Background: Obesity is currently viewed as a state of chronic low-grade inflammation in which there is a pro-inflammatory alteration in the serum adipocytokine profile as well as an infiltration of white adipose tissue by activated macrophages. The etiology of this inflammation, however, is poorly understood. Methods: Hypothesizing that local hypoxia within expanding white adipose tissue depots may contribute to obesity-related inflammation, we compared body composition, serum inflammatory marker concentrations and the expression of several hypoxia-regulated genes in white adipose tissue derived from lean, dietary-induced obese (DIO) and ob/ob male C57BL/6J mice. We also examined white adipose tissue for the presence of hypoxia using both a pimonidazole-based antibody system and a fiberoptic sensor for real-time pO 2 quantification in vivo. Finally, using cell-specific leukocyte antibodies, we performed immunohistochemistry and flow cytometric analyses to further characterize the cellular nature of adipose inflammation. Results: We determined that obesity in male C57BL/6J mice is associated with increased expression of HIF (hypoxia-inducible factor) isoforms and GLUT-1, and that white adipose tissue hypoxia was present in the obese mice. Immunohistochemistry revealed hypoxic areas to colocalize predominantly with F4/80 þ macrophages. Interestingly, CD3 þ T cells were present in large numbers within the adipose of both DIO and ob/ob obese mice, and flow cytometry revealed their adipose to possess significantly more CD8 þ T cells than their lean cohort. Conclusions: White adipose hypoxia and cytotoxic T-cell invasion are features of obesity in C57BL/6J mice and are potential contributors to their local and generalized inflammatory state.

Study objective-To determine whether premature ovarian insufficiency (POI) associated with classic galactosemia results from a true deficiency of ovarian function or from aberrant follicle stimulating hormone (FSH). Design-Cross-sectional study Setting-University research laboratoryPatients or other participants-Study subjects included 35 girls and women with galactosemia and 43 control girls and women between the ages of <1 yrs to 51 yrs.Interventions-Blood sampling and medical and reproductive histories were obtained.Main outcome measures-We determined FSH and anti-Müllerian hormone (AMH) levels in subjects with and without classic galactosemia. FSH bioactivity was measured in a subset of girls and women with and without galactosemia who were not on hormone therapy.Results-FSH levels were significantly higher and AMH levels were significantly lower in our galactosemic cases relative to controls. FSH bioactivity did not significantly differ between cases and controls.Conclusions-Close to 90% of girls and women with classic galactosemia have a profound absence of ovarian function, a deficit which is evident shortly after birth, if not before. These patients have no evidence of abnormally functioning FSH. AMH levels can be assessed prior to menarche or

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