[ Diabetes Solutions ]

Diabetes and Inflammation

Low-grade inflammation caused by obesity is widely believed to contribute to insulin resistance and type 2 diabetes. But now a study by researchers in Sweden shows us how to reduce our level of inflammation and bring down our blood sugar level as well. Recent developments reveal a crucial role for the autophagy pathway under conditions of oxidative stress and inflammation. Overtime, these selective pressures gave us the ability to withstand starvation and disease. Results: A total of 39367 participants were enrolled in the study and 1634 (4.2%) subjects with missing information on T2D and the inflammatory diseases were excluded. A chromatin immunoprecipitation assay was performed to analyze the effects of Klotho signaling on interleukin-8 and monocyte chemoattractant protein-1 promoter recruitment of RelA and RelA serine (Ser)536. Frederik Paulsen Chair at the Salk Institute.

Moreover, diabetic patients, constituting about 15% to 20% of patients presenting with acute coronary syndromes, are at considerably increased risk of excess morbidity and mortality, as compared with nondiabetic patients, as diabetics’ risk of adverse events is twice that of nondiabetics, even in the most recent experimental or observational clinical studies. CONCLUSIONS We demonstrate, for the first time, a possible contribution of ambient air pollution to systemic inflammation in Indian type 2 diabetic patients. Furthermore, women with higher levels of C-reactive protein were at 15.7 times greater risk of developing diabetes. After adjusting their findings for known risk factors, the researchers reported that the women with the highest levels of interleukin-6 were 2.3 times more likely to become diabetics, while those with highest levels of Creactive protein were 4.2 times more likely to develop diabetes. But where does all of the inflammation come from? This widespread and sneaky inflammation stems from an accumulation of fat and waste debris in and around every cell in your body that affects every single organ in your body. It also prevents your mitochondria (those specialized subunits in all of your cells that produce energy like little batteries) from generating the energy you need.

Diabetics are predisposed to all of these conditions so an increase of NETs at the source of a wound is especially troubling. As a result, your damaged mitochondria hinder proper insulin secretion, which leads to the development of diabetes.3 And sooner or later, the breakdown of your mitochondria will cause all kinds of other diseases as well, including heart disease, stroke, and even cancer. This process makes the human body less responsive to insulin, and more likely to develop insulin resistance. In conclusion, high circulating concentrations of glucose and FFAs may explain, at least in part, the oxidative and inflammatory derangements during acute illness; insulin may exert its anti-inflammatory action by ameliorating glucose and lipid parameters.

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