Impact of Alcohol on Glycemic Control and Insulin Action

Steiner, Jennifer L.; Crowell, Kristen T.; Lang, Charles H.

doi:10.3390/biom5042223

Cited by 78 publications

(80 citation statements)

References 159 publications

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“…It is well-recognized and reviewed elsewhere [63] that chronic alcohol intake can impair insulin action and glucose tolerance; therefore, changes in these measures will not be reiterated herein [7,22,23,33,64]. However, adipose tissue, in addition to liver and skeletal muscle, is a primary site of glucose disposal.…”

Section: Regulation Of Lipid Balancementioning

confidence: 99%

Alcohol, Adipose Tissue and Lipid Dysregulation

Steiner

Lang

2017

Biomolecules

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Chronic alcohol consumption perturbs lipid metabolism as it increases adipose tissue lipolysis and leads to ectopic fat deposition within the liver and the development of alcoholic fatty liver disease. In addition to the recognition of the role of adipose tissue derived fatty acids in liver steatosis, alcohol also impacts other functions of adipose tissue and lipid metabolism. Lipid balance in response to long-term alcohol intake favors adipose tissue loss and fatty acid efflux as lipolysis is upregulated and lipogenesis is either slightly decreased or unchanged. Study of the lipolytic and lipogenic pathways has identified several regulatory proteins modulated by alcohol that contribute to these effects. Glucose tolerance of adipose tissue is also impaired by chronic alcohol due to decreased glucose transporter-4 availability at the membrane. As an endocrine organ, white adipose tissue (WAT) releases several adipokines that are negatively modulated following chronic alcohol consumption including adiponectin, leptin, and resistin. When these effects are combined with the enhanced expression of inflammatory mediators that are induced by chronic alcohol, a pro-inflammatory state develops within WAT, contributing to the observed lipodystrophy. Lastly, while chronic alcohol intake may enhance thermogenesis of brown adipose tissue (BAT), definitive mechanistic evidence is currently lacking. Overall, both WAT and BAT depots are impacted by chronic alcohol intake and the resulting lipodystrophy contributes to fat accumulation in peripheral organs, thereby enhancing the pathological state accompanying chronic alcohol use disorder.

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Section: Regulation Of Lipid Balancementioning

confidence: 99%

Alcohol, Adipose Tissue and Lipid Dysregulation

Steiner

Lang

2017

Biomolecules

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“…Alcohol is known to reduce insulin-mediated glucose uptake upon acute ingestion, 5 although data on the effects of chronic alcohol intake are conflicting. 60 Iron deposition within the liver was shown to interfere with the ability of insulin to suppress hepatic glucose production. 61 In NAFLD, insulin resistance is mediated by multiple mechanisms.…”

Section: Insulin Resistancementioning

confidence: 99%

Hepatogenous diabetes: Is it time to separate it from type 2 diabetes?

Orsi

Grancini

Menini

et al. 2016

Liver International

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By definition, hepatogenous diabetes is directly caused by loss of liver function, implying that it develops after cirrhosis onset. Therefore, it should be distinguished from type 2 diabetes developing before cirrhosis onset, in which specific causes of liver disease play a major role, in addition to traditional risk factors. Currently, although hepatogenous diabetes shows distinct pathophysiological and clinical features, it is not considered as an autonomous entity. Recent evidence suggests that the failing liver exerts an independent "toxic" effect on pancreatic islets resulting in β-cell dysfunction. Moreover, patients with hepatogenous diabetes usually present with normal fasting glucose and haemoglobin A levels and abnormal response to an oral glucose tolerance test, which is therefore required for diagnosis. This article discusses the need to separate hepatogenous diabetes from type 2 diabetes occurring in subjects with chronic liver disease and to identify individuals suffering from this condition for prognostic and therapeutic purposes.

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“…Alcohol has profound effects on muscle and whole-body fuel metabolism, thus contributing to increased morbidity and mortality in people with alcohol dependence (Steiner et al, 2015). In fact, alcohol abuse increases the synthesis and secretion of various catabolic agents, such as inflammatory cytokines and glucocorticoids, as well as the production of oxidative metabolites generated by the hepatic metabolism of ethanol (Avogaro and Tiengo, 1993; Gonzalez-Reimers et al, 2011).…”

Section: Melanocortin-dependent Impairment Of Glial Cells and Its Conmentioning

confidence: 99%

New Implications for the Melanocortin System in Alcohol Drinking Behavior in Adolescents: The Glial Dysfunction Hypothesis

Orellana

Cerpa

Carvajal

et al. 2017

Front. Cell. Neurosci.

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Alcohol dependence causes physical, social, and moral harms and currently represents an important public health concern. According to the World Health Organization (WHO), alcoholism is the third leading cause of death worldwide, after tobacco consumption and hypertension. Recent epidemiologic studies have shown a growing trend in alcohol abuse among adolescents, characterized by the consumption of large doses of alcohol over a short time period. Since brain development is an ongoing process during adolescence, short- and long-term brain damage associated with drinking behavior could lead to serious consequences for health and wellbeing. Accumulating evidence indicates that alcohol impairs the function of different components of the melanocortin system, a major player involved in the consolidation of addictive behaviors during adolescence and adulthood. Here, we hypothesize the possible implications of melanocortins and glial cells in the onset and progression of alcohol addiction. In particular, we propose that alcohol-induced decrease in α-MSH levels may trigger a cascade of glial inflammatory pathways that culminate in altered gliotransmission in the ventral tegmental area and nucleus accumbens (NAc). The latter might potentiate dopaminergic drive in the NAc, contributing to increase the vulnerability to alcohol dependence and addiction in the adolescence and adulthood.

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Impact of Alcohol on Glycemic Control and Insulin Action

Cited by 78 publications

References 159 publications

Alcohol, Adipose Tissue and Lipid Dysregulation

Alcohol, Adipose Tissue and Lipid Dysregulation

Hepatogenous diabetes: Is it time to separate it from type 2 diabetes?

New Implications for the Melanocortin System in Alcohol Drinking Behavior in Adolescents: The Glial Dysfunction Hypothesis

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