By C. Huang
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Extra resources for Advanced Bariatric and Metabolic Surgery
2011) reported that such a drug ameliorated dyslipidemia but not the insulin resistance due to diet-induced obesity in mice. 12 Glutathione peroxidase 3 [GPX-3] GPX-3 along with glutathione reductase are enzymes involved in the removal of hydrogen peroxide formed in mitochondria and are thus able to reduce the level of reactive oxygen species in cells (Haddad and Harb, 2005). , 1999) and slightly lower in obese humans as well (Lee et al, 2008b). However, negative effects of GPX-3 knockout studies in mice on the development of obesity (Yang et al, 2009) and of obesity in women on circulating levels of GPX-3 (Fain, 2011) suggest that the role of this enzyme in obesity is unclear.
1998). These data suggest that increased formation of the TNFR2 is part of a feedback system designed to reduce the effects of TNF since the soluble TNFR2 protein binds to and thus reduces the level of active TNF. , 2002). , 2009). , (2004) had previously reported that obesity decreased adipose tissue oxygenation in humans. Thus the question is why in obesity the reduced pO2 in the expanding fat mass does not result in release of VEGF and growth of more blood vessels to enhance pO2. , 2003).
1994) and its absence leads to massive obesity in mice and men as well as delayed sexual maturation and immune defects (Dagogo-Jack, 2001; Gautron and Elmquist, 2011). , 1996). , 2001). , 2001). Their report and many others have amply demonstrated that elevated body fat content is associated with a proinflammatory state and enhanced circulating levels of leptin. , (2011) recently suggested that leptin might have a pathophysiological role in the development of hypertension and vascular heart disease in obesity.