Journal
DIABETOLOGIA
Volume 51, Issue 10, Pages 1901-1911Publisher
SPRINGER
DOI: 10.1007/s00125-008-1118-5
Keywords
clinical science; cytokines; gastro-entero pancreatic factors; human; insulin sensitivity and resistance; other hormones; other islet cells/hormones; weight regulation and obesity
Categories
Funding
- NATIONAL CENTER FOR ADVANCING TRANSLATIONAL SCIENCES [UL1TR000002] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR COMPLEMENTARY &ALTERNATIVE MEDICINE [R21AT002599, R21AT002993, R21AT000293] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [UL1RR024146] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL075675] Funding Source: NIH RePORTER
- NCATS NIH HHS [UL1 TR000002] Funding Source: Medline
- NCCIH NIH HHS [R21 AT002993, AT 002599, AT 00293, R21 AT002599] Funding Source: Medline
- NCRR NIH HHS [UL1 RR 024146, UL1 RR024146] Funding Source: Medline
- NHLBI NIH HHS [R01 HL075675, HL 075675] Funding Source: Medline
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Aims/hypothesis Bariatric surgery is an effective treatment for severe obesity, as in addition to dramatic weight loss, co-morbidities such as type 2 diabetes are frequently resolved. Although altered gastrointestinal peptide hormone secretion and its relationship with post-surgical improvements in insulin sensitivity has been studied, much less is known about long-term changes in pancreatic and adipose tissue-derived hormones. Our objective was to conduct a comprehensive longitudinal investigation of the endocrine changes following Roux-en-Y gastric bypass surgery (RYGBP), focusing on pancreatic and adipocyte hormones and systemic markers of inflammation. Methods Nineteen severely obese women (BMI 45.6 +/- 1.6 kg/m(2)) were studied prior to RYGBP, and at 1, 3, 6, and 12 months after RYGBP. Body composition was assessed before surgery and at 1 and 12 months. Results Pre-surgical adiposity was correlated with circulating adipocyte hormones (leptin, visfatin) and inflammatory molecules (IL-6, high sensitivity C-reactive protein [hsCRP], monocyte chemoattractant protein-1). As expected, RYGBP reduced fat mass and fasting insulin and glucose concentrations. In addition, reductions of fasting pancreatic polypeptide (PP) and glucagon concentrations were observed at 1 and 3 months, respectively. In the 12 months following RYGBP, concentrations of most adipocyte hormones (leptin, acylation-stimulating hormone and visfatin, but not retinol-binding hormone-4) and inflammatory molecules (IL-6, hsCRP and soluble intracellular adhesion molecule-1) were significantly reduced. Reductions of insulin resistance (measured by homeostasis model assessment of insulin resistance) were independently associated with changes of glucagon, visfatin and PP. Pre-surgical HMW adiponectin concentrations independently predicted losses of body weight and fat mass. Conclusions/interpretation These results suggest that pancreatic and adipocyte hormones may contribute to the long-term resolution of insulin resistance after RYGBP.
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