Longitudinal changes in pancreatic and adipocyte hormones following Roux-en-Y gastric bypass surgery.
OBJECTIVE
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
These results suggest that pancreatic and adipocyte hormones may contribute to the long-term resolution of insulin resistance after RYGBP.
Swarbrick
M M
MM
Department of Molecular Biosciences, School of Veterinary Medicine, University of California-Davis, One Shields Ave, Davis, CA 95616-5270, USA.
Stanhope
K L
KL
Austrheim-Smith
I T
IT
Van Loan
M D
MD
Ali
M R
MR
Wolfe
B M
BM
Havel
P J
PJ
D017667:Adipocytes / Q000378:metabolism*; D000328:Adult; D002097:C-Reactive Protein / Q000378:metabolism; D018932:Chemokine CCL2 / Q000378:metabolism; D005260:Female; D015390:Gastric Bypass / Q000379:methods*; D005934:Glucagon / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006801:Humans; D015850:Interleukin-6 / Q000378:metabolism; D020738:Leptin / Q000378:metabolism; D008137:Longitudinal Studies; D009767:Obesity, Morbid / Q000378:metabolism / Q000473:pathology / Q000601:surgery*; D010179:Pancreas / Q000378:metabolism*; D054839:Retinol-Binding Proteins, Plasma / Q000378:metabolism; D013997:Time Factors
D018932:Chemokine CCL2; D015850:Interleukin-6; D020738:Leptin; C101326:RBP4 protein, human; D054839:Retinol-Binding Proteins, Plasma; D002097:C-Reactive Protein; D005934:Glucagon; D005947:Glucose