Abstract
Increasing evidence supports the role of appetite-regulating pathways, including ghrelin and leptin, in alcoholism. This study tested the hypothesis that intravenous exogenous ghrelin administration acutely decreases endogenous serum leptin levels, and that changes in leptin levels negatively correlate with alcohol craving. This was a double-blind, placebo-controlled human laboratory study. Non-treatment-seeking, alcohol-dependent, heavy drinkers (n=45) were randomized to receive intravenous ghrelin or placebo, followed by a cue-reactivity procedure, during which participants were exposed to neutral (juice) and alcohol trial cues. There was a main effect for intravenous ghrelin administration, compared with placebo, in reducing serum leptin levels (P<0.01). Post hoc analysis showed significant differences in serum leptin levels at the alcohol trial (P<0.05) that persisted at the end of the experiment (P<0.05). By contrast, there were no significant differences in serum leptin levels at the juice trial (P=not significant (NS)). The change of serum leptin level at the alcohol trial correlated with the increase in alcohol urge (P<0.05), whereas urge to drink juice was not correlated with the leptin change at the juice trial (P=NS). These findings provide preliminary evidence of ghrelin–leptin cross-talk in alcoholic individuals and suggest that their relationship may have a role in alcohol craving.
Highlights
Alcohol dependence (AD) is a leading cause of preventable morbidity and mortality worldwide.[1,2] Medications currently approved by the Food and Drug Administration to treat AD exhibit limited efficacy.[3]
Consistent with our hypotheses, the main findings of this analysis were that intravenous ghrelin administration significantly decreased serum leptin levels, and ghrelin-induced changes in leptin levels significantly negatively correlated with increased alcohol craving in AD heavy drinkers
We believe this is the first study in which the effects of exogenous intravenous ghrelin administration on endogenous serum leptin levels were assessed in the context of alcohol craving studied in AD individuals
Summary
Alcohol dependence (AD) is a leading cause of preventable morbidity and mortality worldwide.[1,2] Medications currently approved by the Food and Drug Administration to treat AD exhibit limited efficacy.[3]. A longitudinal clinical study revealed a positive correlation between blood ghrelin levels and both alcohol craving and risk of relapse in AD patients.[9] More recent clinical research indicated that intravenous administration of exogenous ghrelin acutely increased cue-induced alcohol craving in heavy-drinking AD individuals.[10]. Serum leptin levels were found to be elevated in AD individuals and associated with increased craving for alcohol.[11,12] in AD patients, treatment with naltrexone and/or acamprosate was associated with lower leptin levels, suggesting leptin may serve as a possible biomarker for medication response.[13] Two other peripherally secreted adipose hormones are resistin, a 108-aa protein produced in the stromal vascular fraction of adipose tissue and peripheral blood monocytes[14] and visfatin, a 491-aa peptide produced by the visceral adipose tissue.[15] Leptin, resistin and visfatin may have important roles in metabolism and energy balance in several endocrine disorders
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