open access

Vol 69, No 5 (2018)
Review Article
Published online: 2018-09-12
Submitted: 2018-08-08
Accepted: 2018-08-12
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Endocrine implications of obesity and bariatric surgery

Michał Dyaczyński, Colin Guy Scanes, Helena Koziec, Helena Koziec, Krystyna Pierzchała-Koziec
DOI: 10.5603/EP.2018.0059
·
Pubmed: 30379322
·
Endokrynologia Polska 2018;69(5):574-597.

open access

Vol 69, No 5 (2018)
Review Article
Published online: 2018-09-12
Submitted: 2018-08-08
Accepted: 2018-08-12

Abstract

Introduction: Obesity is a highly prevalent disease in the world associated with the disorders of endocrine system. Recently, it may be concluded that the only effective treatment of obesity remains bariatric surgery. The aim of the review was to compare the concepts of appetite hormonal regulation, reasons of obesity development and bariatric procedures published over the last decade. Material and methods: The reviewed publications had been chosen on the base on: 1. reasons and endocrine consequences of obesity; 2. development of surgery methods from the first bariatric to present and future less aggressive procedures; 3. impact of surgery on the endocrine status of patient. Results: The most serious endocrine disturbances during obesity are dysfunctions of hypothalamic circuits responsible for appetite regulation, insulin resistance, changes in hormones activity and abnormal activity of adipocytes hormones. The currently recommended bariatric surgeries are Roux-en-Y gastric bypass, sleeve gastrectomy and adjustable gastric banding. Bariatric surgical procedures, particularly combination of restrictive and malabsorptive, decrease the body weight and eliminate several but not all components of metabolic syndrome. Conclusions: 1.Hunger and satiety are mediated by an interplay of nervous and endocrine signals. 2. Healthy adipose tissue secretion of adipokines is coordinated in an anti-inflammatory, insulin-sensitizing and cardioprotective pattern. However, with increasing fat mass this secretion pattern is changed into a proinflammatory, insulin resistant, atherogenic and fatal systemic environment . 3. Bariatric surgery is not a solution of the obesity problem for everyone. 4. Long term postsurgical observations of the hormonal profile changes are necessary and should be obligatory.

Abstract

Introduction: Obesity is a highly prevalent disease in the world associated with the disorders of endocrine system. Recently, it may be concluded that the only effective treatment of obesity remains bariatric surgery. The aim of the review was to compare the concepts of appetite hormonal regulation, reasons of obesity development and bariatric procedures published over the last decade. Material and methods: The reviewed publications had been chosen on the base on: 1. reasons and endocrine consequences of obesity; 2. development of surgery methods from the first bariatric to present and future less aggressive procedures; 3. impact of surgery on the endocrine status of patient. Results: The most serious endocrine disturbances during obesity are dysfunctions of hypothalamic circuits responsible for appetite regulation, insulin resistance, changes in hormones activity and abnormal activity of adipocytes hormones. The currently recommended bariatric surgeries are Roux-en-Y gastric bypass, sleeve gastrectomy and adjustable gastric banding. Bariatric surgical procedures, particularly combination of restrictive and malabsorptive, decrease the body weight and eliminate several but not all components of metabolic syndrome. Conclusions: 1.Hunger and satiety are mediated by an interplay of nervous and endocrine signals. 2. Healthy adipose tissue secretion of adipokines is coordinated in an anti-inflammatory, insulin-sensitizing and cardioprotective pattern. However, with increasing fat mass this secretion pattern is changed into a proinflammatory, insulin resistant, atherogenic and fatal systemic environment . 3. Bariatric surgery is not a solution of the obesity problem for everyone. 4. Long term postsurgical observations of the hormonal profile changes are necessary and should be obligatory.
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Keywords

obesity; endocrine dysfunctions; bariatric surgery; gastrointestinal hormones

About this article
Title

Endocrine implications of obesity and bariatric surgery

Journal

Endokrynologia Polska

Issue

Vol 69, No 5 (2018)

Pages

574-597

Published online

2018-09-12

DOI

10.5603/EP.2018.0059

Pubmed

30379322

Bibliographic record

Endokrynologia Polska 2018;69(5):574-597.

Keywords

obesity
endocrine dysfunctions
bariatric surgery
gastrointestinal hormones

Authors

Michał Dyaczyński
Colin Guy Scanes
Helena Koziec
Helena Koziec
Krystyna Pierzchała-Koziec

References (89)
  1. Friedman JM. Obesity in the new millennium. Nature. 2000; 404(6778): 632–634.
  2. Dhillo WS. Appetite regulation: an overview. Thyroid. 2007; 17(5): 433–445.
  3. de Lima-Júnior JC, Velloso LA, Geloneze B. The Obese Brain--Effects of Bariatric Surgery on Energy Balance Neurocircuitry. Curr Atheroscler Rep. 2015; 17(10): 57.
  4. World Health Organization. Report of a WHO Consultation. Obesity: preventing and managing the global epidemic Geneva, Switzerland WHO, 2000.
  5. World Health Organisation. Ten facts on obesity 2013 (5/9/2013). http://www.who.int/features/factfiles/obesity/en/index.html.
  6. Caballero B. The global epidemic of obesity: an overview. Epidemiol Rev. 2007; 29: 1–5.
  7. Kozakowski J, Lebovitz HE, Zgliczyński W, et al. Gastric Contractility Modulation - a novel method for the treatment of type 2 diabetes mellitus and obesity. Endokrynol Pol. 2017; 68(5): 579–584.
  8. Rucker D, Padwal R, Li SK, et al. Long term pharmacotherapy for obesity and overweight: updated meta-analysis. BMJ. 2007; 335(7631): 1194–1199.
  9. Rodgers S, Burnet R, Goss A, et al. Jaw wiring in treatment of obesity. Lancet. 1977; 1(8024): 1221–1222.
  10. Buchwald H, Oien DM. Metabolic/bariatric surgery Worldwide 2008. Obes Surg. 2009; 19(12): 1605–1611.
  11. Beck B. Neuropeptides and obesity. Nutrition. 2000; 16(10): 916–923.
  12. Steele CA, Cuthbertson DJ, MacFarlane IA, et al. Hypothalamic obesity: prevalence, associations and longitudinal trends in weight in a specialist adult neuroendocrine clinic. Eur J Endocrinol. 2013; 168(4): 501–507.
  13. Menyhért J, Wittmann G, Hrabovszky E, et al. Interconnection between orexigenic neuropeptide Y- and anorexigenic alpha-melanocyte stimulating hormone-synthesizing neuronal systems of the human hypothalamus. Brain Res. 2006; 1076(1): 101–105.
  14. Williams KW, Elmquist JK. Lighting up the hypothalamus: coordinated control of feeding behavior. Nat Neurosci. 2011; 14(3): 277–278.
  15. Zhan C, Zhou J, Feng Q, et al. Acute and long-term suppression of feeding behavior by POMC neurons in the brainstem and hypothalamus, respectively. J Neurosci. 2013; 33(8): 3624–3632.
  16. Lei L, Gu Y, Murphy JG, et al. Brainstem raphe pallidus and the adjacent area contain a novel action site in the melanocortin circuitry regulating energy balance. Life Sci J. 2008; 5(3): 1–13.
  17. Cummings DE, Overduin J. Gastrointestinal regulation of food intake. J Clin Invest. 2007; 117(1): 13–23.
  18. Bloomgarden ZT. Gut and adipocyte peptides. Diabetes Care. 2006; 29(2): 450–456.
  19. Ockander L, Hedenbro JL, Rehfeld JF, et al. Jejunoileal bypass changes the duodenal cholecystokinin and somatostatin cell density. Obes Surg. 2003; 13(4): 584–590.
  20. Matson CA, Reid DF, Cannon TA, et al. Cholecystokinin and leptin act synergistically to reduce body weight. Am J Physiol Regul Integr Comp Physiol. 2000; 278(4): R882–R890.
  21. Whitmore TE, Holloway JL, Lofton-Day CE, et al. Human secretin (SCT): gene structure, chromosome location, and distribution of mRNA. Cytogenet Cell Genet. 2000; 90(1-2): 47–52.
  22. Baldwin GS, Patel O, Shulkes A. Evolution of gastrointestinal hormones: the cholecystokinin/gastrin family. Curr Opin Endocrinol Diabetes Obes. 2010; 17(1): 77–88.
  23. Sanger GJ, Wang Y, Hobson A, et al. Motilin: towards a new understanding of the gastrointestinal neuropharmacology and therapeutic use of motilin receptor agonists. Br J Pharmacol. 2013; 170(7): 1323–1332.
  24. Lang R, Gundlach AL, Holmes FE, et al. Physiology, signaling, and pharmacology of galanin peptides and receptors: three decades of emerging diversity. Pharmacol Rev. 2015; 67(1): 118–175.
  25. Amato A, Baldassano S, Mulè F. GLP2: an underestimated signal for improving glycaemic control and insulin sensitivity. J Endocrinol. 2016; 229(2): R57–R66.
  26. Nauck M, Schmidt WE, Ebert R, et al. Insulinotropic properties of synthetic human gastric inhibitory polypeptide in man: interactions with glucose, phenylalanine, and cholecystokinin-8. J Clin Endocrinol Metab. 1989; 69(3): 654–662.
  27. Seufert J, Gallwitz B. The extra-pancreatic effects of GLP-1 receptor agonists: a focus on the cardiovascular, gastrointestinal and central nervous systems. Diabetes Obes Metab. 2014; 16(8): 673–688.
  28. Vidal J, de Hollanda A, Jiménez A. GLP-1 is not the key mediator of the health benefits of metabolic surgery. Surg Obes Relat Dis. 2016; 12(6): 1225–1229.
  29. Gourcerol G, St-Pierre DH, Taché Y. Lack of obestatin effects on food intake: should obestatin be renamed ghrelin-associated peptide (GAP)? Regul Pept. 2007; 141(1-3): 1–7.
  30. le Roux CW, Batterham RL, Aylwin SJB, et al. Attenuated peptide YY release in obese subjects is associated with reduced satiety. Endocrinology. 2006; 147(1): 3–8.
  31. Laferrère B, Swerdlow N, Bawa B, et al. Rise of oxyntomodulin in response to oral glucose after gastric bypass surgery in patients with type 2 diabetes. J Clin Endocrinol Metab. 2010; 95(8): 4072–4076.
  32. Willesen MG, Kristensen P, Rømer J. Co-localization of growth hormone secretagogue receptor and NPY mRNA in the arcuate nucleus of the rat. Neuroendocrinology. 1999; 70(5): 306–316.
  33. Kojima M, Hosoda H, Date Y, et al. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature. 1999; 402(6762): 656–660.
  34. Date Y, Kojima M, Hosoda H, et al. Ghrelin, a novel growth hormone-releasing acylated peptide, is synthesized in a distinct endocrine cell type in the gastrointestinal tracts of rats and humans. Endocrinology. 2000; 141(11): 4255–4261.
  35. Pournaras DJ, le Roux CW. Ghrelin and metabolic surgery. Int J Pept. 2010; 2010.
  36. Dickson SL, Egecioglu E, Landgren S, et al. The role of the central ghrelin system in reward from food and chemical drugs. Mol Cell Endocrinol. 2011; 340(1): 80–87.
  37. Benarroch EE. Endogenous opioid systems: current concepts and clinical correlations. Neurology. 2012; 79(8): 807–814.
  38. Gosnell BA, Levine AS. Reward systems and food intake: role of opioids. Int J Obes (Lond). 2009; 33 Suppl 2: S54–S58.
  39. Davis CA, Levitan RD, Reid C, et al. Dopamine for. Obesity (Silver Spring). 2009; 17(6): 1220–1225.
  40. Guillemin R. Somatostatin: the beginnings, 1972. Mol Cell Endocrinol. 2008; 286(1-2): 3–4.
  41. Rigamonti AE, Cella SG, Bonomo SM, et al. Effect of somatostatin infusion on peptide YY secretion: studies in the acute and recovery phase of anorexia nervosa and in obesity. Eur J Endocrinol. 2011; 165(3): 421–427.
  42. Martinez V. Somatostatin. Handbook of Biologically Active Peptides. 2013: 1320–1329.
  43. Ando H. Somatostatin. Handbook of Hormones. 2016: 36-e5–4.
  44. Ottaviani E, Malagoli D, Franceschi C. The evolution of the adipose tissue: a neglected enigma. Gen Comp Endocrinol. 2011; 174(1): 1–4.
  45. Bilir BE, Güldiken S, Tunçbilek N, et al. The effects of fat distribution and some adipokines on insulin resistance. Endokrynol Pol. 2016; 67(3): 277–282.
  46. García-Solís P, García OP, Hernández-Puga G, et al. Thyroid hormones and obesity: a known but poorly understood relationship. Endokrynol Pol. 2018; 69(3): 292–303.
  47. Fonseca-Alaniz MH, Takada J, Alonso-Vale MI, et al. Adipose tissue as an endocrine organ: from theory to practice. J Pediatr (Rio J). 2007; 83(5 Suppl): S192–S203.
  48. Trayhurn P, Bing C, Wood IS. Adipose tissue and adipokines--energy regulation from the human perspective. J Nutr. 2006; 136(7 Suppl): 1935S–1939S.
  49. Krysiak R, Żmuda W, Marek B, et al. Age may determine the effect of hypolipidemic agents on plasma adipokine levels in patients with elevated low-density lipoprotein cholesterol levels. Endokrynol Pol. 2016; 67(3): 271–276.
  50. Baranowska-Bik A, Baranowska B, Martyńska L, et al. Adipokine profile in patients with anorexia nervosa. Endokrynol Pol. 2017; 68(4): 422–429.
  51. Sirbu AE, Buburuzan L, Kevorkian S, et al. Adiponectin expression in visceral adiposity is an important determinant of insulin resistance in morbid obesity. Endokrynol Pol. 2018; 69(3): 252–258.
  52. Friedman JM, Halaas JL. Leptin and the regulation of body weight in mammals. Nature. 1998; 395(6704): 763–770.
  53. Khan SM, Hamnvik OPR, Brinkoetter M, et al. Leptin as a modulator of neuroendocrine function in humans. Yonsei Med J. 2012; 53(4): 671–679.
  54. Hwa JJ, Fawzi AB, Graziano MP, et al. Leptin increases energy expenditure and selectively promotes fat metabolism in ob/ob mice. Am J Physiol. 1997; 272(4 Pt 2): R1204–R1209.
  55. Steppan CM, Lazar MA. Resistin and obesity-associated insulin resistance. Trends Endocrinol Metab. 2002; 13(1): 18–23.
  56. Steppan CM, Bailey ST, Bhat S, et al. The hormone resistin links obesity to diabetes. Nature. 2001; 409(6818): 307–312.
  57. Goldstein BJ, Scalia R. Adiponectin: A novel adipokine linking adipocytes and vascular function. J Clin Endocrinol Metab. 2004; 89(6): 2563–2568.
  58. Wojciechowska C, Jacheć W, Romuk E, et al. The effect of BMI, serum leptin, and adiponectin levels on prognosis in patients with non-ischaemic dilated cardiomyopathy. Endokrynol Pol. 2017; 68(1): 26–34.
  59. Matsuzawa Y. Adiponectin: Identification, physiology and clinical relevance in metabolic and vascular disease. Atheroscler Suppl. 2005; 6(2): 7–14.
  60. Siemińska L, Borowski A, Marek B, et al. Serum concentrations of adipokines in men with prostate cancer and benign prostate hyperplasia. Endokrynol Pol. 2018; 69(2): 120–127.
  61. Kadowaki T, Yamauchi T. Adiponectin and adiponectin receptors. Endocr Rev. 2005; 26(3): 439–451.
  62. Fukuhara A, Matsuda M, Nishizawa M, et al. Visfatin: a protein secreted by visceral fat that mimics the effects of insulin. Science. 2005; 307(5708): 426–430.
  63. Davutoglu M, Ozkaya M, Guler E, et al. Plasma visfatin concentrations in childhood obesity: relationships with insulin resistance and anthropometric indices. Swiss Med Wkly. 2009; 139(1-2): 22–27.
  64. Auguet T, Quintero Y, Riesco D, et al. New adipokines vaspin and omentin. Circulating levels and gene expression in adipose tissue from morbidly obese women. BMC Med Genet. 2011; 12: 60.
  65. Blüher M. Vaspin in obesity and diabetes: pathophysiological and clinical significance. Endocrine. 2012; 41(2): 176–182.
  66. Tham JCh, leRoux CW. Benefits of bariatric surgery and perioperative surgical safety. EMJ Diabet. 2015; 3: 66–71.
  67. Colquitt JL, Picot J, Loveman E, et al. Surgery for obesity. Cochrane Database Syst Rev. 2009(2): CD003641.
  68. Lucchese M, Scopinaro N. Metabolic surgery. In: Buchwald H. ed. Minimally invasive bariatric and metabolic surgery: principles and technical aspects. Springer 2015: 69–79.
  69. Buchwald H. Overview of bariatric surgery. J Am Coll Surg. 2002; 194(3): 367–375.
  70. Moshiri M, Osman S, Robinson TJ, et al. Evolution of bariatric surgery: a historical perspective. AJR Am J Roentgenol. 2013; 201(1): W40–W48.
  71. Chang SH, Stoll CRT, Song J, et al. The effectiveness and risks of bariatric surgery: an updated systematic review and meta-analysis, 2003-2012. JAMA Surg. 2014; 149(3): 275–287.
  72. Melissas J. The bariatric multidisciplinary center.Lucchese M, Scopinaro N. ed. Minimally invasive bariatric and metabolic surgery: principles and technical aspects 2015: 59–67.
  73. le Roux CW, 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(5): 780–785.
  74. Demirpence M, Yilmaz H, Colak A, et al. The effect of sleeve gastrectomy on serum irisin levels in patients with morbid obesity. Endokrynol Pol. 2016; 67(5): 481–486.
  75. Laferrère B, Teixeira J, McGinty J, et al. Effect of weight loss by gastric bypass surgery versus hypocaloric diet on glucose and incretin levels in patients with type 2 diabetes. J Clin Endocrinol Metab. 2008; 93(7): 2479–2485.
  76. Chan JL, Mun EC, Stoyneva V, et al. Peptide YY levels are elevated after gastric bypass surgery. Obesity (Silver Spring). 2006; 14(2): 194–198.
  77. Beckman LM, Beckman TR, Earthman CP. Changes in gastrointestinal hormones and leptin after Roux-en-Y gastric bypass procedure: a review. J Am Diet Assoc. 2010; 110(4): 571–584.
  78. Cummings DE, Weigle DS, Frayo RS, et al. Plasma ghrelin levels after diet-induced weight loss or gastric bypass surgery. N Engl J Med. 2002; 346(21): 1623–1630.
  79. Reinehr T, Roth CL, Schernthaner GH, et al. Peptide YY and glucagon-like peptide-1 in morbidly obese patients before and after surgically induced weight loss. Obes Surg. 2007; 17(12): 1571–1577.
  80. Zwirska-Korczala K, Konturek SJ, Sodowski M, et al. Basal and postprandial plasma levels of PYY, ghrelin, cholecystokinin, gastrin and insulin in women with moderate and morbid obesity and metabolic syndrome. J Physiol Pharmacol. 2007; 58 Suppl 1: 13–35.
  81. Christou NV, Look D, McLean AP. Pre- and post-prandial plasma ghrelin levels do not correlate with satiety or failure to achieve a successful outcome after Roux-en-Y gastric bypass. Obes Surg. 2005; 15(7): 1017–1023.
  82. Gonzalez-Campoy JM, Richardson B, Richardson C, et al. Bariatric endocrinology: principles of medical practice. Int J Endocrinol. 2014; 2014: 917813.
  83. Lutz TA, Bueter M. The Use of Rat and Mouse Models in Bariatric Surgery Experiments. Front Nutr. 2016; 3: 25.
  84. Dirksen C, Jørgensen NB, Bojsen-Møller KN, et al. Gut hormones, early dumping and resting energy expenditure in patients with good and poor weight loss response after Roux-en-Y gastric bypass. Int J Obes (Lond). 2013; 37(11): 1452–1459.
  85. Pierzchała-Koziec K, Scanes CG, Zubel-łojek J, et al. Met-enkephalin-like peptides and ghrelin mitigate negative effects of bariatric surgery in rats. Acta Biol Cracovien ser Zool. 2014; 55/56: 100–107.
  86. Clements RH, Gonzalez QH, Long CI, et al. Hormonal changes after Roux-en Y gastric bypass for morbid obesity and the control of type-II diabetes mellitus. Am Surg. 2004; 70(1): 1–4; discussion 4.
  87. Fernández-Soto ML, Martín-Leyva A, González-Jiménez A, et al. Remission of type 2 diabetes mellitus after bariatric surgery - comparison between procedures. Endokrynol Pol. 2017; 68(1): 18–25.
  88. Meek CL, Lewis HB, Reimann F, et al. The effect of bariatric surgery on gastrointestinal and pancreatic peptide hormones. Peptides. 2016; 77: 28–37.
  89. Ochner CN, Gibson C, Shanik M, et al. Changes in neurohormonal gut peptides following bariatric surgery. Int J Obes (Lond). 2011; 35(2): 153–166.

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