Central obesity is associated with insulin resistance and dyslipidemia. Thus, the mechanisms that control fat distribution and its impact on systemic metabolism have importance for understanding risk for diabetes and cardiovascular disease. Hypercortisolemia at the systemic (Cushing’s syndrome) or local levels (due to adipose-specific overproduction via 11β-Hydroxysteroid dehydrogenase 1) results in the preferential expansion of central, especially visceral fat depots. At the same time, peripheral subcutaneous depots can become depleted. The biochemical and molecular mechanisms underlying the depot-specific actions of glucocorticoids (GCs) on adipose tissue function remain poorly understood. GCs exert pleiotropic effects on adipocyte metabolic, endocrine and immune function, and dampen adipose tissue inflammation. GCs also regulate multiple steps in the process of adipogenesis. Acting synergistically with insulin, GCs increase the expression of numerous genes involved in fat deposition. Variable effects of GC on lipolysis are reported, and GC can improve or impair insulin action depending on the experimental conditions. Thus, the net effect of GC on fat storage appears to depend on the physiologic context. The preferential effects of GC on visceral adipose tissue have been linked to higher cortisol production and glucocorticoid receptor expression, but the molecular details of the depot-dependent actions of GCs are only beginning to be understood. In addition, increasing evidence underlines the importance of circadian variations in GCs in relationship to the timing of meals for determining their anabolic actions on the adipocyte. In summary, although the molecular mechanisms remain to be fully elucidated, there is increasing evidence that GCs have multiple, depot-dependent effects on adipocyte gene expression and metabolism that promote central fat deposition.

More data have become available on the burden from metabolic complications associated with SGAs. New and effective treatment options are required in the near future to improve cardiovascular health in this susceptible population.

articles Bariatric surgery vitamin D reserve as body fat mass declines after surgery. The purpose of this study is to determine the amount of vitamin D in adipose tissue of severely obese patients at the time of RYGB, and to describe changes in serum 25(OH)D during a follow-up period of up to 1 year as it relates to the subject's initial fat vitamin D content and amount of fat mobilization as determined by weight loss. Methods and ProceduresThe study was reviewed and approved by the institutional review board of Boston University Medical Center, and written informed consent was obtained from each subject. Severely obese patients from the Nutrition and Weight Management Center at Boston Medical Center in Boston, MA (latitude 42° 19' N) who were already scheduled to undergo RYGB surgery, as part of their treatment, were invited to participate in this prospective, observational study. Patients whose plan of obesity treatment did not include surgery were not invited. Subjects were not compensated for participating in this study. Exclusion criteria included age of less than 18 years old, pregnancy, liver disease, and kidney disease.At the preoperative visit, patients were consented and demographic and medical history was obtained. Subjects were asked to provide blood which was used to determine 25(OH)D level. All surgeries were performed by a single surgeon at Boston University Medical Center from years 2003 to 2007. RYGB was performed with approximate roux limb length of 100 cm, gastric pouch size of 30 ml, and gastrojejunostomy anastomosis size of 10-11 mm. Discarded abdominal subcutaneous, omental, and mesenteric adipose tissue was obtained at the time of surgery, and was flash frozen using liquid nitrogen and stored at −80 °C for determination of vitamin D concentration.Subjects were scheduled for study visits at 3, 6, 9, and 12 months after surgery and were contacted to reschedule if they missed an appointment. At each visit, patients were weighed, BMI was calculated, and blood was drawn and used to determine serum 25(OH)D. Amount of vitamin D intake was assessed at each visit by patient self-report and their medical and prescription records. Subjects who were found to be vitamin D deficient were treated at the discretion of the physician, either before or during the study period. Treatment regimen used at this institution was 50,000 IU of vitamin D 2 , taken continuously at a weekly interval (4).