TY - JOUR
T1 - Longitudinal changes in pancreatic and adipocyte hormones following Roux-en-Y gastric bypass surgery
AU - Swarbrick, M. M.
AU - Stanhope, K. L.
AU - Austrheim-Smith, I. T.
AU - Van Loan, M. D.
AU - Ali, M. R.
AU - Wolfe, B. M.
AU - Havel, P. J.
N1 - Funding Information:
Acknowledgements We acknowledge the expert technical assistance of J. Graham and E. Nuñez. This study was supported by a grant award from the University of California Davis Health Care Systems. It was also supported by the UC Davis Clinical and Translational Science Center (grant number UL1 RR024146) and from the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH) and NIH Roadmap for Medical Research. The content of this manuscript is solely the responsibility of the authors and does not necessarily represent the official view of NCRR or NIH. P. J. Havel’s laboratory receives research support from NIH grants: HL-075675, AT-002599, AT-00293, and the American Diabetes Association. M. M. Swarbrick is supported by a New Investigator Award from NAASO, The Obesity Society.
PY - 2008/10
Y1 - 2008/10
N2 - 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/m2) 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.
AB - 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/m2) 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.
KW - Clinical science
KW - Cytokines
KW - Gastro-entero pancreatic factors
KW - Human
KW - Insulin sensitivity and resistance
KW - Other hormones
KW - Other islet cells/hormones
KW - Weight regulation and obesity
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U2 - 10.1007/s00125-008-1118-5
DO - 10.1007/s00125-008-1118-5
M3 - Article
C2 - 18704364
AN - SCOPUS:51249119175
SN - 0012-186X
VL - 51
SP - 1901
EP - 1911
JO - Diabetologia
JF - Diabetologia
IS - 10
ER -