Increased Circulating Leptin Levels in Chronic Alcoholism

Nicolás, Josep M.; Fernández‐Solà, Joaquim; Fatjó, Francesc; Casamitjana, Roser; Bataller, Ramón; Sacanella, Emilio; Tobías, Ester; Badı́a, Eva; Estruch, Ramón

doi:10.1111/j.1530-0277.2001.tb02130.x

Cited by 126 publications

(87 citation statements)

References 25 publications

(34 reference statements)

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“…5,29 We recently reported evidence that this CAG trinucleotide repeat in the coding region of the androgen receptor is Figure 2 CAG repeat length (short (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18), intermediate (19)(20)(21)(22)(23) and long (24)(25)(26)(27)(28)(29)(30)(31)(32) and Obsessive Compulsive Drinking Scale-total (OCDS-to). One-way analysis of variance and post hoc analysis (Bonferroni) revealed significant differences between the groups (F ¼ 3.312, P ¼ 0.040), 'short' versus 'long' (P ¼ 0.034).…”

Section: Discussionmentioning

confidence: 99%

“…It is clear that it is especially involved in glucose metabolism, as well as in normal sexual maturation and reproduction. 10 Its plasma levels are elevated during chronic alcohol consumption, 11 normalize after cessation of drinking 12 and are associated with craving in alcohol withdrawal, which has been shown by multiple studies. [13][14][15][16] Thus, the aim of this study was to further elucidate whether leptin mediates the effect of the mentioned polymorphism on craving in men undergoing alcohol withdrawal.…”

Section: Introductionmentioning

confidence: 99%

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The modulating effect of the androgen receptor on craving in alcohol withdrawal of men is partially mediated by leptin

et al. 2009

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We reported recently that a functional relevant CAG trinucleotide repeat of the androgen receptor influences craving of men in alcohol withdrawal. It is known to modulate serum concentrations of leptin, which affects hypothalamic appetite regulation. Its plasma levels are elevated during chronic alcohol consumption, normalize within periods of abstinence and are associated with craving. The aim of this study was to further elucidate the role of leptin in mediating the effects of the mentioned polymorphism on craving in men undergoing alcohol withdrawal. We included 110 male in-patients who were admitted for detoxification treatment. Each one had an established diagnosis of alcohol dependence according to the DSM-IV. Our results show on the one hand negative associations between the number of CAG repeats and (i) leptin serum levels (Po0.01) and (ii) craving (Po0.05), and on the other hand, a positive association between leptin and craving of man in alcohol withdrawal (Po0.001). The path analysis revealed direct and mediated effects of the number of CAG repeats on alcohol craving, direct effects (r ¼ À0.144) accounting for 60% and indirect, leptin-mediated effects (r ¼ À0.096) accounting for 40% of the total effect. Dysregulation of sexual hormones influences human metabolism and seems to affect leptin homeostasis. This report suggests that the investigated polymorphism mediates its effect on craving of men in alcohol withdrawal mostly through the regulation of leptin. Nevertheless future studies are needed to further explore the functionality of the androgen receptor gene in terms of craving.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The modulating effect of the androgen receptor on craving in alcohol withdrawal of men is partially mediated by leptin

et al. 2009

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“…The results appear to be in agreement with a previous report that circulating leptin levels are increased in chronic alcoholism regardless of nutritional status or the presence of liver disease. 30 Ethanol-induced hyperhomocysteinemia has been proposed to play a role in alcoholic liver injury. 31,32 As shown in Fig.…”

Section: A Hsf Diet Attenuated Hepatic Steatosis and Reversed Alaninementioning

confidence: 99%

Role of adiponectin in the protective action of dietary saturated fat against alcoholic fatty liver in mice

et al. 2005

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The protective effect of dietary saturated fatty acids against the development of alcoholic liver disease has long been known, but the underlying mechanism is not completely understood. We examined the involvement of the adipocyte hormone adiponectin. Circulating adiponectin levels were significantly elevated by chronic ethanol administration to mice consuming a diet high in saturated fat. The increase in circulating adiponectin was associated with the activation a set of hepatic signaling pathways mediated through AMP-activated protein kinase, PPAR-␣, and PPAR-␥ coactivator ␣, which in turn led to markedly increased rates of fatty acid oxidation, prevention of hepatic steatosis, and alleviation of liver enzyme changes. Furthermore, treatment of rat 3T3-L1 adipocytes with saturated fatty acids (palmitic or stearic acids) in the presence of ethanol increased secretion of adiponectin and enhanced activity of a mouse adiponectin promoter. In conclusion, the protective action of saturated fat against the development of alcoholic fatty liver in mice is partially mediated through induction of adiponectin. The present findings suggest a novel paradigm for dietary fatty acids in the pathogenesis of alcoholic liver disease and provide a promising therapeutic strategy-nutritional modulation of adiponectin-in treating human alcoholic fatty liver disease. (HEPATOLOGY 2005;42:568 -577.)

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“…In the population of low-tomoderate alcohol drinkers considered in the present study, the degree of hyperinsulinemia/insulin resistance increases across categories of LS in men after controlling for body composition variables and other risk factors for hepatic fat accretion, but this relationship appears to be mediated by increased serum concentrations of leptin. Serum leptin has been reported to increase with alcohol consumption in a dose-dependent manner (32), and to correlate with the degree of LS in subjects with normal transaminase levels, in NASH and in chronic hepatitis C, but not with transaminase concentrations, inflammation or fibrosis (4, 7, 32 -35). This suggests that hyperleptinemia and leptin resistance may be involved in the first steps of the pathogenesis of LS, but not necessarily on its progression to steatohepatitis.…”

Section: Relationship Among Leptin Insulin and Lsmentioning

confidence: 99%

Relationship between leptin, insulin, body composition and liver steatosis in non-diabetic moderate drinkers with normal transaminase levels

Valtueña¹,

Numeroso²,

Ardigò³

et al. 2005

eur j endocrinol

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Objective: Obesity and insulin resistance play a major role in the development of liver steatosis (LS), but also relative leptin resistance has been reported to correlate with LS in humans. Our objective was to investigate the relationship between serum leptin, insulin, obesity and LS in non-diabetic males (n ¼ 74) and postmenopausal females (n ¼ 50) with normal transaminase levels and low-tomoderate alcohol intake. Methods: A medical history to retrieve information about health status, current medications, alcohol consumption and history of viral or toxic hepatitis; a physical examination including height, weight, waist circumference and blood pressure; a fasting blood draw for the determination of glucose, insulin, leptin, lipid profile, transaminases and uric acid; an oral glucose tolerance test to exclude type 2 diabetes; a dual-energy X-ray absorptiometry scan to assess fat mass (FM) and lean body mass (LBM), and an echography of the liver to assess LS. Results: Fasting leptin and insulin were highly correlated with FM in men (R ¼ 0.767 and R ¼ 0.495 respectively, P , 0.001) and women (R ¼ 0.713 and R ¼ 0.526 respectively, P , 0.001). After correction for FM, leptin showed a significant negative correlation with LBM in men (R ¼ 2 0.240, P ¼ 0.039), but not in women (R ¼ 2 0.214, P ¼ 0.132). The positive relationship observed between leptin, insulin and LS persisted after adjustment of leptin and insulin for body composition only in men (R ¼ 0.415, P , 0.001 and R ¼ 0.339, P ¼ 0.003 respectively for leptin and insulin vs LS). Adjusted means (95% confidence intervals) of leptin increased significantly across categories of LS in men even when insulin was considered in the model (absent ¼ 7.1 ng/ml (5.6-8.5), mild ¼ 8.2 ng/ml (7.2 -9.2), moderate/severe ¼ 12.1 ng/ml (10.3 -14.0); P , 0.001), whereas no significant relationship was observed between insulin and LS after leptin was accounted for. Conclusion: Serum concentrations of leptin and insulin are positively correlated in men independently of body composition, but not in postmenopausal women. In men, the steatogenic effect of hyperinsulinemia/insulin resistance in the context of low-to-moderate alcohol consumption appears to be mediated by high concentrations of serum leptin, whereas body fat alone could identify postmenopausal women at high risk for LS. European Journal of Endocrinology 153 283-290

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Increased Circulating Leptin Levels in Chronic Alcoholism

Abstract: Circulating leptin levels are increased in a dose-dependent manner in chronic alcoholism, regardless of nutritional status or the presence of compensated liver disease.

Cited by 126 publications

References 25 publications

The modulating effect of the androgen receptor on craving in alcohol withdrawal of men is partially mediated by leptin

The modulating effect of the androgen receptor on craving in alcohol withdrawal of men is partially mediated by leptin

Role of adiponectin in the protective action of dietary saturated fat against alcoholic fatty liver in mice

Relationship between leptin, insulin, body composition and liver steatosis in non-diabetic moderate drinkers with normal transaminase levels

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