Featured Articles

Volume 4 | No. 10 | October 2015

E4orf1 induction in adipose tissue promotes insulin-independent signaling in the adipocyteKusminski and colleagues study the different branches of the insulin signaling pathway by generating and characterizing an inducible mouse model of E4orf1 expression in adipocytes. Expression of the 14-kDa adenoviral polypeptide results in 'insulin-sparing' characteristics during glucose tolerance tests. This phenomenon arises from activation of a Ras-ERK-MAPK signaling pathway that enhances insulin-independent p-Akt activation.

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NF-κB drives survival of adipose tissue macrophages in an obesogenic environmentDuring obesity, macrophages accumulate in adipose tissue (AT) and correlate with adiposity, systemic inflammation and insulin resistance. Hill and colleagues now establish a recruitment-independent mechanism contributing to this accumulation. They demonstrate that during obesity, activation of NF-κB in AT macrophages promotes cell survival.

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The role of GluN2A and GluN2B NMDA Receptor Subunits in AgRP and POMC Neurons on Body Weight and Glucose HomeostasisHypothalamic agouti-related peptide (AgRP) and pro-opiomelanocortin (POMC) producing neurons play important roles in the regulation of body weight homeostasis and get glutamatergic input via n-methyl-D-aspartate (NMDA) receptors. Üner and colleagues investigate the role of the specific NMDA receptor subunits GluN2A and GluN2B. They show that GluN2B expression in hypothalamic AgRP neurons is required for normal control of caloric intake and body weight in lean animals and can influence leptin sensitivity and glucose balance under obese and diabetic conditions.

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Moderate voluntary exercise attenuates the metabolic syndrome in melanocortin-4 receptor-deficient ratsMelanocortin-4 receptor (MC4R) loss-of-function mutations are the most commonly observed monogenetic associations with the metabolic syndrome in humans. Obici and colleagues demonstrate in rats that MC4R-deficiency results in reduced voluntary wheel running, associated with dysregulation of the mesolimbic dopamine system. They also show that voluntary wheel running can normalize several characteristic phenotypes of MC4R deficiency, including body weight gain, hyperphagia, insulin insensitivity, hypercholesterolemia, and hepatic steatosis.

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Leptin modulates nutrient reward via inhibitory galanin action on orexin neuronsLaque and colleagues uncover a novel neuronal circuit where leptin receptor (LepRb) and galanin (GAL) co-expressing neurons in the lateral hypothalamus directly innervate orexin as well as noradrenergic locus coeruleus neurons. Dysregulation of this system by deleting LepRb from GAL neurons causes increased nutrient reward value and consumption for sucrose, while fat consumption is decreased.

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Distribution and characterisation of Glucagon-like peptide-1 receptor expressing cells in the mouse brainCork and colleagues detail the distribution of Glucagon-like peptide-1 receptor (GLP-1R) expressing cells throughout the mouse brain using a novel transgenic model, in which cre-recombinase is expressed under the control of the Glp1r gene. This mouse model can also be used to manipulate specific subsets of GLP-1R expressing cells with cre-dependent viral gene transfer in vivo.

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Molecular regulation of urea cycle function by the liver glucocorticoid receptorGlucocorticoid (GC) treatment is an effective and thus often prescribed immunosuppressive therapy, but also has negative side effects such as lean tissue wasting. Okun and colleagues now demonstrate that the liver glucocorticoid receptor (GR) coordinates proper urea cycle function. In particular, the liver GR upregulates the expression of Arginase I during dexamethasone treatment, aiding in the disposal of excess amino acid N yielded from lean tissue wasting and preventing accumulation of ammonia and associated neuromuscular dysfunction.

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TIMP3 interplays with apelin to regulate cardiovascular metabolism in hypercholesterolemic miceTissue inhibitor of metalloproteinase 3 (TIMP3) is an extracellular matrix bound protein, which is downregulated in human subjects and experimental models with cardiometabolic disorders, such as type 2 diabetes mellitus, hypertension and atherosclerosis. Stöhr and colleagues report that ApoE-/-TIMP3-/- mice show decreased lifespan and reduced resistance to cardiac stress. Based on metabolite profiling and gene/protein expression analyses, they conclude that loss of TIMP3 results in a perturbation of metabolic flexibility in the heart and arrhythmias, phenomena that may underlie the increased rates of cardiovascular death in this model.

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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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