Obesity and diabetes: the link between adipose tissue dysfunction and glucose homeostasis

Nutrition Research Reviews - Tập 28 Số 2 - Trang 121-132 - 2015
Monise Viana Abranches1, F. C. E. de Oliveira2, Lisiane Lopes da Conceição3, Maria do Carmo Gouveia Pelúzio3
1Instituto de Ciências Biológicas e da Saúde, Universidade Federal de Viçosa Campus de Rio Paranaíba, Rodovia MG-230 – Km 7, Rio Paranaíba, MG, 38810-000, Brazil
2Departamento de Enfermagem, Faculdade de Ciências Sociais Aplicadas de Sinop, Sinop, MT, 78550-000, Brazil
3Departamento de Nutrição e Saúde, Universidade Federal de Viçosa, Campus Universitário, Edifício Centro de Ciências Biológicas II, s/n, Viçosa, MG, 36571-900, Brazil

Tóm tắt

Abstract

Obesity and type 2 diabetes mellitus (T2DM) epidemics, which have already spread, imply the possibility of both conditions being closely related. Thus, the goal of the present review was to draw a parallel between obesity, adipose tissue (AT) changes, and T2DM development. To this end, a search was conducted in PubMed, MEDLINE and SciELO databases, using the following key words and their combinations: obesity; diabetes; insulin resistance; diet; weight loss; adipocin; inflammation markers; and interleukins. Based on a literature review, AT dysfunction observed in obesity is characterised by adipocyte hypertrophy, macrophage infiltration, impaired insulin signalling and insulin resistance. In addition, there is release of inflammatory adipokines and an excessive amount of NEFA promoting ectopic fat deposition and lipotoxicity in muscle, liver and pancreas. Recent evidence supports the hypothesis that the conception of AT as a passive energy storage organ should be replaced by a dynamic endocrine organ, which regulates metabolism through a complex adipocyte communication with the surrounding microenvironment. The present review demonstrates how glucose homeostasis is changed by AT dysfunction. A better understanding of this relationship enables performing nutritional intervention strategies with the goal of preventing T2DM.

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