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• W3149849218 abstract "Dysregulation of the homeostatic control of appetite and hepatic glucose production, and the imbalance of the interrelation between the gut microbiota and the innate immune system, are currently believed to be the main causes of obesity. Most of these mechanisms function by interacting with one another, rendering high levels of complexity in continual maintainance of a stable body weight. Understand the molecule that acts specifically or having a regulatory role in each of the pathway, is therefore crucial in effective management of obesity development. A number of function-specific mechanisms and pathways of the hypothalamus and the gut have been identified as potential therapeutic targets. The arcuate nucleus (ARC) of the hypothalamus is particularly important in the integration of central and peripheral signals that regulate appetite. The ARC houses two neuronal circuits, ie. the appetite- and the satiety-stimulating circuits, which signal using specific neurotransmitters to modulate feeding behavior and energy expenditure. Gut hormones have long been recognised as the primary peripheral signals that determine the release of specific central neuropeptides [1]. Most recently, favourable outcome from bariatric surgeries has led to a rejuvenated interest in the gut and the gut-brain neuronal axis. Bariatric surgeries performed on obese, non-diabetic patients caused a reduction in acyl-ghrelin, and significant increase in anorexigenic peptides such as peptide YY 3-36 (PYY 3-36 ) and glucagonlike peptide (GLP)-1 [2]. Because bariatric surgery is currently the only clinically used obesity treatment that has resulted in significant long-term weight loss, these hormones may be critical in the regulation of body weight. However, ghrelin receptor is widely expressed in the central nervous system, and exerts different effects in different areas of the brain. Infusion of ghrelin receptor antagonist into the cerebral ventricles decreases caloric intake and weight gain [3], but chronic antagonism of ghrelin receptor in the paraventricular nucleus (PVN) increases the animal’s preference for high fat-diet (HFD) and their body weight gain [4]. Therefore, unless the inhibitor of ghrelin receptor can be designed to reach brain regions other than the PVN, its use may be of limited beneficial effects. GLP-1 is effective in reducing appetite and body weight [5], but has unwanted side effect, ie. it may cause hypoglycaemia in non-diabetic subjects [6]. Compare with ghrelin and GLP-1, PYY 3-36 may be a more promising target. Daily, intermittent intravenous infusion of PYY 3-36 has been reported to cause a sustained reduction in daily food intake and body weight [7]. Since PYY 3-36 has higher affinity to the ARC Y 2 than other Y receptors, peripheral administration of suitable dose of PYY 3-36 to specifically target Y 2 receptor may be effective in long-term body weight control." @default.
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• W3149849218 date "2014-01-01" @default.
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• W3149849218 title "Modulating Specific Central and Peripheral Pathways to Effectively Treat" @default.
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