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REVIEW
Year : 2012  |  Volume : 5  |  Issue : 2  |  Page : 99-122

An update on the pathogenesis of type 2 diabetes mellitus


1 Institute for Clinical Diabetology, German Diabetes Centre, Leibniz Institute for Diabetes Research at Heinrich-Heine University, Düsseldorf, Germany
2 Institute for Clinical Diabetology, German Diabetes Centre, Leibniz Institute for Diabetes Research at Heinrich-Heine University, Düsseldorf, Germany; Department of Metabolic Diseases, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany; Karl-Landsteiner Institute for Endocrinology and Metabolism, Vienna, Austria

Correspondence Address:
Michael Roden
Institute for Clinical Diabetology, German Diabetes Center, Department of Metabolic Diseases, Heinrich-Heine University, Düsseldorf

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Source of Support: None, Conflict of Interest: None


DOI: 10.7707/hmj.v5i2.167

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The most common form of diabetes mellitus, type 2 diabetes mellitus (T2DM), is characterized by impaired insulin sensitivity of skeletal muscle, liver and adipose tissue, termed insulin resistance (IR), and by inadequate insulin secretion by pancreatic β cells, termed β-cell dysfunction. Recent studies propose that the brain may also contribute to IR and to the pathogenesis of T2DM. There is growing evidence that IR is the earliest detectable abnormality, whereas β-cell exhaustion is mandatory for manifesting overt T2DM. The current concepts of possible mechanisms underlying IR are lipid overflow (lipotoxicity), abnormal energy balance and mitochondrial function, subclinical inflammation, and central neuronal mechanisms. Here we review the relative roles of these mechanisms for the development of T2DM.


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