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Journal ArticleDOI

Insulin resistance: Review of the underlying molecular mechanisms

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TLDR
A review of a number of major mechanisms, including oxidative stress, inflammation, insulin receptor mutations, endoplasmic reticulum stress, and mitochondrial dysfunction, considered the role these cellular mechanisms play in the development of IR.
Abstract
Most human cells utilize glucose as the primary substrate, cellular uptake requiring insulin. Insulin signaling is therefore critical for these tissues. However, decrease in insulin sensitivity due to the disruption of various molecular pathways causes insulin resistance (IR). IR underpins many metabolic disorders such as type 2 diabetes and metabolic syndrome, impairments in insulin signaling disrupting entry of glucose into the adipocytes, and skeletal muscle cells. Although the exact underlying cause of IR has not been fully elucidated, a number of major mechanisms, including oxidative stress, inflammation, insulin receptor mutations, endoplasmic reticulum stress, and mitochondrial dysfunction have been suggested. In this review, we consider the role these cellular mechanisms play in the development of IR.

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Molecular Mechanisms Linking Oxidative Stress and Diabetes Mellitus.

TL;DR: This review presents the molecular mechanisms by which the oxidative milieu contributes to the pathophysiology of insulin resistance and diabetes mellitus through several molecular mechanisms.
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TL;DR: The present review summarizes recent developments in nanodelivery of natural antioxidants and its application to combat pathological conditions associated with oxidative stress.
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TL;DR: This review consolidates and discusses the latest research in pathogenesis, diagnosis, and treatments of diabetes and sarcopenic obesity.
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Mechanisms of Non-Alcoholic Fatty Liver Disease in the Metabolic Syndrome. A Narrative Review.

TL;DR: In this paper, the authors consider the risk of metabolic syndrome as a risk factor for cardiovascular disease, regardless of age, sex, smoking habit, cholesterolemia, and other elements of MS, and suggest that lifestyle modifications (diet, physical exercise, and weight loss) determine an improvement in IR, MS and both clinical and histologic liver picture.
References
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Journal ArticleDOI

Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance.

TL;DR: It is proposed that obesity-related insulin resistance is, at least in part, a chronic inflammatory disease initiated in adipose tissue, and that macrophage-related inflammatory activities may contribute to the pathogenesis of obesity-induced insulin resistance.
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IDF Diabetes Atlas: Global estimates for the prevalence of diabetes for 2015 and 2040.

TL;DR: Diabetes prevalence, deaths attributable to diabetes, and health expenditure due to diabetes continue to rise across the globe with important social, financial and health system implications.
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Increased oxidative stress in obesity and its impact on metabolic syndrome

TL;DR: It is suggested that increased oxidative stress in accumulated fat is an early instigator of metabolic syndrome and that the redox state in adipose tissue is a potentially useful therapeutic target for obesity-associated metabolic syndrome.
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A Novel Serum Protein Similar to C1q, Produced Exclusively in Adipocytes

TL;DR: A novel 30-kDa secretory protein, Acrp30 (adipocyte complement-related protein of 30 kDa), that is made exclusively in adipocytes and whose mRNA is induced over 100-fold during adipocyte differentiation is described.
Journal ArticleDOI

A central role for JNK in obesity and insulin resistance

TL;DR: It is shown that JNK activity is abnormally elevated in obesity and an absence of JNK1 results in decreased adiposity, significantly improved insulin sensitivity and enhanced insulin receptor signalling capacity in two different models of mouse obesity.
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