Featured Articles

Volume 5 | No. 6 | June 2016

PI3K p110β subunit is required for the acute hypophagia induced by endotoxemia Systemic inflammation triggered by bacterial endotoxin is characterized by increased cytokines, altered energy balance via suppression of food consumption, and body weight loss. Borges and colleagues show that bacterial lipopolysaccharide (LPS) stimulates phosphoinositide 3-kinase (PI3K) and signal transducer and activator of transcription 3 (STAT3) signalling pathways in hypothalamic leptin receptor (LepR) expressing cells. Central PI3K inhibition or double deletion of PI3K p110α and p110β in LepR cells prevent LPS-induced hypophagia.

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Triggering the adaptive immune system with gut bacteria protects against insulin resistanceIt has been shown before that changes in the ecology of gut bacteria characterize metabolic disease. Pomié et al. demonstrate that targeting the adaptive immune system by specific luminal ileum microbiota extracts allows the intestinal immune system to control gut microbiota most likely through the activation of CD4 T cells and the production of IgA. This mechanism is largely documented where a change in gut microbiota, by the mean of antibiotics or prebiotics and by germ free mouse colonization, is responsible for the glycemic control. The authors propose that the immunization process impacts the glycemic control by a mechanism involving the adaptive intestinal immune system.

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A lipidomic screen of pancreatic β-cells defines novel features of glucose-stimulated turnover of neutral lipids, sphingolipids and plasmalogensAlthough it has been recognized for more than 40 years that β-cell lipids are acutely remodelled following glucose stimulation, these changes remain poorly defined. Pearson and colleagues apply mass spectrometry to conduct the first comprehensive and unbiased characterization of how glucose acutely regulates the turnover of phospholipids, sphingolipids, and neutral lipids in β-cells. Their results point to remodelling of all three lipid classes in response to glucose, which impacts the overall accumulation of separate diacylglycerol and monoacylglycerol species, phosphatidylcholine plasmalogens, and various sphingolipid metabolites. The findings shed new light on metabolic stimulus-secretion coupling in β-cells.

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Role of mitochondrial uncoupling protein-2 (UCP2) in higher brain functions, neuronal plasticity and network oscillationMitochondria support energy demanding processes like neural transmission and synaptogenesis and are thus promising points of broadening interest in the energetics underlying the neurobiology of mental illness. Using an animal model of mitochondrial dysfunction, UCP2 KO, Hermes and colleagues explore responses to NMDA receptor blockade, synaptic density, auditory gating, and gamma power. These measures and markers relevant to the pathophysiology of mental illnesses, reveal a significant vulnerability in animals with UCP2 deficiency.

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Raptor/mTORC1 loss in adipocytes causes lipodystrophy and fatty liver disease White adipose tissue (WAT) functions both as the body’s major energy storage site, and as a critical endocrine tissue. Lack of adipose tissue or lipodystrophy associates with severe metabolic complications. Lee et al. investigate the in vivo role of mTORC1 in mature adipocytes by deleting Raptor with Adiponectin-Cre. They conclude that mTORC1 activity in white adipocytes is dispensable for early postnatal WAT growth but becomes essential for normal adipose tissue expansion with age. Adipocyte Raptor KO mice consuming a high fat diet are hyperphagic yet resistant to obesity. These mice appear to have a defect in adipose tissue expansion, which redistributes lipids to the liver resulting in severe hepatomegaly and hepatic steatosis and causes a dietary lipid absorption defect.

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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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