The oversupply of calories and sedentary lifestyle has resulted in a rapid increase of diabetes prevalence worldwide. During the past two decades, lines of evidence suggest that mitochondrial dysfunction plays a key role in the pathophysiology of diabetes. Mitochondria are vital to most of the eukaryotic cells as they provide energy in the form of adenosine triphosphate by oxidative phosphorylation. In addition, mitochondrial function is an integral part of glucose‐stimulated insulin secretion in pancreatic β‐cells. In the present article, we will briefly review the major functions of mitochondria in regard to energy metabolism, and discuss the genetic and environmental factors causing mitochondrial dysfunction in diabetes. In addition, the pathophysiological role of mitochondrial dysfunction in insulin resistance and β‐cell dysfunction are discussed. We argue that mitochondrial dysfunction could be the central defect causing the abnormal glucose metabolism in the diabetic state. A deeper understanding of the role of mitochondria in diabetes will provide us with novel insights in the pathophysiology of diabetes. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2010.00047.x, 2010)

Purpose: To identify vitreous proteins that were differentially expressed in patients suffering from proliferative diabetic retinopathy with active neovascularization. Methods: The vitreous samples of 15 active proliferative diabetic retinopathy patients were analyzed by two-dimensional gel electrophoresis and mass spectrometry, and the results were compared with those from age-matched patients with macular hole. Results: Twenty-five protein spots were identified in the two-dimensional gel electrophoresis gels. Eight proteins (pigmented epithelium derived factor, serine protease inhibitor, apolipoprotein A-IV precursor, prostaglandin-H2 D-isomerase, α₁-antitrypsin precursor, ankyrin repeat domain 15 protein, alpha2-HS-glycoprotein, and beta V spectrin) in the 25 spots were expressed significantly differently between the macular hole and proliferative diabetic retinopathy patients (p value < 0.05). Five proteins were upregulated in the proliferative diabetic retinopathy patients, and three were downregulated (p value < 0.05). Conclusions: We constructed vitreous protein profiles for proliferative diabetic retinopathy patients and identified eight candidate proteins believed to be involved in the pathogenesis of proliferative diabetic retinopathy.

Lee HK. Diabetes Metab J. 2011 Jun;35(3):207-215. https://doi.org/10.4093/dmj.2011.35.3.207

Summary: From the lectures presented at the 2nd International Workshop on Obesity and Environmental Contaminants, which was held in Uppsala, Sweden, on 8–9 October 2015, it became evident that the findings from numerous animal and epidemiological studies are consistent with the hypothesis that environmental contaminants could contribute to the global obesity epidemic. To increase awareness of this important issue among scientists, regulatory agencies, politicians, chemical industry management, and the general public, the authors summarize compelling scientific evidence that supports the hypothesis and discuss actions that could restrict the possible harmful effects of environmental contaminants on obesity.