The following is a list of Diabetes research studies:
1. Lowell, B. B., & Shulman, G. I. (2005). Mitochondrial dysfunction and type 2 diabetes. Science, 307(5708), 384-387. Abstract conclusion: Maintenance of normal blood glucose levels depends on a complex interplay between the insulin responsiveness of skeletal muscle and liver and glucose-stimulated insulin secretion by pancreatic β cells. Defects in the former are responsible for insulin resistance, and defects in the latter are responsible for progression to hyperglycemia. Emerging evidence supports the potentially unifying hypothesis that both of these prominent features of type 2 diabetes are caused by mitochondrial dysfunction.
2. Kim, J. A., Wei, Y., & Sowers, J. R. (2008). Role of mitochondrial dysfunction in insulin resistance. Circulation research, 102(4), 401-414. Abstract conclusion: Reactive oxygen species formation may have maladaptive consequences that increase the rate of mutagenesis and stimulate proinflammatory processes. In addition to reactive oxygen species formation, genetic factors, aging, and reduced mitochondrial biogenesis all contribute to mitochondrial dysfunction. These factors also contribute to insulin resistance in classic and nonclassic insulin target tissues. Insulin resistance emanating from mitochondrial dysfunction may contribute to metabolic and cardiovascular abnormalities and subsequent increases in cardiovascular disease. Furthermore, interventions that improve mitochondrial function also improve insulin resistance. Collectively, these observations suggest that mitochondrial dysfunction may be a central cause of insulin resistance and associated complications. In this review, we discuss mechanisms of mitochondrial dysfunction related to the pathophysiology of insulin resistance in classic insulin-responsive tissue, as well as cardiovascular tissue.
3. Schrauwen, P., & Hesselink, M. K. (2004). Oxidative capacity, lipotoxicity, and mitochondrial damage in type 2 diabetes. Diabetes, 53(6), 1412-1417. Abstract conclusion: We propose that accumulation of fatty acids inside mitochondria might lead to increased production of lipid peroxides and damage to mitochondria. Mitochondrial uncoupling, by UCP3 or other unidentified mechanisms, might play an important role in the protection of mitochondria against these lipid peroxides by lowering the production of ROS. Therefore, in the search for the mechanisms underlying the reduced oxidative capacity observed in type 2 diabetes and aging, the putative role of mitochondrial uncoupling per se, and UCP3 in particular, in the prevention of peroxide-induced mitochondrial damage deserves in-depth investigation.
4. Kelley, D. E., He, J., Menshikova, E. V., & Ritov, V. B. (2002). Dysfunction of mitochondria in human skeletal muscle in type 2 diabetes. Diabetes, 51(10), 2944-2950. Abstract conclusion: As measured by electron microscopy, skeletal muscle mitochondria were smaller in type 2 diabetic and obese subjects than in muscle from lean volunteers (P < 0.01). We conclude that there is an impaired bioenergetic capacity of skeletal muscle mitochondria in type 2 diabetes, with some impairment also present in obesity.
5. Suzuki, S., Hinokio, Y., Komatu, K., Ohtomo, M., Onoda, M., Hirai, S., ... & Akai, H. (1999). Oxidative damage to mitochondrial DNA and its relationship to diabetic complications. Diabetes research and clinical practice, 45(2), 161-168. Abstract conclusion: Oxidative mtDNA damage is speculated to contribute to the pathogenesis of diabetic complications though a defect in mitochondrial oxidative phosphorylation or other mechanisms. 8-OHdG and Delta mtDNA(4977) are useful markers to evaluate oxidative mtDNA damage in the diabetic patients.
6. Green, K., Brand, M. D., & Murphy, M. P. (2004). Prevention of mitochondrial oxidative damage as a therapeutic strategy in diabetes. Diabetes, 53(suppl 1), S110-S118. Abstract conclusion: mitochondrial radical production in response to hyperglycemia contributes to both the progression and pathological complications of diabetes. Consequently, strategies to decrease mitochondrial radical production and oxidative damage may have therapeutic potential. This could be achieved by the use of antioxidants or by decreasing the mitochondrial membrane potential. Here, we outline the background to these strategies and discuss how antioxidants targeted to mitochondria, or selective mitochondrial uncoupling, may be potential therapies for diabetes.
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