Featured Articles

Volume 2 | No. 4 | November 2013

Moderate metabolic consequences of an ObRa deletionThe leptin receptor is a cytokine family receptor that is spliced into multiple forms. The ObRa form expresses a short cytoplasmic region that lacks motifs required for leptin signal transduction. The results of Li and colleagues provide in-vivo evidence that ObRa plays a small but statistically significant role in mediating leptin action suggesting that ObRa could play a role in mediating leptin’s transport, internalization or signal transduction in extra-hypothalamic sites.

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Seven transmembrane G protein-coupled receptors regulate ghrelin secretionAlthough much is known about how food and circadian rhythmicity affect circulating ghrelin levels, the molecular mechanisms within the ghrelin cell, which receives the stimulatory and inhibitory secretion signals, remain unknown. In the present study, Engelstoft and colleagues identify the full repertoire of gastric ghrelin cell 7-transmembrane receptors and heterotrimeric GTP-binding protein Gα subunits and functionally characterize them in respect to their effects on ghrelin secretion.

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Interaction of cannabinoid and leptin receptors in astrocytesDue to their locations between blood vessels and neurons, astrocytes are involved in supplying energy to neurons and sensing peripheral energy state. In this study, Bosier and colleagues demonstrate that astroglial CB1 cannabinoid receptors participate in the control of astroglial energy storage functions through the maintenance of functional leptin signaling.

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The role of RPM1l in endoplasmic reticulum stress responseThe Ppm1l gene has recently been shown to exhibit a causal effect on obesity. However, the molecular mechanisms and the role in metabolic disorders remained unclear. Lu and colleagues now demonstrate that the Ppm1l gene encodes an endoplasmic reticulum (ER) targeted protein phosphatase with high specificity for IRE-1, which is a key regulator in the ER stress signaling pathway.

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Snacking decreases serotonin transportersIn today’s society there is increasing snacking behavior and it has been shown that snacking is associated with obesity. Koopman and colleagues now demonstrate that overeating by regularly snacking fat and sugar decreases serotonin transporters in the hypothalamic region, which is a key regulatory brain centre for energy balance.

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Loss of neurotensin receptor-1 (NtsR1) promotes hedonic feedingAcute treatment with neurotensin (Nts) decreases food intake while acute blockade of NtsR1 promotes feeding, suggesting a role for Nts/NtsR1 signaling in energy balance. The results of Opland and colleagues suggest that NtsR1KO mice overeat specifically in response to a palatable diet and exhibit increased sucrose preference indicating that a loss of NtsR1 disrupts the control of the mesolimbic dopamine system by leptin.

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Phenotypes of mouse strains developing hepatosteatosisThe contribution of genetic and environmental factors to the development of non-alcoholic fatty liver disease is not clearly understood. In their study, Kahle and colleagues systematically assess physiological and molecular hepatic adaptations in four widely used inbred mouse strains.

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The role of hepatic lipogenesis in the development of obesityBile acids are known to reduce triglyceride levels and increase energy expenditure by activating thyroid hormone in brown adipose tissue. Bochkis and colleagues now demonstrate that the loss of hepatic Foxa2, a transcription factor regulating genes encoding bile acid transporters, leads to increased hepatic lipogenesis and overall adiposity.

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Cholesteryl ester transfer protein (CETP) protects against insulin resistanceGut bile acids are known to improve liver and muscle glucose metabolism. CETP delivers cholesteryl esters to the liver, where they are converted into bile acids. The results of Cappel and colleagues show that CETP expression protects female mice from insulin resistance associated with obesity.

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Peptide lipidation improves diabetes and obesitySingle molecule peptides capable of balanced action at multiple receptors should provide enhanced efficacy in the treatment of diabetes, obesity and the metabolic syndrome. The results of Ward and colleagues suggest that lipid-acylated glucagon analogs provide enhanced pharmacodynamics and reduce body weight and plasma glucose.

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Low birth weight – coenzyme Q10 prevents cardiac agingIncreased oxidative stress and cellular aging are thought to play an important role in the developing of the metabolic syndrome and cardiovascular disease in low birth weight babies. The results of Tarry-Adkins and colleagues demonstrate that postnatal antioxidant intervention with coenzyme Q10 ameliorates programmed cardiac aging, cellular senescence and apoptosis.

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TrkB plays a crucial role in hyperphagic obesityBrain-derived neurotrophic factor (BDNF) and its receptor TrkB play a role in the regulation of eating behavior and energy homeostasis. The results of Liao and colleagues demonstrate that the deletion of the TrkB gene in many hypothalamic neurons and a small number of cortical and striatal neurons lead to hyperphagic obesity. This indicates that BDNF regulates appetite through TrkB-expressing neurons in the hypothalamus.

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Bone resorption is a determinant of glucose metabolismOsteocalcin, a bone derived hormone, is known to stimulate insulin secretion, to increase insulin sensitivity and to regulate energy metabolism. Lacombe and colleagues now provide evidence that bone resorption by osteoclasts contributes to the decarboxylation and activation of osteocalcin and to the control of whole body glucose metabolism by this hormone.

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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.



Flaminia Fanelli
University of Bologna, Italy
Referring article

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