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Molecular Aspects of Obesity and Insulin Resistance in Metabolic Syndrome and Neurological Disorders

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Metabolic Syndrome
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Abstract

It is becoming increasingly evident that obesity is mediated by dysfunction of feeding centers in hypothalamus, imbalance in energy intake and expenditure, and genetic variations. Obesity is an essential component of the MetS, which is characterized by abnormalities in glucose and lipid metabolism, low-grade inflammation, hypertension, and insulin resistance. Obesity is mediated by a variety of mediators, such as leptin, insulin, and different adipocytokines. Leptin resistance is closely associated with obesity and diabetes. In contrast, adiponectin produces anti-inflammatory effects and reduces obesity by regulating food intake and therefore exerting a direct effect on energy balance and weight control. Other cytokines and chemokines contribute to low-grade inflammation and initial adipose macrophage infiltration, which promote impairment in adipocyte insulin signaling and induction of insulin resistance through the interference of insulin/insulin-like growth factor 1 receptor (IGF-IR) signaling pathways. Oxidative stress and low-grade inflammation are caused by an imbalance between increased production of ROS and/or reduced antioxidant activity and secretion of adipocytokines and cytokines, respectively. Collective evidence suggests that obesity is closely associated with changes in the serum levels of leptin, insulin, glucose, and corticosterone/cortisol.

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Farooqui, A.A. (2013). Molecular Aspects of Obesity and Insulin Resistance in Metabolic Syndrome and Neurological Disorders. In: Metabolic Syndrome. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-7318-3_5

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