Interest in the control feeding and has increased as a result of the obesity epidemic and rising incidence of metabolic diseases. The brain detects alterations in energy stores and triggers metabolic and behavioral responses designed to maintain energy balance. Energy homeostasis is controlled mainly by neuronal circuits in the hypothalamus and brainstem, whereas reward and motivation aspects of eating behavior are controlled by neurons in limbic regions and cerebral cortex. This article provides an integrated perspective on how metabolic signals emanating from the gastrointestinal tract, adipose tissue and other peripheral organs target the brain to regulate feeding, energy expenditure and hormones. Knowledge of these complex pathways is crucial to the pathogenesis and treatment of obesity and abnormalities of glucose and lipid metabolism. KeywordsNervous system; appetite; metabolism; adipokine; neuropeptide Historical perspectiveOur survival depends on the ability to procure food for immediate metabolic needs and to store excess energy in the form of fat to meet metabolic demands during fasting. Eating behavior is stimulated by hunger, cravings, and hedonic sensations and also controlled by homeostatic processes. Knowledge of how the brain interacts with peripheral organs to control feeding and energy balance dates back to earlier descriptions of the "adiposogenital syndrome" in patients with pituitary tumors encroaching on the base of the brain [1]. Affected individuals manifested a voracious appetite, morbid obesity and hypogonadism [1]. Thus, it was posited that the brain was critical in the negative feedback regulation of appeite and weight. The adiposogenital syndrome was subsequently recapitulated in rats by lesioning the ventromedial hypothalamus [2]. In contrast, lesions of the lateral hypothalamus prevented spontaneous feeding, resulting in starvation [2]. These seminal observations led to the concept of a "dual center model", in which the "satiety center" was located in the ventromedial hypothalamus and the "feeding center" was located in the lateral hypothalamus. It soon became apparent that the classic hypothalamic lesions were imprecise and often damaged adjacent brain regions and nerve tracts passing through [1]. Nonetheless, this concept formed the basis of later studies linking the brain and peripheral organs.
Diets with high fat content induce steatosis, insulin resistance, and type 2 diabetes. The lipid droplet protein adipose differentiation-related protein (ADRP) mediates hepatic steatosis, but whether this affects insulin action in the liver or peripheral organs in diet-induced obesity is uncertain. We fed C57BL/6J mice a high-fat diet and simultaneously treated them with an antisense oligonucleotide (ASO) against ADRP for 4 wk. Glucose homeostasis was assessed with clamp and tracer techniques. ADRP ASO decreased the levels of triglycerides and diacylglycerol in the liver, but fatty acids, long-chain fatty acyl CoAs, ceramides, and cholesterol were unchanged. Insulin action in the liver was enhanced after ADRP ASO treatment, whereas muscle and adipose tissue were not affected. ADRP ASO increased the phosphorylation of insulin receptor substrate (IRS)1, IRS2, and Akt, and decreased gluconeogenic enzymes and PKCepsilon, consistent with its insulin-sensitizing action. These results demonstrate an important role for ADRP in the pathogenesis of diet-induced insulin resistance.
Moringa oleifera is a multipurpose plant used in Ghana and most parts of Africa. Its high mineral, protein, and vitamins content has enabled its use as a nutraceutical and panacea for various diseases. This study aimed at measuring the micro- and macroelements content of dried Moringa oleifera leaves using energy dispersive X-ray fluorescence spectroscopic (EDXRF) and assessing its toxicological effect in rats. Acute toxicity (5000 mg/kg) and a subacute toxicity studies of the leaf (40 mg/kg to 1000 mg/kg) extract were conducted in rats. Blood samples were assessed for biochemical and haematological parameters. Results showed significant levels of thirty-five (35) elements (14 macroelements and 21 microelements) in M. oleifera extract. There were no observed overt adverse reactions in the acute and subacute studies. Although there were observed elevations in liver enzymes ALT and ALP (P < 0.001) and lower creatinine levels in the extract treated groups, no adverse histopathological findings were found. Moringa oleifera dried leaf extract may, therefore, be reasonably safe for consumption. However, the consumption of Moringa oleifera leaves should not exceed a maximum of 70 grams per day to prevent cumulative toxicity of these essential elements over long periods.
HighlightsPSN was assessed by symptoms, examination and quantitative assessment.High burden of PSN in diabetes patients in Ghana.The major determinants of PSN using different assessment methods were reported.
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