MAP4K4 and IL-6+ Th17 cells play important roles in non-obese type 2 diabetes.

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obesity 330 (collection): /2017AbstractObesity is a causal factor of type 2 diabetes (T2D); however, people without obesity (including lean, normal weight, or overweight) may still develop T2D. Non-obese T2D is prevalent in
obesity 540 Asia and also frequently occurs in Europe. Recently, multiple evidences oppose the notion that either obesity or central obesity (visceral fat accumulation) promotes non-obese T2D. Several factors such as inflammation
obesity 559 frequently occurs in Europe. Recently, multiple evidences oppose the notion that either obesity or central obesity (visceral fat accumulation) promotes non-obese T2D. Several factors such as inflammation and environmental
obesity 2129 BMI < 30) by WHO criteria, and 50% of those in Europe and Britain are also non-obese [[1]]. Even when the obesity criteria for Asia is adjusted from BMI ≥ 30 to BMI ≥ 27.5, more than 60% of T2D patients
obesity 2344 Asia are still classified as having non-obese T2D [[1]]. While BMI > 30 is considered to be morbid obesity , the population of non-obese T2D in Asia might be underestimated. In addition, the Obesity in Asia Collaboration
obesity 2611 increasing BMI and T2D in Asians compared with that in Caucasians [[2]]. Thus, other factors instead of obesity may contribute to the development of non-obese T2D. Central obesity (visceral fat accumulation) was
obesity 2679 Thus, other factors instead of obesity may contribute to the development of non-obese T2D. Central obesity (visceral fat accumulation) was thought to be the main cause of both non-obese and obese T2D [[3]];
obesity 2878 T2D [[3]]; however, several recent reports using clinical data or animal models indicate that central obesity is not associated with non-obese T2D. Recently, a door has been opened to understanding of non-obese
obesity 3727 slim people suffer from T2D.To date, most attention and resources have been directed toward studying obesity -induced T2D. However, the pathogenesis of non-obese T2D cannot be readily revealed using samples from
obesity 4891 pathogenesis of non-obese T2D.The controversy of visceral fat accumulation in non-obese T2DCentral obesity as determined by increased visceral fat accumulation was thought to be a risk of T2D in both Europeans
obesity 6371 demonstrates that the association between insulin resistance and T2D incident is independent of central obesity (waist circumferences) and obesity (BMI) [[15]]. Surprisingly, insulin resistance of normal-weight T2D
obesity 6406 between insulin resistance and T2D incident is independent of central obesity (waist circumferences) and obesity (BMI) [[15]]. Surprisingly, insulin resistance of normal-weight T2D subjects is not positively (but
obesity 6549 resistance of normal-weight T2D subjects is not positively (but inversely) correlated with central obesity (gynoid fat mass, measured by dual-energy X-ray absorptiometry (DAX)), as well as BMI [[15]]. Consistently,
obesity 12531 [[35]]. Furthermore, the methylation frequencies are correlated with OGTT glucose levels independent of obesity ; this correlation is particularly higher in the patient subgroup with BMI < 23 compared to those
obesity 14289 These findings indicate that the pathogenic IL-6+IL17+ T cell population for T2D is not induced by obesity . Collectively, these results also suggest that IL-6+ Th17 cells and IFN-γ+ T cells are important causes
obesity 14423 results also suggest that IL-6+ Th17 cells and IFN-γ+ T cells are important causes of non-obese T2D and obesity -induced T2D, respectively. In addition, IL-17 and IFN-γ levels from T cells of T2D patients from the
obesity 14951 cells may cross-talk with Th17 cells in T2D patients. Thus, it is likely that the people with both obesity and MAP4K4 dysfunction may be susceptible to earlier or worse T2D.Prevention and therapeutic strategies
obesity 19375 dysfunction of MAP4K4 in T cells. In conclusion, MAP4K4-downregulated, inflammatory Th17 cells and obesity contribute to non-obese T2D and obese T2D, respectively (Fig. 2). Furthermore, both IL-6+ Th17 cells
obesity 19489 contribute to non-obese T2D and obese T2D, respectively (Fig. 2). Furthermore, both IL-6+ Th17 cells and obesity may occur in the same individuals, leading to exacerbated T2D. In addition, inflammatory IL-6+ Th17
obesity 20673 leading to insulin resistance of the insulin-targeted cells. In obese T2D, high-fat diet is a cause of obesity and visceral fat accumulation, resulting in overproduction of the proinflammatory cytokine IFN-γ from

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