Featured Articles

Volume 5 | No. 2 | February 2016

Ataxin-10 is part of a cachexokine cocktail triggering cardiac metabolic dysfunctionCancer cachexia represents a severe clinical condition for which no effective diagnostic, preventive or therapeutic measures are available. The studies of Schäfer and colleagues provide a first unbiased and functional screening setup for the discovery of bona fide cachexokines with both sufficient and necessary cachexogenic properties. The researchers find a signature of seven secreted proteins that act in a combined manner to provoke cardiac atrophy and aberrant fatty acid oxidation.

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Muscle mitochondrial stress adaptation operates independently of endogenous FGF21 actionThe endocrine acting pleiotropic protein fibroblast growth factor 21 (FGF21) is proposed as key metabolic mediator of the mitochondrial stress adaptation. Ost, Coleman and colleagues confirm that white adipose tissue (WAT) is a major target of circulating myokine FGF21. In contrast to prior expectations, the present study shows that the adaptive metabolic stress response operates independently of both WAT browning and FGF21 action.

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Bdnf is required to establish normal patterns of afferent GABAergic connectivity and responses to hypoglycemiaThe ventromedial nucleus of the hypothalamus (VMH) is a focal point for examination of neural circuits underlying regulation of food intake and body weight. Kamitakahara and colleagues demonstrate that expression of brain-derived neurotrophic factor (BDNF) by steroidogenic factor 1 (SF1) neurons is required for normal patterns of GABA innervation in the VMH. The loss of BDNF from SF1 neurons results in increased GABAergic innervation in the ventrolateral part of the VMH, as well as reduced glucagon secretion in response to insulin-induced hypoglycemia.

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Mediobasal hypothalamic overexpression of DEPTOR protects against obesityThe mechanistic target of rapamycin (mTOR) plays an important role in the hypothalamic regulation of energy balance. DEP-domain containing mTOR-interacting protein (DEPTOR) is a recently discovered component. Caron et al. report that systemic overexpression of DEPTOR prevents high-fat diet-induced obesity, improves glucose metabolism and protects against the development of metabolic disturbances. These phenotypes are associated with a reduction in feed efficiency.

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Blockade of gamma-secretase, but not inhibition of Notch activity, reduces adipose insulin sensitivityObesity is associated with reactivated liver Notch signaling, which, in turn, increases hepatic insulin resistance, opening up therapeutic avenues for Notch inhibitors to be repurposed for type 2 diabetes (T2D). Sparling and colleagues demonstrate that Notch likely does not play an active role in maintenance of adipocyte function or local/systemic insulin sensitivity. On the contrary, γ-secretase appears to sensitize adipocytes to insulin action, by both biochemical (insulin signaling) and pharmacologic (insulin tolerance testing) proofs. Thus, specific Notch inhibitors are likely to fare better for treatment of T2D than γ-secretase inhibitors.

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IL-13 improves beta-cell survival and protects against IL-1beta-induced beta-cell deathRütti et al. show for the first time that interleukin-13 (IL-13) can directly affect human beta-cell survival and that IL-13 protects beta-cells from interleukin-1beta induced apoptosis, a cytokine known to play an important role in type 2 diabetes. These positive effects are mediated via the IRS2/Akt pathway and the regulation of genes implicated in the cellular stress response. IL-13 may be an important new player in helping beta-cells survive cytokine attack in both major forms of diabetes.

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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
University of Michigan Health System, Ann Arbor, USA
Referring article

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