Featured Articles

Volume 5 | No. 12 | December 2016

Hypoxia-inducible gene 2 promotes fat deposition and insulin resistanceHypoxia-inducible gene 2 (Hig2) has been identified as a protein that localizes to lipid droplets (LDs) in hepatocytes and promotes hepatic lipid deposition by inhibiting lipolysis. In this present study, DiStefano and colleagues observed that Hig2 is highly expressed in the adipocyte fraction of adipose tissue samples. They demonstrate that Hig2 also localizes to LDs in adipocytes, and its expression is increased with both adipogenic differentiation and fat deposition in vitro. Observations in mice harboring an adipocyte-specific deletion of Hig2 suggest that adipocyte-specific Hig2 promotes adipocyte lipid deposition and glucose intolerance.

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Fat and gut microbiota interactions determine obesity in miceThe gut microbial ecosystem, positioned at the interface between diet and host energy metabolism, can affect energy balance. In the present study, Kübeck et al. assessed the impact of dietary fat source and the gut microbiota on diet-induced obesity (DIO) by performing comprehensive phenotyping of the host combined with metabolite profiling. This was achieved by feeding high-fat diets to germfree and specific pathogen free mice. This work assessed host energy balance in response to different dietary fat sources in combination with metabolite profiling, qPCR, and high-throughput sequencing approaches, providing novel insights into the physiological relevance of gut microbiota and cholesterol-derived metabolites interactions.

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Gut Microbiota and Glucometabolic Alterations in Response to Sleep Deprivation The last two decades have revealed an increasingly important role of the gut microbiome for human health. Benedict et al. conducted a study in which the impact of sleep loss on the human gut microbiota was assessed in healthy, young normal-weight individuals. This study is the first to provide evidence for sleep deprivation-induced changes in microbial families of bacterial gut species, which have previously been linked to metabolic pathologies.

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Targeting the endocannabinoid/CB1 receptor system for treating obesity Prader-Willi syndrome (PWS) is a complex neurogenetic disorder characterized by childhood-onset hyperphagia-associated obesity and intellectual disability, among other symptoms. The study by Knani and colleagues provides the first evidence that the endocannabinoid (eCB) system may contribute to severe obesity both in PWS children and adults and in an established mouse model for this syndrome. In subjects with PWS, increased circulating eCBs were associated with their metabolic abnormalities. Specifically targeting the peripheral eCB system in obese Magel2-null mice was found to be as efficacious as in diet-induced obese animals. Therefore, it may represent a novel approach to treating obesity and its complications in PWS.

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Impaired histone deacetylases expression mimics the effects of obesity and hypoxia In both human and mice obesity, hypoxia is thought to contribute to impaired adipokine production. Bricambert, Favre, Brajkovic and colleagues have identified altered adipocyte histone deacetylase (Hdac) 5 and Hdac6 expression in obesity and associated hypoxia. Modeling the defect of the two Hdacs in adipocytes by genetic silencing and selective inhibitors mimicked the effect of hypoxia and obesity on the expression of key adipokines. These findings provide a better understanding of the possible mechanism responsible of adipose dysfunction, obesity related insulin resistance, and metabolic complications.

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Islet ChREBP-β is increased in diabetes and controls ChREBP-α and glucose-induced gene expression Carbohydrate-response element-binding protein (ChREBP) is the major transcription factor conferring glucose-induced expression of glycolytic, gluconeogenic, and lipogenic genes. Jing et al. have found that a novel ChREBP-β isoform is increased in diabetic islets, whereas ChREBP-α is decreased. These results suggest that ChREBP-β provides a compensatory response, limiting excessive ChREBP-α-mediated gene expression in the context of diabetes or high glucose conditions. The study sheds new light on the physiological role of this novel β-isoform of ChREBP in pancreatic islets and on the regulation of glucose-induced gene expression in general.

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The 60 Second Metabolist
In this section authors briefly report on their work recently published in Molecular Metabolism.

Watch the most recent interview by clicking the video still. The link "referring article" directs you to this author's publication.



Ursula Neumann
University of British Columbia, Vancouver, Canada
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