Featured Articles

Volume 4 | No. 4 | April 2015

Clic4 sensitizes β-cells to apoptosis

Patel and colleagues show that Clic4 sensitizes beta cells to cytokines- or palmitic acid-induced apoptosis. Reducing Clic4 expression increases beta cell survival. Targeting Clic4 expression or its interaction with specific protein partners may provide a new way to prevent b eta cell apoptosis in the context of diabetes mellitus

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GLP-1 receptor signaling in pancreatic β-cells

Rajan and colleagues demonstrate that chronically elevated glucose acts via PKA to reduce GLP-1R signalling through a SUMO-1-dependent mechanism. Alteration of receptor levels is a likely mechanism for the reduced efficacy of incretin therapies in type 2 diabetes.

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LKB1 and AMPKα1 are required for the normal regulation of glucagon secretion

Sun and colleagues show that LKB1 signalling, at least partly mediated via AMPKα1, is essential for the normal stimulation of glucagon secretion at low glucose levels. Moreover, they show that LKB1 plays a limited if any role in the control of alpha cell size or total alpha cell mass.

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FTO is necessary for the induction of leptin resistance by high-fat feeding

Tung and colleagues report that mice deficient in FTO significantly increase their fat mass in response to HFD and remain sensitive to leptin. They show that genes encoding components of the NFкB signalling pathway are down-regulated in FTO-deficient mice following a HFD. TRIP4, a transcriptional coactivator of NFкB, is identified as a binding partner of FTO.

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TRAP-seq defines markers for novel populations of LepRb neurons

By elucidating the transcriptome of brainstem and hypothalamic LepRb neurons, the TRAP-seq analysis performed by Allison and colleagues reveals markers for numerous subpopulations of LepRb neurons and genes likely to contribute importantly to central leptin action.

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Therapeutic effects of adropin on glucose tolerance and substrate utilization

The study of Gao and colleagues provides a molecular basis for the improvements in glucose homeostasis that are observed with adropin treatment. The data suggest that skeletal muscle is a major organ target in mediating these effects. Adropin may be a promising drug target in developing treatments against diet-induced dysregulation of glucose homeostasis and insulin resistance.

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Enhanced insulin signaling in density-enhanced phosphatase-1 (DEP-1) knockout mice

Krüger and colleagues report that a conventional knockout of DEP-1 results in an improved metabolic phenotype in mice, characterized in particular by enhanced insulin sensitivity and insulin signaling. Knockdown of DEP-1 in skeletal muscle cells leads to an increased insulin-induced glucose uptake. The findings support the notion of DEP-1 as a novel negative regulator of insulin signaling.

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Angiotensin type 1a receptors facilitate leptin-induced weight loss through brown adipose tissue thermogenesis

Young and colleagues show that the subfornical organ, a tiny forebrain structure dense with AT1aR, and recently implicated as an integrative metabolic center, plays a previously unrecognized role in the control of body weight. They demonstrate an interaction between SFO-AT1aR and CNS leptin in the regulation of brown adipose tissue thermogenic metabolism and body weight.

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The expression of dominant negative TCF7L2 causes impaired glucose homeostasis

Shao and colleagues demonstrate that TCF7L2DN expression in Ins-1 cells attenuates cell growth, glucose stimulated insulin secretion (GSIS), and β-cell specific gene expression. Its expression during embryonic development significantly impairs the generation of Pdx-1 and Nkx6.1 positive islet cells, β-cell gene expression, and the function of pancreatic islets in response to GLP-1.

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The LXR inverse agonist SR9238 suppresses fibrosis in a model of non-alcoholic steatohepatitis

Griffett and colleagues show that the LXR inverse agonist SR9238 displays efficacy in reduction of hepatic pathology in a mouse model of diet induced NASH. SR9238 is effective in reducing hepatic steatosis and inflammation and reduces hepatic fibrosis. LXR inverse agonists, such as SR9238, may offer novel therapies to treat NASH.

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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.

Jaqueline Beaudry
Lunenfeld-Tanenbaum Research Institute, Sinai Health System, Toronto, Ontario, Canada
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Non-coding RNAs in Metabolic Diseases
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