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Biochim Biophys Acta Mol Basis Dis. 2017 May;1863(5):1106-1114. doi: 10.1016/j.bbadis.2016.07.019. Epub 2016 Aug 4.

The renin angiotensin system, oxidative stress and mitochondrial function in obesity and insulin resistance.

Author information

1
Department of Nutritional Sciences, Texas Tech University, Lubbock, TX, United States; Obesity Research Cluster, Texas Tech University, Lubbock, TX, United States.
2
Department of Nutritional Sciences, Texas Tech University, Lubbock, TX, United States.
3
Department of Nutrition and Food Sciences, Texas Women's University, Denton, TX, United States.
4
Obesity Research Cluster, Texas Tech University, Lubbock, TX, United States; Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX, United States.
5
Department of Nutritional Sciences, Texas Tech University, Lubbock, TX, United States; Obesity Research Cluster, Texas Tech University, Lubbock, TX, United States; Department of Physiology, Faculty of Medicine, University of Peradeniya, Sri Lanka.
6
Department of Nutritional Sciences, Texas Tech University, Lubbock, TX, United States; Obesity Research Cluster, Texas Tech University, Lubbock, TX, United States. Electronic address: naima.moustaid-moussa@ttu.edu.

Abstract

Obesity is a complex disease characterized by excessive expansion of adipose tissue and is an important risk factor for chronic diseases such as cardiovascular disorders, hypertension and type 2 diabetes. Moreover, obesity is a major contributor to inflammation and oxidative stress, all of which are key underlying causes for diabetes and insulin resistance. Specifically, adipose tissue secretes bioactives molecules such as inflammatory hormone angiotensin II, generated in the Renin Angiotensin System (RAS) from its precursor angiotensinogen. Accumulated evidence suggests that RAS may serve as a strong link between obesity and insulin resistance. Dysregulation of RAS also occurs in several other tissues including those involved in regulation of glucose and whole body homeostasis as well as insulin sensitivity such as muscle, liver and pancreas and heart. Here we review the scientific evidence for these interactions and potential roles for oxidative stress, inflammation and mitochondrial dysfunction in these target tissues which may mediate effects of RAS in metabolic diseases. This article is part of a Special Issue entitled: Oxidative Stress and Mitochondrial Quality in Diabetes/Obesity and Critical Illness Spectrum of Diseases - edited by P. Hemachandra Reddy.

KEYWORDS:

NADPH oxidases; Obesity and insulin resistance; Oxidative stress; Renin angiotensin System

PMID:
27497523
DOI:
10.1016/j.bbadis.2016.07.019
[Indexed for MEDLINE]
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