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Ghrelin and Adipose Tissue Regulatory Peptides: Effect of Gastric Bypass Surgery in Obese Humans
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Medical Sciences.
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2003 In: The Journal of Clinical Endocrinology & Metabolism, ISSN 0021-972X, Vol. 88, no 7, 3177-3183 p.Article in journal (Refereed) Published
Place, publisher, year, edition, pages
2003. Vol. 88, no 7, 3177-3183 p.
Identifiers
URN: urn:nbn:se:uu:diva-97580OAI: oai:DiVA.org:uu-97580DiVA: diva2:172579
Available from: 2008-10-02 Created: 2008-10-02Bibliographically approved
In thesis
1. Gastric Bypass in Morbid Obesity: Postoperative Changes in Metabolic, Inflammatory and Gut Regulatory Peptides
Open this publication in new window or tab >>Gastric Bypass in Morbid Obesity: Postoperative Changes in Metabolic, Inflammatory and Gut Regulatory Peptides
2008 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

This thesis examines the effect of surgical weight loss on gut and adipose tissue peptides involved in appetite regulation and energy homeostasis in morbidly obese humans. Roux-en-Y gastric bypass (RYGBP) is the gold standard operation used for effective long-term weight loss and improved health. The exact mechanisms for this outcome are under investigation.

We measured ghrelin, a recently discovered hunger hormone, insulin, adiponectin and leptin along with anthropometry measures in 66 morbidly obese patients prior to and 6 and 12 months after RYGBP. Impressive weight loss occurred postoperatively as did alterations in the peptides. Consistent correlations were found between weight, leptin, ghrelin and insulin. The main findings were low ghrelin concentrations in obesity and an increase after RYGBP.

We explored inflammatory proteins C-reactive protein (CRP), serum amyloid A and interleukin-6 before and during massive weight loss 6 and 12 months after RYGBP in morbidly obese subjects. The studied proteins declined after surgery and a correlation between CRP and homeostatic model of assessment for insulin resistance, independent of BMI, strongly linked insulin resistance and inflammation. CRP declined most in insulin-sensitive subjects.

We examined the excluded stomach mucosa and vagus nerve by measuring gastrin, pepsinogen I (PGI), pancreatic polypeptide (PP) and ghrelin levels during week 1 and year after RYGBP. Ghrelin levels rose with weight loss but declined 24-hours after surgery, like PP, indicating transient vagal nerve damage. Low levels of gastrin and PGI suggest a resting mucosa.

We evaluated gut peptides: peptide YY (PYY), glucaogon like peptide-1 (GLP-1), pro-neurotensin (pro-NT) and PP, in lean (young and middle-aged), obese and postoperative RYGBP subjects pre- and postprandially. RYGBP subjects had exaggerated levels of PYY and GLP-1 postprandially and higher basal proNT levels, implying a ‘satiety peptide tone’ that may contribute to the maintenance of weight loss.

In summary, RYGBP results in marked weight loss and alterations in gut and adipose tissue peptides involved in appetite regulation and energy homeostasis. These postoperative peptide changes may contribute to impressive weight loss observed after RYGBP.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2008. 59 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 380
Keyword
gastric bypass, morbid obesity, ghrelin, C-reactive protein, pancreatic polypeptide, peptide YY, glucagon-like peptide-1
National Category
Clinical Science
Identifiers
urn:nbn:se:uu:diva-9297 (URN)978-91-554-7293-1 (ISBN)
Public defence
2008-10-25, Enghoffsalen, Entrance 50, University Hospital Uppsala, 09:15
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Available from: 2008-10-02 Created: 2008-10-02Bibliographically approved

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