Coordinated regulation of scopoletin at adipose tissue–liver axis improved alcohol-induced lipid dysmetabolism and inflammation in rats

Lee, Hae-In; Lee, Mi-Kyung

doi:10.1016/j.toxlet.2015.06.016

Cited by 37 publications

(34 citation statements)

References 46 publications

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“…In contrast, chronic alcohol feeding in rats does not consistently increase fat mass potentially due to improper pair-feeding techniques [16,17], differences in macronutrient composition of the diets (i.e., high fat versus low fat), doses of alcohol used, feeding methods (liquid diet, in water, through gastric tube), or the interaction of these methodological variances in the different adipose tissue depots (eWAT vs. sWAT). Of those animals receiving alcohol as part of a complete nutritionally adequate liquid diet, visceral and subcutaneous adipose tissue mass was unchanged [18,19], while eWAT was either unchanged [20] or decreased [19,21]. A high dose of alcohol (5 g/kg/day) administered via a gastric tube to animals consuming a low fat (10%) chow diet increased eWAT and perirenal depots [22].…”

Section: Chronic Alcohol and Adipose Tissue Massmentioning

confidence: 99%

“…Only one other investigation has reported a similar decrease in eWAT from rats after 12 weeks of an alcohol-containing liquid diet [19]. Instead, the majority of work shows HSL phosphorylation, activity or mRNA to be increased [7,9,11,12,14,15,18,45,46] or at least unchanged by alcohol [7,14,18,45]. The preponderance of data indicate that chronic alcohol feeding increases adipose tissue triglyceride lipase (ATGL), the other rate-limiting enzyme in adipose tissue lipolysis, that catalyzes the removal of the first fatty acid from triacylglycerol [7,9,12,14,15,18,19].…”

Section: Regulation Of Lipid Balancementioning

confidence: 99%

“…While the lipolytic effects of alcohol outweigh its lipogenic effects, alcohol does modulate several components of the lipogenic pathway (see Figure 1 for pathway overview). For example, PPARγ which is among the most prominent lipogenic stimulators is generally decreased in WAT after chronic alcohol consumption [7,9,12,15,18,19,49,50]. Treatment with the PPARγ agonist rosiglitazone restored this alcohol-mediated perturbation [12,51].…”

Section: Regulation Of Lipid Balancementioning

confidence: 99%

“…Alcohol suppresses ACC Ser79 phosphorylation in vivo [9,18,19,23,25], while in vitro no change and an increase is observed depending on the dose of alcohol [19,25]. This decrease in ACC phosphorylation is consistent with the concomitant reduction in activity of its protein kinase, AMP kinase (AMPK), observed after chronic alcohol consumption [9,18,23,25]. As AMPK activation in adipose tissue can also suppress lipolysis (basal and stimulated), the alcohol-related decrease in AMPK may similarly lead to enhanced lipolysis.…”

Section: Regulation Of Lipid Balancementioning

confidence: 99%

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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: Chronic Alcohol and Adipose Tissue Massmentioning

confidence: 99%

Section: Regulation Of Lipid Balancementioning

confidence: 99%

Section: Regulation Of Lipid Balancementioning

confidence: 99%

Section: Regulation Of Lipid Balancementioning

confidence: 99%

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Alcohol, Adipose Tissue and Lipid Dysregulation

Steiner

Lang

2017

Biomolecules

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“…Adiponectin has an important role in insulin sensitizing effect by altering the signaling pathway of AMP-activated protein kinase (AMPK) pathway, metabolism of glucose and fatty acid oxidation in tissues. In animal models, many data generated from chronic alcohol liver disease showed the decreased levels of circulating adiponectin [48][49][50][51]. While in humans converse results were obtained, when low or moderate level alcohol was added to the diet for short period, the result suggested serum adiponectin increase in men and women, while in chronic heavy drinker (>50 g/day) adiponectin was decreased.…”

Section: Adipose Tissue and Alcoholmentioning

confidence: 98%

Potential Molecular Mechanism of Probiotics in Alcoholic Liver Disease

Patel¹,

Patel²,

Palash³

2017

J Alcohol Drug Depend

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Alcohol consumption and its abuse are significant prevalent cause for liver diseases and death worldwide. Increased bacterial endotoxin in the portal circulation, the plasma ratio of liver enzymes like alanine aminotransferase (ALT), aspartate aminotransferase (AST) and triglyceride implies the symbiotic relation between the gut and liver plays a key function in alcoholic liver disease (ALD). Consumption of alcohol leads to gut dysbiosis and informalities of the intestinal barrier, hyper gut permeability, oxidative stress, inflammation and adversely affect adipose tissue metabolism, and those are mainly recognized as major factors for progression of alcoholic liver disease. Alteration of gut microbiota is referred to as bacterial overgrowth which leads to the release of bacterial products to change in commercial/pathogenic microbiota equilibrium. Lipopolysaccharide (LPS) derived inflammatory signal renders inflammation in alcoholic liver disease. Increase in concentration of lipopolysaccharide leads to activation of toll-like receptor 4 (TLR4) and alteration in micro RNA (miRNA) expression at the transcription level. Activation of myeloid differentiation factor 88 (MyD88) pathways eventually produces pro inflammatory cytokine activation that is an important mediator of alcoholic liver disease. However, there is no effectual Food and Drug Administration (FDA) approved treatment for any stage of alcoholic liver disease. Thus, the potential therapeutic approach for alcoholic liver disease is restoration and alteration of gut microbiota. With the increasing importance of gut microbiota in the onset and occurrence of a variety of diseases, the potential use of probiotics in ALD is receiving more exploration and clinical attention. Probiotic administration is nontoxic, inexpensive and noninvasive strategy with minimal side effects compared to antibiotic therapy and surgery. Yet, there is no substantial evidence on the efficient molecular mechanism regarding mode of action of probiotics on ALD as therapeutics. This review summarizes the research done on gut liver-axis and potential mechanism of probiotic in alcoholic liver disease.

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Scopoletin Supplementation Ameliorates Steatosis and Inflammation in Diabetic Mice

Choi

Ham

Lee³

et al. 2017

Phytotherapy Research

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Scopoletin is a bioactive component in many edible plants and fruits. This study investigated the effects of scopoletin on hepatic steatosis and inflammation in a high-fat diet fed type 1 diabetic mice by comparison with metformin. Scopoletin (0.01%, w/w) or metformin (0.5%, w/w) was provided with a high-fat diet to streptozotocin-induced diabetic mice for 11 weeks. Both scopoletin and metformin lowered blood glucose and HbA , serum ALT, TNF-α and IL-6 levels, glucose intolerance, and hepatic lipid accumulation compared with the diabetic control group. Scopoletin or metformin down-regulated hepatic gene expression of triglyceride (Pparg, Plpp2, and Dgat2) and cholesterol (Hmgcr) synthesis as well as inflammation (Tlr4, Myd88, Nfkb1, Tnfa, and Il6), while it up-regulated Cyp7a1 gene. Hepatic PPARγ and DGAT2 protein levels were also down-regulated in scopoletin or metformin group compared with the control group. Scopoletin or metformin also inhibited hepatic fatty acid synthase and phosphatidate phosphohydrolase activities. These results suggest that scopoletin protects against diabetes-induced steatosis and inflammation by inhibiting lipid biosynthesis and TLR4-MyD88 pathways. Copyright © 2017 John Wiley & Sons, Ltd.

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Coordinated regulation of scopoletin at adipose tissue–liver axis improved alcohol-induced lipid dysmetabolism and inflammation in rats

Cited by 37 publications

References 46 publications

Alcohol, Adipose Tissue and Lipid Dysregulation

Alcohol, Adipose Tissue and Lipid Dysregulation

Potential Molecular Mechanism of Probiotics in Alcoholic Liver Disease

Scopoletin Supplementation Ameliorates Steatosis and Inflammation in Diabetic Mice

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