Featured Articles

Volume 3 | No. 1 | February 2014

Central action of FGF19 improves glucose metabolismRecently, FGF19 has emerged as an important regulator of the postprandial adaptive metabolic response. Marcelin and colleagues report that FGF19-induced signaling in the hypothalamus ameliorates glucose intolerance by improving insulin sensitivity. Their findings support a mechanism by which FGF19 inhibits hypothalamic AGRP/NPY neurons.

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Muscle clock regulates insulin sensitivity and glucose metabolismCircadian rhythms and energy metabolism are inextricably linked. By generating two skeletal muscle-specific Bmal1 knockout models Dyar and colleagues demonstrate that muscle-specific Bmal1 ablation causes muscle insulin resistance and that the muscle clock controls PDH activation and promotes metabolic flexibility.

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High fat diet (HFD) alters the balance of metabolismGiven the complexity of the whole-body response to dietary changes, invertebrate model organisms can serve as useful tools to examine the interplay between genes, signaling pathways, and metabolism. Heinrichsen and colleagues report that in Drosophila melanogaster, HFD alters expression of genes in amino acid metabolism, including CG9510.The role of this gene at the junction of carbon and nitrogen metabolism identifies a mechanism by which HFD impacts the regulation of metabolic balance.

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Irs2 and Irs4 synergize in non-LepRb neuronsThe various IRS-proteins have distinct physiologic functions. The results of Sadagurski and colleagues provide evidence that Irs2 and Irs4 synergize in non-LepRb neurons and that deletion of Irs2 in the CNS in mice lacking whole body Irs4 causes obesity, hyperglycemia, and impaired energy homeostasis.

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AgRP neurons mediate regulatory actions of ghrelinAgRP neurons localized to the arcuate nucleus have been hypothesized to play a role in the orexigenic effects of ghrelin. Using a mouse model for spatiotemporal gene manipulation in AgRP neurons Wang and colleagues now demonstrate that AgRP neuron-selective GHSR expression allows a partial eating response to ghrelin.

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Leptin deficiency leads to high reward value of sucrose in miceIn humans, food hedonics (“liking”) is measured with a subjective rating scale, but this scale cannot be used in studies of animals that cannot self-report. Using an optogenetic assay for testing the reward value of food Domingos and colleagues show that leptin rescue in ob/ob mice suppresses the reward value of sucrose even before weight loss is achieved.

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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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