Rojdmark S. Inhibitory effect of alcohol on ghrelin secretion in normal man

Department of Endocrinology, Metabolism and Diabetology, Karolinska University Hospital, Stockholm, Sweden.
European Journal of Endocrinology (Impact Factor: 4.07). 06/2005; 152(5):743-7. DOI: 10.1530/eje.1.01905
Source: PubMed


Human appetite is stimulated by alcohol but the underlying mechanism is unknown. It is possible that hunger-stimulating hormones are mediators of this effect of alcohol. Ghrelin stimulates hunger, but how alcohol affects human ghrelin secretion has never been studied before.
To investigate whether alcohol ingestion exerts an acute influence on serum ghrelin concentrations in healthy subjects.
Eight healthy non-obese subjects participated in the study. All were investigated on two occasions (experiments A and B). Alcohol (0.55 g ethanol/kg body weight) was ingested in experiment A, and drinking-water in experiment B. Venous blood was collected before, and 30 and 60 min after consumption of the drinks. Serum concentrations of ghrelin, cortisol and ethanol were determined and neuropeptide Y (NPY) concentrations were determined in plasma.
Alcohol lowered the ghrelin level by 13.9+/-5.0% at 30 min and by 17.5+/-2.6% at 60 min, in contrast to drinking-water which was without significant effect. Serum levels of cortisol and insulin were similar after alcohol and water as was plasma NPY.
Alcohol has an acute inhibitory influence on human ghrelin secretion but no measurable effect on the secretion of NPY and cortisol. Hence, none of these hormones mediate the orexigenic effect of the drug.

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Available from: Kerstin Brismar, Mar 18, 2014
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    • "Studies showing alterations in plasma levels of ghrelin in patients with alcohol dependence as well as in high- and low-alcohol preferring rats support a role for ghrelin signaling in alcohol mediated behaviors. Initially it was shown that acute oral alcohol intake reduces the secretion of ghrelin in healthy volunteers [69–71]. Interestingly, the reduction of ghrelin by acute oral alcohol intake is not affected by gastroprotective sucralfate, implying that the appetite-stimulating effect of alcohol is not mediated by ghrelin [72]. "
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    ABSTRACT: Food intake and appetite are regulated by various circulating hormones including ghrelin and glucagon-like-peptide 1 (GLP-1). Ghrelin, mainly released from the stomach, increases food intake, induces appetite, enhances adiposity as well as releases growth hormone. Hypothalamic "ghrelin receptors" (GHS-R1A) have a critical role in food intake regulation, but GHS-R1A are also expressed in reward related areas. GLP-1 is produced in the intestinal mucosa as well as in the hindbrain in response to nutrient ingestion. This gut-brain hormone reduces food intake as well as regulates glucose homeostasis, foremost via GLP-1 receptors in hypothalamus and brain stem. However, GLP-1 receptors are expressed in areas intimately associated with reward regulation. Given that regulation of food and drug intake share common neurobiological substrates, the possibility that ghrelin and GLP-1 play an important role in reward regulation should be considered. Indeed, this leading article describes that the orexigenic peptide ghrelin activates the cholinergic-dopaminergic reward link, an important part of the reward systems in the brain associated with reinforcement and thereby increases the incentive salience for motivated behaviors via this system. We also review the role of ghrelin signaling for reward induced by alcohol and addictive drugs from a preclinical, clinical and human genetic perspective. In addition, the recent findings showing that GLP-1 controls reward induced by alcohol, amphetamine, cocaine and nicotine in rodents are overviewed herein. Finally, the role of several other appetite regulatory hormones for reward and addiction is briefly discussed. Collectively, these data suggest that ghrelin and GLP-1 receptors may be novel targets for development of pharmacological treatments of alcohol and drug dependence.
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    • "In summary, human laboratory studies conducted with rigorous experimental designs and under well-controlled conditions have consistently shown that oral administration of alcohol results in reduced circulating ghrelin. These studies have all examined changes in ghrelin levels after an oral alcohol administration (Calissendorff et al., 2005, 2006, 2012; Zimmermann et al., 2007). Given that ghrelin is primarily produced in the stomach (Inui et al., 2004), an additional question never explored is whether bypassing the gastrointestinal tract by using alcohol administered intravenously (IV) has the same inhibitory effect on ghrelin levels. "
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    ABSTRACT: Ghrelin is a 28-amino acid peptide produced mainly by mucosal neuroendocrine cells lining the fundus of the stomach. Preclinical and clinical studies suggest that ghrelin plays a role in alcoholism. Furthermore, human laboratory studies indicate that acute oral administration of alcohol results in reduced circulating ghrelin. As ghrelin is primarily produced in the stomach, one question never previously explored is whether alcohol administered intravenously (IV) results in similar decrease in ghrelin levels. Thus, this study analyzed the potential effects of IV alcohol administration on plasma ghrelin levels in healthy nonsmoking social drinkers (n=44) who received either a 180-min IV infusion of 6% (v/v) alcohol or 0.9% normal saline in two separate counterbalanced sessions. At each session, participants arrived having fasted for ∼7h and received a light breakfast 60min before the infusion. The percent change (%Δ) in ghrelin levels was 4.5-fold less in the alcohol condition than the saline condition. In fact, there was only a modest change in ghrelin levels from baseline in the IV alcohol condition (9.6%Δghrelin) while in the IV saline condition there was a robust change (43.4%Δghrelin). There was a trend toward significance in %Δghrelin in the alcohol condition compared to the placebo condition (F[1,33]=3.3, p=0.07). While the exact mechanisms by which alcohol influences ghrelin levels are unclear, alcohol may act directly in the stomach by inhibiting ghrelin secretion and/or release, and may also attenuate ghrelin levels systemically. Although IV alcohol did not reduce circulating ghrelin levels, as seen in previous studies with oral alcohol administration, the present findings suggest that, despite bypassing the stomach, alcohol still attenuated circulating ghrelin levels, i.e. the fasting-induced increase in circulating ghrelin was blunted by IV alcohol administration. These findings lead us to hypothesize that alcohol might affect ghrelin signaling not only via a local effect on the stomach mucosa, but also via a systemic effect.
    Full-text · Article · Sep 2013 · Psychoneuroendocrinology
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    • "The aetiology of the metabolic syndrome is complex, determined by the interplay of both genetic and environmental factors (Ala et al, 2009). Alcohol is a significant source of calories, with its inherent properties as well as by stimulating appetite (Calissendorff et al., 2005) and greater consumption of fatty products (cheese, meat) in drinkers. An association between alcohol consumption and a greater waist circumference has been consistently reported (Buja et al., 2010). "
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    ABSTRACT: Background: Substance abuse, alcohol in particular, is associated with increased risk of diabetes and metabolic syndrome (MS). The relationship between the substance abuse and MS is complex and the literature is sparse. Objective: The present research was aimed to study the prevalence and predictors of MS among inpatients with substance dependence. Method: The study was conducted in tertiary care centre in North India, in which all consecutive patients with substance dependence were recruited, who were admitted from 1st January, 2011 to 31st December, 2011. MS was assessed using International Diabetes Federation (IDF) and Modified NCEP ATP-III criteria. Results: Out of 256 subjects, 24 (9.4%) subjects met the IDF criteria and 28 (10.9%) subjects met the modified NCEP criteria for MS with higher prevalence of MS in patients with alcohol and opioid dependence (26.7%) compared to alcohol (13.1%) or opioid dependence (9.6%). The commonest abnormalities were increased triglycerides (37.5%) and increased blood pressure (33.6%). On regression analysis, body mass index was found to be the most significant predictor for the development of MS. Conclusions: MS was highest in subjects with alcohol and opioid dependence with the commonest abnormality of triglyceride and blood pressure. Hence routine screening is advisable in this population to address emerging MS.
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