Food Restriction on Ghrelin in Normal‐Cycling Female Rats and in Pregnancy

Gualillo, Oreste; Caminos, Jorge Eduardo; Nogueiras, Rubén; Seoane, Luísa M.; Arvat, E.; Ghigo, Ezio; Casanueva, Felipe F.; Diéguez, Carlos

doi:10.1038/oby.2002.92

Cited by 92 publications

(62 citation statements)

References 27 publications

(35 reference statements)

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“…Additionally, ghrelin augments cocaine-induced reward as measured by locomotor activity and conditioned place preference, and elevated ghrelin levels are associated with cocaine-seeking in rats (Davis et al 2007;Tessari et al 2007;Wellman et al 2005). Food restriction, that increases ghrelin levels (Gualillo et al 2002), augments cocaine-as well as amphetamine-induced locomotor stimulation, enhances cocaineseeking behaviour and increases the self-administration of cocaine or amphetamine in rats (Carroll et al 1979). In human genetic studies a ghrelin gene haplotype has been associated with paternal heredity of alcohol-use disorder (Landgren et al 2010) and with increased weight in alcohol dependent individuals (Landgren et al 2008).…”

Section: The Central Ghrelin Signalling System Integrates With a Key mentioning

confidence: 99%

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 System Integrates With a Key mentioning

confidence: 99%

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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“…Effect of chronic food restriction on stomach mucosa GOAT and ghrelin mRNA expression Male rats were randomly assigned on day 1 to one of two dietary groups as previously described (Gualillo et al 2002): rats fed ad libitum and a restricted group of rats fed with 30% of the amount of food that ad libitum rats ate the previous day. Male rats at different days of restriction were killed and stomach mucosa samples were collected at 8, 12, 16, and 21 days of food restriction.…”

Section: Effect Of Acute Food Restriction and Leptinmentioning

confidence: 99%

“…Plasma leptin levels were measured by RIA as previously described (Gualillo et al 2002, López et al 2008a) using reagents provided in commercial kits (Rat leptin RIA, Linco Research Inc., St Charles, MO, USA).…”

Section: Plasma Leptin Levelsmentioning

confidence: 99%

Influence of chronic undernutrition and leptin on GOAT mRNA levels in rat stomach mucosa

González¹,

Vázquez²,

López³

et al. 2008

Journal of Molecular Endocrinology

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The most unique feature of ghrelin is the acyl-modification of a hydroxyl group of the Ser3 in the N-terminus. The Ser3 is commonly modified by n-octanoic acid in vertebrates being needed for its biological effects, at least in terms of feeding. Therefore, a critical question regarding the role of ghrelin was to characterize the mechanism involved in its acylation. The acyltransferase that catalyzes ghrelin octanoylation has been recently identified and named ghrelin O-acyltransferase (GOAT). The aim of this study was to clarify the physiological implications of GOAT in the regulation of energy balance, by assessing the effect of undernutrition, as well as fasting in adult male rats. We have determined GOAT mRNA expression levels by real time-PCR in the stomach mucosa. Our results show that chronic food restriction led to an increase in GOAT mRNA, particularly following long-term chronic malnutrition (21 days). Furthermore, following 48 h complete fasting, a situation with high-circulating ghrelin levels, we found similar mRNA expression of GOAT in fed and fasted rats; exogenous leptin administration markedly increase GOAT mRNA levels in the stomach mucosa of fasted rats. These findings suggest that increased GOAT mRNA levels may have a role in mediating the physiological responses to chronic undernutrition and could represent an adaptive response to prevent long-lasting alterations in energy balance and body weight homeostasis. Furthermore, our data also offer mechanistic insights into the reason why during fasting acylated ghrelin levels are not increased at a time when a marked increase in an orexigenic signal as important as acylated ghrelin will be expected.

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“…The stomach peptide ghrelin is an endogenous ligand for the growth-hormone secretagogue receptor (Kojima et al, 1999;Tschop et al, 2000) and functions as an orexigen receptor (Ariyasu et al, 2001;Inui et al, 2004;Naleid et al, 2005;Wren et al, 2001a;Wren et al, 2001b). Plasma levels of ghrelin are elevated by FR, whereas administration of ghrelin elicits eating (Ariyasu et al, 2001;Asakawa et al, 2003;Bagnasco et al, 2003;Diano et al, 2006;Gualillo et al, 2002;Inui et al, 2004;Naleid et al, 2005;Tolle et al, 2002;Wren et al, 2001a;Wren et al, 2001b). Ghrelin can gain entry into the CNS (Banks et al, 2002;Diano et al, 2006) and ICV infusions of ghrelin can stimulate locomotion and induce dopamine overflow within the nucleus accumbens (Jerlhag et al, 2006).…”

mentioning

confidence: 99%

Systemic ghrelin sensitizes cocaine-induced hyperlocomotion in rats

Wellman

Hollas

Elliott

2008

Regulatory Peptides

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The feeding-relevant pathway by which food restriction (FR) augments cocaine action is unknown. Systemic administration of the 28-amino acid acylated peptide ghrelin (1−10 nMol) increases food intake in rats and circulating levels of rat ghrelin are up-regulated by FR. The present experiment examined the impact of repeated administration of ghrelin or vehicle on the subsequent capacity of cocaine to enhance locomotion in rats. Male Sprague-Dawley rats were pretreated daily for seven days with 0, 5 or 10 nMol rat ghrelin (i.p.) in the home cage. On the 8 th day, rats were transported to a testing room, placed in a locomotion chamber for 15 min, and then injected (i.p.) with 0, 7.5, or 15 mg/kg cocaine hydrochloride. Locomotor activity was monitored over a 45 min post-cocaine period. Pretreatment with 5 or 10 nMol ghrelin alone did not significantly increase basal locomotion relative to that of the 0 nMol ghrelin group. Rats pretreated with 5 nMol or 10 nMol ghrelin showed an enhanced locomotor response after treatment with 15 mg/kg cocaine relative to rats treated with 0 nMol ghrelin. These results indicate that acute injection of ghrelin, at a feeding-relevant dose, can augment the acute effects of cocaine on locomotion in rats. KeywordsFood deprivation; Locomotion; Growth Hormone Food restriction (FR) is known to augment the locomotor actions of psychostimulant drugs such as cocaine or amphetamine (Bell et al., 1997;Campbell and Carroll, 2001;Carr, 2002;Carroll and Meisch, 1980, 1981). Additionally, FR acts to facilitate the acquisition of cocaine or amphetamine self-administration (Carroll, 1985) and augments the acquisition of cocaineinduced conditioned place preference (Bell et al., 1997). When animals already trained to selfadminister cocaine are deprived of food, their daily drug intake increases and FR can facilitate the reinstatement of cocaine-seeking behavior (Carroll, 1985). Conversely, food satiation can delay the acquisition of cocaine self-administration (Carroll and Lac, 1998). These findings suggest that feeding and drug addiction may share common pathways (DiLeone et al., 2003).The neural substrate through which the hyperlocomotor and reinforcing actions of drugs such as cocaine or amphetamine are enhanced by FR remains unknown (Carr, 2002). The stomach peptide ghrelin is an endogenous ligand for the growth-hormone secretagogue receptor (Kojima et al., 1999;Tschop et al., 2000) and functions as an orexigen receptor (Ariyasu et al. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Inui et al., 2004;Naleid et al., 2005;Wren et al., 2001a;Wren et al.,...

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Effect of Food Restriction on Ghrelin in Normal‐Cycling Female Rats and in Pregnancy

Cited by 92 publications

References 27 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

Influence of chronic undernutrition and leptin on GOAT mRNA levels in rat stomach mucosa

Systemic ghrelin sensitizes cocaine-induced hyperlocomotion in rats

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