Featured Articles

Volume 3 | No. 4 | July 2014

Rictor regulates energy and glucose homeostasisRictor is known to be a critical downstream mediator of insulin signal transduction. In their study, Kocalis and colleagues deleted Rictor in all neurons and specifically in POMC or AgRP arcuate neurons. As neuronal Rictor deletion led to an obesity and diabetes phenotype, they reveal a key role for Rictor in CNS regulation of energy and glucose homeostasis.

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Mitochondrial dysfunction influences insulin actionOne of the most contentious issues in metabolic research is the role of mitochondrial dysfunction in the development of insulin resistance. Martin and colleagues now provide evidence that impairments in mitochondrial function are sufficient for insulin resistance in a cell type-dependent manner. The spatial location of mitochondrial impairment determines the impact on insulin action.

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Inhibition of ACC increases fat accumulation in the liverThe liver plays an important role in the regulation of whole body lipid and carbohydrate homeostasis during fluctuations in nutrient intake. The results of Chow and colleagues suggest that complete inhibition of hepatocyte ACC enzymes triggers the activation of a compensatory pathway that preserves fat storage in the liver due to increased acetylation of key metabolic enzymes and transcriptional regulatory sensors.

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Can defended body weight be reset upward by chronic hyperleptinemia?In weight-stable individuals, circulating leptin concentrations are directly proportional to fat mass. Ravussin and colleagues now demonstrate that chronic elevations of circulating leptin concentrations per se do not result in major changes in defended body weight or diet preference.

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KLF induces food intake and body weightRecent evidence suggests that Krüppel-like factor 4 (KLF4) plays an important role in the central regulation of energy balance. The results of Imbernon and colleagues indicate that KLF4 over-expression in the hypothalamic arcuate nucleus induces food intake and body weight via AgRP. Silencing KLF4 in the hypothalamic ARC inhibits fasting-induced hyperphagia.

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Glut4 neurons are enriched in olfacto-sensory receptorsIn this study, Ren and colleagues set out to investigate the nature of Glut4 neurons in the hypothalamus, a key regulatory site for appetite and glucose homeostasis. Their data define hypothalamic Glut4 neurons as a cell population with characteristics of hormone responsiveness, and with the potential to link insulin signaling to olfacto-sensory signaling.

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Method-specific interpretations of the effects of dietary interventions upon RMRBurnett and colleagues postulate that sole reliance upon respirometric methods may lead pharmaceutical researchers to inappropriately waste effort pursuing ultimately ineffective modulators of resting metabolic rate (RMR), or to prematurely discard promising new targets and modulators. To test this hypothesis, they placed mice on a sequential dietary program of chow, high fat diet, then back to chow, and simultaneously measured RMR during each phase using both respirometry and direct calorimetry.

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FABP4 regulates insulin secretion during obesityFatty acid binding protein 4 (FABP4) has a plethora of roles in metabolic regulation. The results of Wu and colleagues suggest that FABP4 is secreted from adipocytes and potentiates insulin secretion, that the secretion is inhibited by insulin, revealing endocrine feedback regulation, and that the signaling by FABP4 and insulin may coordinate glucose-stimulated insulin secretion with adiposity during obesity

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VEGF-A activates brown adipose tissueRecent studies indicated that local overexpression of VEGF-A in a physiological range in white adipose tissue protects against diet-induced obesity and metabolic dysfunction. The results of Sun and colleagues now suggest that VEGF-A stimulates angiogenesis in brown fat tissue and that it can up-regulate both PGC-1α and UCP1 expression, thus increasing thermogenesis and energy expenditure.

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Metabolic memory of β-cells controls insulin secretionIn this study, Santos and colleagues investigated whether pancreatic β-cells acquire and store information contained in calcium pulses as a form of "metabolic memory". Their results indicate that metabolic memory of β-cell depends on Ca2+/calmodulin-dependent protein kinase II (CaMKII).

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Measurement of BAT thermogenesisCurrent in vivo methods aiming to assess the capacity for BAT activation in animals are indirect and complex, which hinders the rapid preclinical development of new obesity therapies. Using a simple, non-invasive method of measuring changes in BAT activity, Crane and colleagues now demonstrate that the surface thermal signature of BAT in mice after β 3 -adrenergic challenge reflects the activity of UCP1.

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Importance of adapted experimental proceduresIn this study, Hebert-Chatelain and colleagues hypothesized that the discrepant results regarding the presence of cannabinoid type 1 receptors on brain mitochondrial membranes, obtained in different laboratories might be caused by different experimental approaches, further underlying the specific cautions that should be taken when addressing brain bioenergetics processes.

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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.



Giles Yeo
University of Cambridge, UK
Referring article

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