Featured Articles

Volume 6 | No. 2 | February 2017

Kinase Suppressor of Ras 2 expression in the brain regulates energy balance Kinase Suppressor of Ras 2 (KSR2) is a molecular scaffold coordinating Raf/MEK/ERK signaling that potently regulates energy consumption and expenditure. Guo, Costanzo-Garvey, Smith et al. show that brain-specific disruption of KSR2 is sufficient to reduce body temperature, promote cold intolerance, cause obesity, and impair glucose homeostasis, while elevating fasting insulin and free fatty acid levels in blood. These data demonstrate that KSR2 functions centrally to regulate energy balance through effects on feeding behavior and adaptive thermogenesis.

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Blocking iNOS and ER Stress Improves Insulin ResistanceThe interactions between inducible nitric oxide synthase (iNOS) and endplasmatic reticulum (ER) stress are complex and bidirectional. Zanotto and colleagues demonstrate that in high fat diet fed mice, iNOS-induced alteration in insulin signaling is an essential mechanism of insulin resistance in muscle. However, in liver and adipose tissue, ER stress and insulin resistance can be induced by both iNOS-dependent and iNOS-independent mechanisms. These results reinforce the tissue-specific regulation of insulin signaling in obesity.

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Carnitine acetyltransferase expression is dispensable for nutrient stress sensing and inflammationCarnitine acetyltransferase (CrAT) regulates fatty acid oxidation and mitochondrial acetyl-CoA balance. Goldberg and Dixit report that loss of CrAT expression in myeloid-lineage cells has no impact on total body glucose metabolism or adipose tissue inflammation in conditions of high-fat diet. These findings reveal that, unlike muscle cells, macrophages have a unique metabolic substrate requirement machinery where CrAT expression is dispensable for regulating adipose tissue inflammation and whole body glucose metabolism under conditions of metabolic stress.

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Dipeptidyl peptidase-4 inhibitor induces a greater increase in bioactive GIP plasma levels than GLP-1Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are incretins released from the gut that promote insulin secretion. Both incretin hormones are rapidly cleaved after secretion by dipeptidyl peptidase-4 (DPP-4) into truncated forms that are no longer insulinotropic. DPP-4 inhibitors are widely used to improve glycemic control in patients with type 2 diabetes mellitus. Yanagimachi et al. find that ELISAs may typically underestimate the levels of bioactive incretins. Moreover, they find that DPP-4 inhibitor treatment has a much greater impact on plasma bioactive GIP levels than bioactive GLP-1 levels in healthy subjects.

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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.

Randy J. Seeley, Henriette Frikke-Schmidt
Department of Surgery, University of Michigan, Ann Arbor, USA
Referring article

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