Skip to main content
Hauptrubriken
CME Facharzt-Training Webinare Zeitschriften Bücher e.Medpedia Podcast
Service
Jobbörse Info & Hilfe
Fachgebiete
Anästhesiologie Allgemeinmedizin Arbeitsmedizin Augenheilkunde Chirurgie Dermatologie Gynäkologie und Geburtshilfe HNO Innere Medizin Kardiologie Neurologie Onkologie und Hämatologie Orthopädie und Unfallchirurgie Pädiatrie Pathologie Psychiatrie Radiologie Rechtsmedizin Urologie Zahnmedizin
Themen
Klimawandel und Gesundheit Neues aus dem Markt COVID-19 Praxis und Beruf Seltene Erkrankungen GOÄ & EBM Panorama
Sammlungen
Kasuistiken Algorithmen & Infografiken Blickdiagnosen Arthropedia FlapFinder (für Dermatochirurgen) Videos Kongressberichterstattung Medizin für Apothekerinnen und Apotheker Für Ärztinnen und Ärzte in Weiterbildung Für Medizinstudierende

Live-Webinar: Aktuelle Leitlinien bei Herz-Kreislauf-Erkrankungen

Konkret geht es um den Diabetes-Patienten mit kardiovaskulären Erkrankungen oder Risiken, die Herzinsuffizienz sowie die kardiovaskuläre Primär- und Sekundärprävention. Sind Sie hier schon auf dem neuesten Stand? Unsere Experten beleuchten, wo und warum das bisherige Procedere geändert werden soll und was in der Praxis sinnvoll ist. Holen Sie sich Ihr Update und 2 CME-Punkte beim MMW-Webinar am 24. April von 17.30 bis 19 Uhr. 
Erweiterte Suche
Anmelden
nach oben
Obesity Surgery
Erschienen in: Obesity Surgery 9/2019

11.06.2019 | Review Article

Targeting Islets: Metabolic Surgery Is More than a Bariatric Surgery

verfasst von: Xi Chen, Jingjing Zhang, Zhiguang Zhou

Erschienen in: Obesity Surgery | Ausgabe 9/2019

Einloggen, um Zugang zu erhalten

Abstract

Metabolic surgery is an effective therapy for diabetic patients with obesity. The main mechanisms underlying the effects of metabolic surgery include food intake restriction and the accompanying reduced daily caloric intake and changes in gut hormones and bile acid. Insulin resistance and impaired β-cell function contribute to the development of type 2 diabetes. An increasing number of studies have focused on the central role of islet function in type 2 diabetes. In this article, we review the related high-quality literature and summarize the following mechanisms and principles underlying metabolic surgery in the context of islet function protection: (1) reduced glucotoxicity and chronic inflammation help facilitate better β-cell function and the preservation of β-cell mass following metabolic surgery; (2) based on the increased levels of GLP-1 and PYY after metabolic surgery, gut hormones appear to play a significant role in improving β-cell function through the GLP-1R signaling pathways; (3) the bile acid signaling pathway could affect β-cell function; and (4) the GLP-1R and bile acid signaling pathways could also cause other endocrine cells to contribute to islet function.
Literatur
1.
Cho NH, Shaw JE, Karuranga S. IDF diabetes atlas: global estimates of diabetes prevalence for 2017 and projections for 2045. Diabetes Res Clin Pract. 2018;138:271–81.PubMedCrossRef
2.
Yang W, Lu J, Weng J. Prevalence of diabetes among men and women in China. N Engl J Med. 2010;362(12):1090–101.CrossRefPubMed
3.
NCD-RisC NRFC. Trends in adult body-mass index in 200 countries from 1975 to 2014: a pooled analysis of 1698 population-based measurement studies with 19·2 million participants. Lancet. 2016;387(10026):1377–96.CrossRef
4.
Ramos-Levi AM, Rubio MA. Comment on Rubino et al. metabolic surgery in the treatment algorithm for type 2 diabetes: a joint statement by International Diabetes Organizations. Diabetes Care 2016;39:861–877. Diabetes Care. 2017;40(7):e90–1.PubMedCrossRef
5.
ADA. Standards of medical care in diabetes--2009. Diabetes Care. 2009;32 Suppl 1:S13–61.
6.
7.
Accili D. Lilly lecture 2003: the struggle for mastery in insulin action: from triumvirate to republic. Diabetes. 2004;53(7):1633–42.PubMedCrossRef
8.
9.
Donath MY. Targeting inflammation in the treatment of type 2 diabetes: time to start. Nat Rev Drug Discov. 2014;13(6):465–76.PubMedCrossRef
10.
Shu CJ, Benoist C, Mathis D. The immune system’s involvement in obesity-driven type 2 diabetes. Semin Immunol. 2012;24(6):436–42.PubMedCrossRef
11.
Ferrannini E. Insulin resistance versus insulin deficiency in non-insulin-dependent diabetes mellitus: problems and prospects. Endocr Rev. 1998;19(4):477–90.PubMedCrossRef
12.
Donath MY, Shoelson SE. Type 2 diabetes as an inflammatory disease. Nat Rev Immunol. 2011;11(2):98–107.PubMedCrossRef
13.
Cerf ME. Beta cell dysfunction and insulin resistance. Front Endocrinol (Lausanne). 2013;4:37.CrossRef
14.
Heit JJ, Karnik SK, Kim SK. Intrinsic regulators of pancreatic beta-cell proliferation. Annu Rev Cell Dev Biol. 2006;22:311–38.PubMedCrossRef
15.
Vangoitsenhoven R, Mathieu C, Van der Schueren B. GLP1 and cancer: friend or foe? Endocr Relat Cancer. 2012;19(5):F77–88.PubMedCrossRef
16.
17.
Kalupahana NS, Moustaid-Moussa N, Claycombe KJ. Immunity as a link between obesity and insulin resistance. Mol Asp Med. 2012;33(1):26–34.CrossRef
18.
Lee BC, Lee J. Cellular and molecular players in adipose tissue inflammation in the development of obesity-induced insulin resistance. Biochim Biophys Acta. 2014;1842(3):446–62.PubMedCrossRef
19.
Butler PC, Meier JJ, Butler AE. The replication of beta cells in normal physiology, in disease and for therapy. Nat Clin Pract Endocrinol Metab. 2007;3(11):758–68.PubMedCrossRef
20.
Talchai C, Lin HV, Kitamura T. Genetic and biochemical pathways of beta-cell failure in type 2 diabetes. Diabetes Obes Metab. 2009;11(Suppl 4):38–45.PubMedCrossRef
21.
Merino B, Alonso-Magdalena P, Lluesma M. Pancreatic alpha-cells from female mice undergo morphofunctional changes during compensatory adaptations of the endocrine pancreas to diet-induced obesity. Sci Rep. 2015;5:11622.PubMedPubMedCentralCrossRef
22.
Liu H, Javaheri A, Godar RJ. Intermittent fasting preserves beta-cell mass in obesity-induced diabetes via the autophagy-lysosome pathway. Autophagy. 2017;13(11):1952–68.PubMedPubMedCentralCrossRef
23.
Tang C, Ahmed K, Gille A. Loss of FFA2 and FFA3 increases insulin secretion and improves glucose tolerance in type 2 diabetes. Nat Med. 2015;21(2):173–7.PubMedCrossRef
24.
Larsen CM, Faulenbach M, Vaag A. Interleukin-1-receptor antagonist in type 2 diabetes mellitus. N Engl J Med. 2007;356(15):1517–26.CrossRefPubMed
25.
Bunck MC, Diamant M, Corner A. One-year treatment with exenatide improves beta-cell function, compared with insulin glargine, in metformin-treated type 2 diabetic patients: a randomized, controlled trial. Diabetes Care. 2009;32(5):762–8.PubMedPubMedCentralCrossRef
26.
Xu W, Bi Y, Sun Z. Comparison of the effects on glycaemic control and beta-cell function in newly diagnosed type 2 diabetes patients of treatment with exenatide, insulin or pioglitazone: a multicentre randomized parallel-group trial (the CONFIDENCE study). J Intern Med. 2015;277(1):137–50.PubMedCrossRef
27.
Yang Z, Zhou Z, Li X. Rosiglitazone preserves islet beta-cell function of adult-onset latent autoimmune diabetes in 3 years follow-up study. Diabetes Res Clin Pract. 2009;83(1):54–60.PubMedCrossRef
28.
Zhao Y, Yang L, Xiang Y. Dipeptidyl peptidase 4 inhibitor sitagliptin maintains beta-cell function in patients with recent-onset latent autoimmune diabetes in adults: one year prospective study. J Clin Endocrinol Metab. 2014;99(5):E876–80.PubMedCrossRef
29.
30.
Karamanakos SN, Vagenas K, Kalfarentzos F. 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(3):401–7.CrossRefPubMed
31.
Peterli R, Wolnerhanssen B, Peters T. Improvement in glucose metabolism after bariatric surgery: comparison of laparoscopic Roux-en-Y gastric bypass and laparoscopic sleeve gastrectomy: a prospective randomized trial. Ann Surg. 2009;250(2):234–41.CrossRefPubMed
32.
Peterli R, Borbely Y, Kern B. Early results of the Swiss Multicentre Bypass or Sleeve Study (SM-BOSS): a prospective randomized trial comparing laparoscopic sleeve gastrectomy and roux-en-Y gastric bypass. Ann Surg. 2013;258(5):690–694, 695.PubMedCrossRef
33.
Peterli R, Wolnerhanssen BK, Vetter D. Laparoscopic sleeve gastrectomy versus Roux-Y-gastric bypass for morbid obesity-3-year outcomes of the prospective randomized Swiss Multicenter Bypass or Sleeve Study (SM-BOSS). Ann Surg. 2017;265(3):466–73.PubMedCrossRef
34.
Ochner CN, Gibson C, Shanik M. Changes in neurohormonal gut peptides following bariatric surgery. Int J Obes. 2011;35(2):153–66.CrossRef
35.
Lee WJ, Chen CY, Chong K. Changes in postprandial gut hormones after metabolic surgery: a comparison of gastric bypass and sleeve gastrectomy. Surg Obes Relat Dis. 2011;7(6):683–90.PubMedCrossRef
36.
Thaler JP, Cummings DE. Minireview: hormonal and metabolic mechanisms of diabetes remission after gastrointestinal surgery. Endocrinology. 2009;150(6):2518–25.PubMedCrossRef
37.
Cummings DE, Weigle DS, Frayo RS. Plasma ghrelin levels after diet-induced weight loss or gastric bypass surgery. N Engl J Med. 2002;346(21):1623–30.CrossRefPubMed
38.
Holdstock C, Engstrom BE, Ohrvall M. Ghrelin and adipose tissue regulatory peptides: effect of gastric bypass surgery in obese humans. J Clin Endocrinol Metab. 2003;88(7):3177–83.CrossRefPubMed
39.
Stoeckli R, Chanda R, Langer I. Changes of body weight and plasma ghrelin levels after gastric banding and gastric bypass. Obes Res. 2004;12(2):346–50.PubMedCrossRef
40.
Rubino F, Gagner M, Gentileschi P. The early effect of the Roux-en-Y gastric bypass on hormones involved in body weight regulation and glucose metabolism. Ann Surg. 2004;240(2):236–42.PubMedPubMedCentralCrossRef
41.
Clements RH, Gonzalez QH, Long CI. 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. 4-5PubMed
42.
DePaula AL, Macedo AL, Schraibman V. Hormonal evaluation following laparoscopic treatment of type 2 diabetes mellitus patients with BMI 20-34. Surg Endosc. 2009;23(8):1724–32.PubMedCrossRef
43.
Farey JE, Preda TC, Fisher OM. Effect of laparoscopic sleeve gastrectomy on fasting gastrointestinal, pancreatic, and adipose-derived hormones and on non-esterified fatty acids. Obes Surg. 2017;27(2):399–407.PubMedCrossRef
44.
Jahansouz C, Xu H, Hertzel AV. Bile acids increase independently from hypocaloric restriction after bariatric surgery. Ann Surg. 2016;264(6):1022–8.PubMedCrossRef
45.
Jorgensen NB, Dirksen C, Bojsen-Moller KN. Improvements in glucose metabolism early after gastric bypass surgery are not explained by increases in total bile acids and fibroblast growth factor 19 concentrations. J Clin Endocrinol Metab. 2015;100(3):E396–406.PubMedCrossRef
46.
Khan FH, Shaw L, Zhang W. Fibroblast growth factor 21 correlates with weight loss after vertical sleeve gastrectomy in adolescents. Obesity (Silver Spring). 2016;24(11):2377–83.CrossRef
47.
Steinert RE, Peterli R, Keller S. Bile acids and gut peptide secretion after bariatric surgery: a 1-year prospective randomized pilot trial. Obesity (Silver Spring). 2013;21(12):E660–8.CrossRef
48.
49.
Ding L, Sousa KM, Jin L. Vertical sleeve gastrectomy activates GPBAR-1/TGR5 to sustain weight loss, improve fatty liver, and remit insulin resistance in mice. Hepatology. 2016;64(3):760–73.PubMedCrossRef
50.
McGavigan AK, Garibay D, Henseler ZM. TGR5 contributes to glucoregulatory improvements after vertical sleeve gastrectomy in mice. Gut. 2017;66(2):226–34.PubMedCrossRef
51.
52.
Ley RE, Turnbaugh PJ, Klein S. Microbial ecology: Human gut microbes associated with obesity. Nature. 2006;444(7122):1022–3.PubMedCrossRef
53.
Liou AP, Paziuk M, Luevano JJ. Conserved shifts in the gut microbiota due to gastric bypass reduce host weight and adiposity. Sci Transl Med. 2013;5(178):141r–78r.CrossRef
54.
Li JV, Ashrafian H, Bueter M. Metabolic surgery profoundly influences gut microbial-host metabolic cross-talk. Gut. 2011;60(9):1214–23.PubMedCrossRef
55.
56.
Furet JP, Kong LC, Tap J. Differential adaptation of human gut microbiota to bariatric surgery-induced weight loss: links with metabolic and low-grade inflammation markers. Diabetes. 2010;59(12):3049–57.PubMedPubMedCentralCrossRef
57.
58.
59.
Puri S, Akiyama H, Hebrok M. VHL-mediated disruption of Sox9 activity compromises beta-cell identity and results in diabetes mellitus. Genes Dev. 2013;27(23):2563–75.PubMedPubMedCentralCrossRef
60.
61.
Wang Z, York NW, Nichols CG. Pancreatic beta cell dedifferentiation in diabetes and redifferentiation following insulin therapy. Cell Metab. 2014;19(5):872–82.PubMedPubMedCentralCrossRef
62.
Cinti F, Bouchi R, Kim-Muller JY. Evidence of beta-cell dedifferentiation in human type 2 diabetes. J Clin Endocrinol Metab. 2016;101(3):1044–54.PubMedCrossRef
63.
Savage PJ, Bennion LJ, Flock EV. Diet-induced improvement of abnormalities in insulin and glucagon secretion and in insulin receptor binding in diabetes mellitus. J Clin Endocrinol Metab. 1979;48(6):999–1007.PubMedCrossRef
64.
Greenwood RH, Mahler RF, Hales CN. Improvement in insulin secretion in diabetes after diazoxide. Lancet. 1976;1(7957):444–7.PubMedCrossRef
65.
Wajchenberg BL. Beta-cell failure in diabetes and preservation by clinical treatment. Endocr Rev. 2007;28(2):187–218.PubMedCrossRef
66.
Zhou X, Qian B, Ji N. Pancreatic hyperplasia after gastric bypass surgery in a GK rat model of non-obese type 2 diabetes. J Endocrinol. 2016;228(1):13–23.PubMedCrossRef
67.
Qian B, Zhou X, Li B. Reduction of pancreatic beta-cell dedifferentiation after gastric bypass surgery in diabetic rats. J Mol Cell Biol. 2014;6(6):531–4.PubMedCrossRef
68.
Roslin MS, Dudiy Y, Weiskopf J. Comparison between RYGB, DS, and VSG effect on glucose homeostasis. Obes Surg. 2012;22(8):1281–6.PubMedCrossRef
69.
Mari A, Manco M, Guidone C. Restoration of normal glucose tolerance in severely obese patients after bilio-pancreatic diversion: role of insulin sensitivity and beta cell function. Diabetologia. 2006;49(9):2136–43.CrossRefPubMed
70.
Nannipieri M, Mari A, Anselmino M. The role of beta-cell function and insulin sensitivity in the remission of type 2 diabetes after gastric bypass surgery. J Clin Endocrinol Metab. 2011;96(9):E1372–9.CrossRefPubMed
71.
Chiellini C, Iaconelli A, Familiari P. Study of the effects of transoral gastroplasty on insulin sensitivity and secretion in obese subjects. Nutr Metab Cardiovasc Dis. 2010;20(3):202–7.PubMedCrossRef
72.
Bosello O, Armellini F, Pelloso M. Glucose tolerance in jejunoileal bypass for morbid obesity: a fifteen month follow-up. Diabete Metab. 1978;4(3):159–62.PubMed
73.
Sirinek KR, O’Dorisio TM, Hill D. Hyperinsulinism, glucose-dependent insulinotropic polypeptide, and the enteroinsular axis in morbidly obese patients before and after gastric bypass. Surgery. 1986;100(4):781–7.PubMed
74.
Karayiannakis AJ, Syrigos KN, Zbar A. The effect of vertical banded gastroplasty on glucose-induced beta-endorphin response. J Surg Res. 1998;80(2):123–8.PubMedCrossRef
75.
Kopp HP, Kopp CW, Festa A. Impact of weight loss on inflammatory proteins and their association with the insulin resistance syndrome in morbidly obese patients. Arterioscler Thromb Vasc Biol. 2003;23(6):1042–7.PubMedCrossRef
76.
Korner J, Inabnet W, Febres G. Prospective study of gut hormone and metabolic changes after adjustable gastric banding and Roux-en-Y gastric bypass. Int J Obes. 2009;33(7):786–95.CrossRef
77.
de Carvalho CP, Marin DM, de Souza AL. GLP-1 and adiponectin: effect of weight loss after dietary restriction and gastric bypass in morbidly obese patients with normal and abnormal glucose metabolism. Obes Surg. 2009;19(3):313–20.PubMedCrossRef
78.
De Paula AL, Stival AR, Halpern A. Improvement in insulin sensitivity and beta-cell function following ileal interposition with sleeve gastrectomy in type 2 diabetic patients: potential mechanisms. J Gastrointest Surg. 2011;15(8):1344–53.PubMedCrossRef
79.
Lee WJ, Ser KH, Chong K. Laparoscopic sleeve gastrectomy for diabetes treatment in nonmorbidly obese patients: efficacy and change of insulin secretion. Surgery. 2010;147(5):664–9.CrossRefPubMed
80.
Umeda LM, Silva EA, Carneiro G. Early improvement in glycemic control after bariatric surgery and its relationships with insulin, GLP-1, and glucagon secretion in type 2 diabetic patients. Obes Surg. 2011;21(7):896–901.PubMedCrossRef
81.
Campos GM, Rabl C, Peeva S. Improvement in peripheral glucose uptake after gastric bypass surgery is observed only after substantial weight loss has occurred and correlates with the magnitude of weight lost. J Gastrointest Surg. 2010;14(1):15–23.PubMedCrossRef
82.
Laferrere B, Heshka S, Wang K. Incretin levels and effect are markedly enhanced 1 month after Roux-en-Y gastric bypass surgery in obese patients with type 2 diabetes. Diabetes Care. 2007;30(7):1709–16.PubMedCrossRef
83.
Cummings DE, Cohen RV. Response to Comment on: Cohen et al. Effects of gastric bypass surgery in patients with type 2 diabetes and only mild obesity. Diabetes Care 2012;35:1420–1428. Diabetes Care. 2013;36(4):e59.PubMedPubMedCentralCrossRef
84.
85.
Ramracheya RD, McCulloch LJ, Clark A. PYY-dependent restoration of impaired insulin and glucagon secretion in type 2 diabetes following Roux-En-Y gastric bypass surgery. Cell Rep. 2016;15(5):944–50.PubMedPubMedCentralCrossRef
86.
Alarcon C, Boland BB, Uchizono Y. Pancreatic beta-cell adaptive plasticity in obesity increases insulin production but adversely affects secretory function. Diabetes. 2016;65(2):438–50.PubMedCrossRef
87.
Martinussen C, Bojsen-Moller KN, Dirksen C. Immediate enhancement of first-phase insulin secretion and unchanged glucose effectiveness in patients with type 2 diabetes after Roux-en-Y gastric bypass. Am J Physiol Endocrinol Metab. 2015;308(6):E535–44.PubMedCrossRef
88.
Ehses JA, Perren A, Eppler E. Increased number of islet-associated macrophages in type 2 diabetes. Diabetes. 2007;56(9):2356–70.PubMedCrossRef
89.
Richardson SJ, Willcox A, Bone AJ. Islet-associated macrophages in type 2 diabetes. Diabetologia. 2009;52(8):1686–8.PubMedCrossRef
90.
Boni-Schnetzler M, Thorne J, Parnaud G. Increased interleukin (IL)-1beta messenger ribonucleic acid expression in beta -cells of individuals with type 2 diabetes and regulation of IL-1beta in human islets by glucose and autostimulation. J Clin Endocrinol Metab. 2008;93(10):4065–74.PubMedPubMedCentralCrossRef
91.
Eguchi K, Manabe I, Oishi-Tanaka Y. Saturated fatty acid and TLR signaling link beta cell dysfunction and islet inflammation. Cell Metab. 2012;15(4):518–33.PubMedCrossRef
92.
Jones HB, Nugent D, Jenkins R. Variation in characteristics of islets of Langerhans in insulin-resistant, diabetic and non-diabetic-rat strains. Int J Exp Pathol. 2010;91(3):288–301.PubMedPubMedCentralCrossRef
93.
Masters SL, Dunne A, Subramanian SL. Activation of the NLRP3 inflammasome by islet amyloid polypeptide provides a mechanism for enhanced IL-1beta in type 2 diabetes. Nat Immunol. 2010;11(10):897–904.PubMedPubMedCentralCrossRef
94.
Youm YH, Adijiang A, Vandanmagsar B. Elimination of the NLRP3-ASC inflammasome protects against chronic obesity-induced pancreatic damage. Endocrinology. 2011;152(11):4039–45.PubMedPubMedCentralCrossRef
95.
Nicol LE, Grant WF, Comstock SM. Pancreatic inflammation and increased islet macrophages in insulin-resistant juvenile primates. J Endocrinol. 2013;217(2):207–13.PubMedPubMedCentralCrossRef
96.
Maedler K, Sergeev P, Ris F. Glucose-induced beta cell production of IL-1beta contributes to glucotoxicity in human pancreatic islets. J Clin Invest. 2017;127(4):1589.PubMedPubMedCentralCrossRef
97.
Cancello R, Rouault C, Guilhem G. Urokinase plasminogen activator receptor in adipose tissue macrophages of morbidly obese subjects. Obes Facts. 2011;4(1):17–25.PubMedPubMedCentralCrossRef
98.
Dillard TH, Purnell JQ, Smith MD. Omentectomy added to Roux-en-Y gastric bypass surgery: a randomized, controlled trial. Surg Obes Relat Dis. 2013;9(2):269–75.PubMedCrossRef
99.
Moschen AR, Molnar C, Geiger S. Anti-inflammatory effects of excessive weight loss: potent suppression of adipose interleukin 6 and tumour necrosis factor alpha expression. Gut. 2010;59(9):1259–64.PubMedCrossRef
100.
Pardina E, Ferrer R, Baena-Fustegueras JA. Only C-reactive protein, but not TNF-alpha or IL6, reflects the improvement in inflammation after bariatric surgery. Obes Surg. 2012;22(1):131–9.PubMedCrossRef
101.
Haider DG, Schindler K, Prager G. Serum retinol-binding protein 4 is reduced after weight loss in morbidly obese subjects. J Clin Endocrinol Metab. 2007;92(3):1168–71.PubMedCrossRef
102.
Baggio LL, Drucker DJ. Biology of incretins: GLP-1 and GIP. Gastroenterology. 2007;132(6):2131–57.PubMedCrossRef
103.
Ye J, Hao Z, Mumphrey MB. GLP-1 receptor signaling is not required for reduced body weight after RYGB in rodents. Am J Physiol Regul Integr Comp Physiol. 2014;306(5):R352–62.PubMedPubMedCentralCrossRef
104.
Wilson-Perez HE, Chambers AP, Ryan KK. Vertical sleeve gastrectomy is effective in two genetic mouse models of glucagon-like Peptide 1 receptor deficiency. Diabetes. 2013;62(7):2380–5.PubMedPubMedCentralCrossRef
105.
Bottcher G, Ahren B, Lundquist I. Peptide YY: intrapancreatic localization and effects on insulin and glucagon secretion in the mouse. Pancreas. 1989;4(3):282–8.PubMedCrossRef
106.
Upchurch BH, Aponte GW, Leiter AB. Expression of peptide YY in all four islet cell types in the developing mouse pancreas suggests a common peptide YY-producing progenitor. Development. 1994;120(2):245–52.PubMed
107.
108.
Boey D, Sainsbury A, Herzog H. The role of peptide YY in regulating glucose homeostasis. Peptides. 2007;28(2):390–5.PubMedCrossRef
109.
Sam AH, Gunner DJ, King A. Selective ablation of peptide YY cells in adult mice reveals their role in beta cell survival. Gastroenterology. 2012;143(2):459–68.PubMedCrossRef
110.
Shi YC, Loh K, Bensellam M. Pancreatic PYY is critical in the control of insulin secretion and glucose homeostasis in female mice. Endocrinology. 2015;156(9):3122–36.PubMedCrossRef
111.
Garibay D, Lou J, Lee SA. Beta cell GLP-1R signaling alters alpha cell proglucagon processing after vertical sleeve gastrectomy in mice. Cell Rep. 2018;23(4):967–73.PubMedPubMedCentralCrossRef
112.
Mokadem M, Zechner JF, Margolskee RF. Effects of Roux-en-Y gastric bypass on energy and glucose homeostasis are preserved in two mouse models of functional glucagon-like peptide-1 deficiency. Mol Metab. 2014;3(2):191–201.CrossRefPubMed
113.
Sachdev S, Wang Q, Billington C. FGF 19 and bile acids increase following Roux-en-Y gastric bypass but not after medical management in patients with type 2 diabetes. Obes Surg. 2016;26(5):957–65.PubMedPubMedCentralCrossRef
114.
Nemati R, Lu J, Dokpuang D. Increased bile acids and FGF19 after sleeve gastrectomy and Roux-en-Y gastric bypass correlate with improvement in type 2 diabetes in a randomized trial. Obes Surg. 2018;28(9):2672–86.PubMedCrossRef
115.
Kohli R, Kirby M, Setchell KD. Intestinal adaptation after ileal interposition surgery increases bile acid recycling and protects against obesity-related comorbidities. Am J Physiol Gastrointest Liver Physiol. 2010;299(3):G652–60.PubMedPubMedCentralCrossRef
116.
Cariou B, van Harmelen K, Duran-Sandoval D. The farnesoid X receptor modulates adiposity and peripheral insulin sensitivity in mice. J Biol Chem. 2006;281(16):11039–49.PubMedCrossRef
117.
Prawitt J, Abdelkarim M, Stroeve JH. Farnesoid X receptor deficiency improves glucose homeostasis in mouse models of obesity. Diabetes. 2011;60(7):1861–71.PubMedPubMedCentralCrossRef
118.
119.
Ryan KK, Kohli R, Gutierrez-Aguilar R. Fibroblast growth factor-19 action in the brain reduces food intake and body weight and improves glucose tolerance in male rats. Endocrinology. 2013;154(1):9–15.PubMedCrossRef
120.
Baud G, Daoudi M, Hubert T. Bile diversion in Roux-en-Y gastric bypass modulates sodium-dependent glucose intestinal uptake. Cell Metab. 2016;23(3):547–53.PubMedCrossRef
121.
Whalley NM, Pritchard LE, Smith DM. Processing of proglucagon to GLP-1 in pancreatic alpha-cells: is this a paracrine mechanism enabling GLP-1 to act on beta-cells? J Endocrinol. 2011;211(1):99–106.PubMedCrossRef
122.
Kumar DP, Rajagopal S, Mahavadi S. Activation of transmembrane bile acid receptor TGR5 stimulates insulin secretion in pancreatic beta cells. Biochem Biophys Res Commun. 2012;427(3):600–5.PubMedPubMedCentralCrossRef
123.
Kumar DP, Asgharpour A, Mirshahi F. Activation of transmembrane bile acid receptor TGR5 modulates pancreatic islet alpha cells to promote glucose homeostasis. J Biol Chem. 2016;291(13):6626–40.PubMedPubMedCentralCrossRef
Metadaten
Titel
Targeting Islets: Metabolic Surgery Is More than a Bariatric Surgery
verfasst von
Xi Chen
Jingjing Zhang
Zhiguang Zhou
Publikationsdatum
11.06.2019
Verlag
Springer US
Erschienen in
Obesity Surgery / Ausgabe 9/2019
Print ISSN: 0960-8923
Elektronische ISSN: 1708-0428
DOI
https://doi.org/10.1007/s11695-019-03979-1

Weitere Artikel der Ausgabe 9/2019

Obesity Surgery 9/2019 Zur Ausgabe

Original Contributions

Reliability and Educational Value of Laparoscopic Sleeve Gastrectomy Surgery Videos on YouTube

Review Article

Endoscopic Gastric Plication for Morbid Obesity: a Systematic Review and Meta-analysis of Published Data over Time

Letter to the Editor

Sleeve-Jejunal Bypass as an Alternative Procedure for Managing Leakage After Laparoscopic Sleeve Gastrectomy: a Case Report

Original Contributions

Endoscopic Internal Drainage Coupled to Prompt External Drainage Mobilization Is an Effective Approach for the Treatment of Complicated Cases of Sleeve Gastrectomy

Brief Communication

Duodenal-Jejunal Bypass Maintains Gut Permeability by Suppressing Gut Inflammation

Brief Communication

Prediction of Airflow Obstruction and the Risk of Complications in Morbidly Obese Patients Undergoing Bariatric Surgery

Neu im Fachgebiet Chirurgie

17.04.2024 | Postoperative nausea and vomiting | Nachrichten

Hochrisiko-Eingriffe für postoperative Übelkeit

16.04.2024 | HNO-Chirurgie | Nachrichten

HNO-Op. auch mit über 90?

16.04.2024 | Infektiologie | Nachrichten

Kein Abstrich bei chronischen Wunden ohne Entzündungszeichen!

10.04.2024 | Postoperative Schmerztherapie | Nachrichten

Chronische Schmerzen nach Op. oft mit neuropathischer Komponente
weitere anzeigen

Update Chirurgie

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.

Newsletter bestellen

Aktuelle BDC Leitlinien-Webinare

S3-Leitlinie „Diagnostik und Therapie des Karpaltunnelsyndroms“

Karpaltunnelsyndrom CME-Kurs
CME: 2 Punkte

Prof. Dr. med. Gregor Antoniadis Das Karpaltunnelsyndrom ist die häufigste Kompressionsneuropathie peripherer Nerven. Obwohl die Anamnese mit dem nächtlichen Einschlafen der Hand (Brachialgia parästhetica nocturna) sehr typisch ist, ist eine klinisch-neurologische Untersuchung und Elektroneurografie in manchen Fällen auch eine Neurosonografie erforderlich. Im Anfangsstadium sind konservative Maßnahmen (Handgelenksschiene, Ergotherapie) empfehlenswert. Bei nicht Ansprechen der konservativen Therapie oder Auftreten von neurologischen Ausfällen ist eine Dekompression des N. medianus am Karpaltunnel indiziert.

Prof. Dr. med. Gregor Antoniadis
Berufsverband der Deutschen Chirurgie e.V.

S2e-Leitlinie „Distale Radiusfraktur“

Radiusfraktur CME-Kurs
CME: 2 Punkte

Dr. med. Benjamin Meyknecht, PD Dr. med. Oliver Pieske Das Webinar S2e-Leitlinie „Distale Radiusfraktur“ beschäftigt sich mit Fragen und Antworten zu Diagnostik und Klassifikation sowie Möglichkeiten des Ausschlusses von Zusatzverletzungen. Die Referenten erläutern, welche Frakturen konservativ behandelt werden können und wie. Das Webinar beantwortet die Frage nach aktuellen operativen Therapiekonzepten: Welcher Zugang, welches Osteosynthesematerial? Auf was muss bei der Nachbehandlung der distalen Radiusfraktur geachtet werden?

PD Dr. med. Oliver Pieske
Dr. med. Benjamin Meyknecht
Berufsverband der Deutschen Chirurgie e.V.

S1-Leitlinie „Empfehlungen zur Therapie der akuten Appendizitis bei Erwachsenen“

Appendizitis CME-Kurs
CME: 2 Punkte

Dr. med. Mihailo Andric
Inhalte des Webinars zur S1-Leitlinie „Empfehlungen zur Therapie der akuten Appendizitis bei Erwachsenen“ sind die Darstellung des Projektes und des Erstellungswegs zur S1-Leitlinie, die Erläuterung der klinischen Relevanz der Klassifikation EAES 2015, die wissenschaftliche Begründung der wichtigsten Empfehlungen und die Darstellung stadiengerechter Therapieoptionen.

Dr. med. Mihailo Andric
Berufsverband der Deutschen Chirurgie e.V.