Zentralbl Chir 2010; 135(1): 28-33
DOI: 10.1055/s-0029-1224697
Übersicht

© Georg Thieme Verlag Stuttgart ˙ New York

Warum Patienten nach bariatrischen Operationen Gewicht abnehmen

Why Patients Lose Weight after Bariatric OperationsM. Bueter1 , F. Seyfried2 , C. T. Germer2
  • 1Imperial College London, Hammersmith Hospital, Department for Investigative Medicine, London, United Kingdom
  • 2Universitätsklinikum Würzburg, Zentrum Operative Medizin (ZOM), Klinik und Poliklinik für Allgemein- und Viszeral-, Gefäß- und Kinderchirurgie, Würzburg, Deutschland
Further Information

Publication History

Publication Date:
05 February 2010 (online)

Zusammenfassung

Die Zunahme des krankhaften Übergewichtes mit seiner assoziierten Morbidität und Mortalität ist in Deutschland und weltweit ein großes sozial-ökonomisches Problem. Zurzeit stellt die bariat­rische Chirurgie die effektivste Therapiemethode mit signifikantem und andauerndem Gewichtsverlust dar. Von den verschiedenen bariatrischen Operationsverfahren wird der Roux-en-Y-Magenbypass weltweit mit am häufigsten durchgeführt. Viele der zugrundeliegenden Mechanismen der Magenbypass-Chirurgie und der Gründe für seine Überlegenheit gegenüber anderen Therapieoptionen sind allerdings noch unklar. Es deutet vieles darauf hin, dass entgegen ursprünglicher Annahmen eine Malabsorption oder eine reduzierte Nahrungsaufnahme durch Restriktion keine oder nur eine untergeordnete Rolle für die Reduktion des Körpergewichtes spielen. Stattdessen scheint der Magenbypass die Physiologie der Gewichts­regulation und des Essverhaltens nachhaltig zu verändern. Die Gewichtsabnahme nach Magenbypass scheint auf komplexen neurophysiologischen und neuro-endokrinologischen Mechanismen zu beruhen, in denen veränderte Spiegel ­verschiedener gastrointestinaler Hormone eine wichtige Rolle einnehmen. Dieser Artikel soll ­einen Überblick über das derzeitige Wissen zur Regulation von Körpergewicht und Essverhalten durch gastrointestinale Hormone geben und ­beleuchten, wie die Magenbypass-Operation in diese Mechanismen eingreift. 

Abstract

The obesity epidemic is in Germany as well as worldwide a major health problem which is associated with increased morbidity and mortality. Bariatric surgery is currently the most effective therapy for significant and sustained weight loss. The most common form of bariatric surgery worldwide is Roux-en-Y gastric bypass surgery. The underlying mechanisms behind the superiority of this procedure are unclear and remain to be elucidated, but recent findings suggest that gastrointestinal hormones play an important role rather than malabsorption or restriction. It appears that gastric bypass surgery alters the physiology of weight regulation and eating behaviour in patients who have undergone the procedure. Gastrointestinal hormones have recently been found to be an important element in the physiol­ogy of appetite regulation due to the signals from the periphery to the brain. It is the purpose of this article to review the current knowledge about the regulation of body weight and eating behaviour by gastrointestinal hormones and how their levels are altered after bariatric surgery. 

Literatur

  • 1 Hedley A A, Ogden C L, Johnson C L et al. Prevalence of overweight and ­obesity among US children, adolescents, and adults, 1999–2002.  JAMA. 2004;  291 2847-2850
  • 2 Visscher T L, Seidell J C. The public health impact of obesity.  Annu Rev Public Health. 2001;  22 355-375
  • 3 Kaplan L M. Pharmacological therapies for obesity.  Gastroenterol Clin North Am. 2005;  34 91-104
  • 4 Adams T D, Gress R E, Smith S C et al. Long-term mortality after gastric bypass surgery.  N Engl J Med. 2007;  357 753-761
  • 5 Sjostrom L, Narbro K, Sjostrom C D et al. Effects of bariatric surgery on mortality in Swedish obese subjects.  N Engl J Med. 2007;  357 741-752
  • 6 Buchwald H, Estok R, Fahrbach K et al. Weight and type 2 diabetes after bariatric surgery: systematic review and meta-analysis.  Am J Med. 2009;  122 248-256
  • 7 Busch P, Wolter S, Rawnaq T et al. Operative Technik und deren Outcome in der metabolischen Chirurgie: Konventioneller und Banded Gastric Bypass.  Zentralbl Chir. 2009;  134 32-37
  • 8 Brolin R E, LaMarca L B, Kenler H A et al. Malabsorptive gastric bypass in patients with superobesity.  J Gastrointest Surg. 2002;  6 195-203
  • 9 Pournaras D J, le Roux C W. After bariatric surgery what vitamins should be measured and what supplements should be given?.  Clin Endocrinol (Oxf). 2009;  71 322-325
  • 10 Crenn P, Morin M C, Joly F et al. Net digestive absorption and adaptive hyperphagia in adult short bowel patients.  Gut. 2004;  53 1279-1286
  • 11 le Roux C W, Welbourn R, Werling M et al. Gut hormones as mediators of appetite and weight loss after Roux-en-Y gastric bypass.  Ann Surg. 2007;  246 780-785
  • 12 Wren A M, Seal L J, Cohen M A et al. Ghrelin enhances appetite and ­increases food intake in humans.  J Clin Endocrinol Metab. 2001;  86 5992
  • 13 Balasubramaniam A, Mullins D E, Lin S et al. Neuropeptide Y (NPY) Y4 receptor selective agonists based on NPY(32-36): development of an anorectic Y4 receptor selective agonist with picomolar affinity.  J Med Chem. 2006;  49 2661-2665
  • 14 Schwartz M W, Woods S C, Porte Jr D et al. Central nervous system control of food intake.  Nature. 2000;  404 661-671
  • 15 Cone R D, Cowley M A, Butler A A et al. The arcuate nucleus as a conduit for diverse signals relevant to energy homeostasis.  Int J Obes Relat ­Metab Disord. 2001;  25 Suppl 5 S63-S67
  • 16 Flier J S. Obesity wars: molecular progress confronts an expanding epidemic.  Cell. 2004;  116 337-350
  • 17 Grill H J, Smith G P. Cholecystokinin decreases sucrose intake in chronic decerebrate rats.  Am J Physiol. 1988;  254 (6 Pt 2) R853-R856
  • 18 Murakami N, Hayashida T, Kuroiwa T et al. Role for central ghrelin in food intake and secretion profile of stomach ghrelin in rats.  J Endocrinol. 2002;  174 283-288
  • 19 Wren A M, Small C J, Abbott C R et al. Ghrelin causes hyperphagia and ­obesity in rats.  Diabetes. 2001;  50 2540-2547
  • 20 Neary N M, Small C J, Wren A M et al. Ghrelin increases energy intake in cancer patients with impaired appetite: acute, randomized, placebo-controlled trial.  J Clin Endocrinol Metab. 2004;  89 2832-2836
  • 21 Cummings D E, Purnell J Q, Frayo R S et al. A preprandial rise in plasma ghrelin levels suggests a role in meal initiation in humans.  Diabetes. 2001;  50 1714-1719
  • 22 le Roux C W, Neary N M, Halsey T J et al. Ghrelin does not stimulate food intake in patients with surgical procedures involving vagotomy.  J Clin Endocrinol Metab. 2005;  90 4521-4524
  • 23 Druce M R, Wren A M, Park A J et al. Ghrelin increases food intake in ­obese as well as lean subjects.  Int J Obes (Lond). 2005;  29 1130-1136
  • 24 Cummings D E, Weigle D S, Frayo R S et al. Plasma ghrelin levels after diet-induced weight loss or gastric bypass surgery.  N Engl J Med. 2002;  346 1623-1630
  • 25 le Roux C W, Patterson M, Vincent R P et al. Postprandial plasma ghrelin is suppressed proportional to meal calorie content in normal-weight but not obese subjects.  J Clin Endocrinol Metab. 2005;  90 1068-1071
  • 26 Holst J J. On the physiology of GIP and GLP-1.  Horm Metab Res. 2004;  36 747-754
  • 27 Abbott C R, Monteiro M, Small C J et al. The inhibitory effects of peripheral administration of peptide YY(3-36) and glucagon-like peptide-1 on food intake are attenuated by ablation of the vagal-brainstem-hypothalamic pathway.  Brain Res. 2005;  1044 127-131
  • 28 Edwards C M, Stanley S A, Davis R et al. Exendin-4 reduces fasting and postprandial glucose and decreases energy intake in healthy volunteers.  Am J Physiol Endocrinol Metab. 2001;  281 E155-E161
  • 29 Gutzwiller J P, Goke B, Drewe J et al. Glucagon-like peptide-1: a potent regulator of food intake in humans.  Gut. 1999;  44 81-86
  • 30 Feinle C, Chapman I M, Wishart J et al. Plasma glucagon-like peptide-1 (GLP-1) responses to duodenal fat and glucose infusions in lean and obese men.  Peptides. 2002;  23 1491-1495
  • 31 Edwards C M, Todd J F, Mahmoudi M et al. Glucagon-like peptide 1 has a physiological role in the control of postprandial glucose in humans: studies with the antagonist exendin 9-39.  Diabetes. 1999;  48 86-93
  • 32 Villanueva-Penacarrillo M L, Marquez L, Gonzalez N et al. Effect of GLP-1 on lipid metabolism in human adipocytes.  Horm Metab Res. 2001;  33 73-77
  • 33 Guerci B, Martin C S. Exenatide: its position in the treatment of type 2 diabetes.  Ann Endocrinol (Paris). 2008;  69 201-209
  • 34 Soltani N, Kumar M, Glinka Y et al. In vivo expression of GLP-1 / IgG-Fc fusion protein enhances beta-cell mass and protects against streptozotocin-induced diabetes.  Gene Ther. 2007;  14 981-988
  • 35 Tatemoto K, Mutt V. Isolation of two novel candidate hormones using a chemical method for finding naturally occurring polypeptides.  Nature. 1980;  285 417-418
  • 36 Adrian T E, Ferri G L, Bacarese-Hamilton A J et al. Human distribution and release of a putative new gut hormone, peptide YY.  Gastroenterology. 1985;  89 1070-1077
  • 37 Adrian T E, Savage A P, Sagor G R et al. Effect of peptide YY on gastric, pancreatic, and biliary function in humans.  Gastroenterology. 1985;  89 494-499
  • 38 le Roux C W, Batterham R L, Aylwin S J et al. Attenuated peptide YY release in obese subjects is associated with reduced satiety.  Endocrinology. 2006;  147 3-8
  • 39 Chelikani P K, Haver A C, Reidelberger R D. Intravenous infusion of pep­tide YY (3-36) potently inhibits food intake in rats.  Endocrinology. 2005;  146 879-888
  • 40 Degen L, Oesch S, Casanova M et al. Effect of peptide YY3-36 on food ­intake in humans.  Gastroenterology. 2005;  129 1430-1436
  • 41 Batterham R L, Cowley M A, Small C J et al. Gut hormone PYY(3-36) phys­i­ologically inhibits food intake.  Nature. 2002;  418 650-654
  • 42 Batterham R L, Cohen M A, Ellis S M et al. Inhibition of food intake in ­obese subjects by peptide YY3-36.  N Engl J Med. 2003;  349 941-948
  • 43 White N E, Dhillo W S, Liu Y L et al. Co-administration of SR141716 with peptide YY3-36 or oxyntomodulin has additive effects on food intake in mice.  Diabetes Obes Metab. 2008;  10 167-170
  • 44 Adrian T E, Savage A P, Bacarese-Hamilton A J et al. Peptide YY abnor­malities in gastrointestinal diseases.  Gastroenterology. 1986;  90 379-384
  • 45 Di F V, Zamboni M, Dioli A et al. Delayed postprandial gastric emptying and impaired gallbladder contraction together with elevated cholecystokinin and peptide YY serum levels sustain satiety and inhibit hunger in healthy elderly persons.  J Gerontol A Biol Sci Med Sci. 2005;  60 1581-1585
  • 46 Creutzfeldt W, Ebert R, Willms B et al. Gastric inhibitory polypeptide (GIP) and insulin in obesity: increased response to stimulation and defective feedback control of serum levels.  Diabetologia. 1978;  14 15-24
  • 47 Baggio L L, Drucker D J. Biology of incretins: GLP-1 and GIP.  Gastroen­ter­ology. 2007;  132 2131-2157
  • 48 Ding W G, Gromada J. Protein kinase A-dependent stimulation of exocytosis in mouse pancreatic beta-cells by glucose-dependent insulinotropic polypeptide.  Diabetes. 1997;  46 615-621
  • 49 Gibbs J, Young R C, Smith G P. Cholecystokinin decreases food intake in rats.  J Comp Physiol Psychol. 1973;  84 488-495
  • 50 Liddle R A, Goldfine I D, Rosen M S et al. Cholecystokinin bioactivity in human plasma. Molecular forms, responses to feeding, and relationship to gallbladder contraction.  J Clin Invest. 1985;  75 1144-1152
  • 51 Moran T H. Cholecystokinin and satiety: current perspectives.  Nutrition. 2000;  16 858-865
  • 52 Batterham R L, le Roux C W, Cohen M A et al. Pancreatic polypeptide reduces appetite and food intake in humans.  J Clin Endocrinol Metab. 2003;  88 3989-3992
  • 53 le Roux C W, Aylwin S J, Batterham R L et al. Gut hormone profiles following bariatric surgery favor an anorectic state, facilitate weight loss, and improve metabolic parameters.  Ann Surg. 2006;  243 108-114
  • 54 Dixon A F, Dixon J B, O’Brien P E. Laparoscopic adjustable gastric banding induces prolonged satiety: a randomized blind crossover study.  J Clin Endocrinol Metab. 2005;  90 813-819
  • 55 Mason E E. The mechanisms of surgical treatment of type 2 diabetes.  Obes Surg. 2005;  15 459-461
  • 56 Patriti A, Facchiano E, Sanna A et al. The enteroinsular axis and the ­recovery from type 2 diabetes after bariatric surgery.  Obes Surg. 2004;  14 840-848
  • 57 Rubino F, Gagner M, Gentileschi P et al. The early effect of the Roux-en-Y gastric bypass on hormones involved in body weight regulation and glucose metabolism.  Ann Surg. 2004;  240 236-242
  • 58 Neary N M, Small C J, Druce M R et al. Peptide YY3-36 and glucagon-like peptide-17-36 inhibit food intake additively.  Endocrinology. 2005;  146 5120-5127
  • 59 Day J W, Ottaway N, Patterson J T et al. A new glucagon and GLP-1 co-agonist eliminates obesity in rodents.  Nat Chem Biol. 2009;  5 749-757
  • 60 Pocai A, Carrington P E, Adams J R et al. GLP-1 / GCGR dual agonism ­reverses obesity in mice.  Diabetes. 2009;  58 2258-2266
  • 61 Holdstock C, Engstrom B E, Ohrvall M et al. Ghrelin and adipose tissue regulatory peptides: effect of gastric bypass surgery in obese humans.  J Clin Endocrinol Metab. 2003;  88 3177-3183
  • 62 Huttl T P, Obeidat F W, Parhofer K G et al. Operative Techniken und deren Outcome in der metabolischen Chirurgie: Sleeve-Gastrektomie.  Zent­ralbl Chir. 2009;  134 24-31
  • 63 Karamanakos S N, Vagenas K, Kalfarentzos F et al. Weight loss, appetite suppression, and changes in fasting and postprandial ghrelin and peptide-YY levels after Roux-en-Y gastric bypass and sleeve gastrectomy: a prospective, double blind study.  Ann Surg. 2008;  247 401-407
  • 64 Kellum J M, Kuemmerle J F, O’Dorisio T M et al. Gastrointestinal hormone responses to meals before and after gastric bypass and vertical banded gastroplasty.  Ann Surg. 1990;  211 763-770
  • 65 Ashrafian H, le Roux C W. Metabolic surgery and gut hormones – A review of bariatric entero-humoral modulation.  Physiol Behav. 2009;  97 620-631

Dr. Marco Bueter

Imperial College London · Hammersmith Hospital · Department for Investigative Medicine

Commonwealth Building, 6th floor

Du Cane Road

W12 0NN London, UK

Phone: 00 44 / (0) 79 70 71 94 53

Fax: 00 44 / (0) 20 83 83 83 20

Email: m.bueter@imperial.ac.uk

    >