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Review
. 2013 Apr 1:6:1-11.
doi: 10.4137/LPI.S10805. eCollection 2013.

Obesity and insulin resistance: an abridged molecular correlation

Affiliations
Review

Obesity and insulin resistance: an abridged molecular correlation

Biswajit Mukherjee et al. Lipid Insights. .

Abstract

A relationship between obesity and type 2 diabetes is now generally well accepted. This relationship represents several major health hazards including morbid obesity and cardiovascular complications worldwide. Diabetes mellitus is a complex metabolic disorder characterized by impaired insulin release and insulin resistance. Lipids play an important physiological role in skeletal muscle, heart, liver and pancreas. Deregulation of fatty acid metabolism is the main culprit for developing insulin resistance and type 2 diabetes. A predominant predisposing factor to developing obesity, insulin resistance and type 2 diabetes is the permanent elevation of free fatty acids in plasma followed by impaired utilization of lipids by muscle. Diabetes-induced inflammation and oxidative stress have also vital role for development of insulin resistance in diabetic patients. The present review is intended to describe the correlation between lipids, obesity and insulin resistance based on current literature, in order to elucidate involved molecular mechanisms in depth.

Keywords: free fatty acids; insulin resistance; lipoproteins; molecular signaling; obesity.

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Figures

Figure 1
Figure 1
Combined impact of genetic makeup, environmental and social factors in the process of development of type 2 diabetes associated with obesity through impaired insulin secretion and insulin action, explaining the progression from insulin resistance to an impaired glucose tolerance test (IGT) and type 2 diabetes.
Figure 2
Figure 2
mTOR/S6K1, AMPK and SHP-1 pathways in the development of insulin resistance.
Figure 3
Figure 3
Inhibitory pathway of GLUT4 translocation by free fatty acids. Abbreviations: FATP1, fatty acid-transport protein 1; ROS, reactive oxygen species.
Figure 4
Figure 4
Predominant biochemical alterations for progression of type 2 diabetes from insulin resistance and due to beta cells dysfunction.

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