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Erschienen in: Obesity Surgery 9/2013

01.09.2013 | Original Contributions

Duodenal–Jejunal Bypass Improves Glucose Metabolism and Adipokine Expression Independently of Weight Loss in a Diabetic Rat Model

verfasst von: Chunxiao Hu, Guangyong Zhang, Dong Sun, Haifeng Han, Sanyuan Hu

Erschienen in: Obesity Surgery | Ausgabe 9/2013

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Abstract

Background

There is accumulating evidence that adipokines lead to a proinflammatory state, which plays crucial roles in insulin resistance and development of type 2 diabetes mellitus (T2DM). Previous studies demonstrated that weight loss after bariatric surgery is accompanied by a suppression of the proinflammatory state. However, the effect of bariatric surgery on adipokine expression beyond weight loss is still elusive. The aim of this study was to investigate the effect of duodenal–jejunal bypass (DJB) on glucose homeostasis and adipokine expression independently of weight loss.

Methods

A T2DM rat model was developed by a high-fat diet and low dose of streptozotocin. Twenty-one diabetic rats and 10 age-matched SD rats were randomly assigned to the DJB group, sham-DJB (S-DJB) group, and control group. For 12 weeks after surgery, their body weight, food intake, glucose homeostasis, lipid parameters, serum adipokine levels, and adipokine gene expression in the mesocolon adipose tissue were measured.

Results

Compared to the S-DJB group, DJB induced significant and sustained glycemic control with improved insulin sensitivity and glucose tolerance independently of weight loss. DJB improved the lipid metabolism by decreasing fasting free fatty acids and triglycerides. Serum leptin and IL-6 significantly decreased 12 weeks after DJB, whereas adiponectin increased and TNF-α remained unchanged. The mRNA expression levels of leptin, TNF-α, and IL-6 decreased, whereas adiponectin increased in the mesocolon adipose tissue.

Conclusion

DJB reduced the proinflammatory adipokines and increased the anti-inflammatory adipokines independently of weight loss, which may contribute to the improvement of insulin sensitivity.
Literatur
1.
Zurück zum Zitat Zimmet P, Alberti KG, Shaw J. Global and societal implications of the diabetes epidemic. Nature. 2001;414(7):782. Epub 2001 Dec 13. PMID: 11742409.PubMedCrossRef Zimmet P, Alberti KG, Shaw J. Global and societal implications of the diabetes epidemic. Nature. 2001;414(7):782. Epub 2001 Dec 13. PMID: 11742409.PubMedCrossRef
2.
Zurück zum Zitat Kopelman PG. Obesity as a medical problem. Nature. 2000;404(6778):635–43. Epub 2000 Apr 6. PMID: 10766250.PubMed Kopelman PG. Obesity as a medical problem. Nature. 2000;404(6778):635–43. Epub 2000 Apr 6. PMID: 10766250.PubMed
3.
Zurück zum Zitat Eckel RH, Grundy SM, Zimmet PZ. The metabolic syndrome. Lancet. 2005;365(9468):1415–28. Epub 2005 Apr 20. PMID: 15836891.PubMedCrossRef Eckel RH, Grundy SM, Zimmet PZ. The metabolic syndrome. Lancet. 2005;365(9468):1415–28. Epub 2005 Apr 20. PMID: 15836891.PubMedCrossRef
4.
Zurück zum Zitat Scherer PE. Adipose tissue: from lipid storage compartment to endocrine organ. Diabetes. 2006;55(6):1537–45. Epub 2006 May 29. PMID: 16731815.PubMedCrossRef Scherer PE. Adipose tissue: from lipid storage compartment to endocrine organ. Diabetes. 2006;55(6):1537–45. Epub 2006 May 29. PMID: 16731815.PubMedCrossRef
5.
Zurück zum Zitat Antuna-Puente B, Feve B, Fellahi S, et al. Obesity, inflammation and insulin resistance: which role for adipokines. Therapie. 2007;62(4):285–92. Epub 2007 Nov 6. PMID: 17983554.PubMedCrossRef Antuna-Puente B, Feve B, Fellahi S, et al. Obesity, inflammation and insulin resistance: which role for adipokines. Therapie. 2007;62(4):285–92. Epub 2007 Nov 6. PMID: 17983554.PubMedCrossRef
6.
Zurück zum Zitat Wellen KE, Hotamisligil GS. Inflammation, stress, and diabetes. J Clin Invest. 2005;115(5):1111–9. Epub 2005 May 03. PMID: 15864338.PubMed Wellen KE, Hotamisligil GS. Inflammation, stress, and diabetes. J Clin Invest. 2005;115(5):1111–9. Epub 2005 May 03. PMID: 15864338.PubMed
7.
Zurück zum Zitat Shoelson SE, Lee J, Goldfine AB. Inflammation and insulin resistance. J Clin Invest. 2006;116(7):1793–801. Epub 2006 Jul 11. PMID: 16823477.PubMedCrossRef Shoelson SE, Lee J, Goldfine AB. Inflammation and insulin resistance. J Clin Invest. 2006;116(7):1793–801. Epub 2006 Jul 11. PMID: 16823477.PubMedCrossRef
8.
Zurück zum Zitat Kahn SE, Hull RL, Utzschneider KM. Mechanisms linking obesity to insulin resistance and type 2 diabetes. Nature. 2006;444(7121):840–6. Epub 2006 Dec 14. PMID: 17167471.PubMedCrossRef Kahn SE, Hull RL, Utzschneider KM. Mechanisms linking obesity to insulin resistance and type 2 diabetes. Nature. 2006;444(7121):840–6. Epub 2006 Dec 14. PMID: 17167471.PubMedCrossRef
9.
Zurück zum Zitat Hotamisligil GS, Shargill NS, Spiegelman BM. Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance. Science. 1993;259(5091):87–91. Epub 1993 Jan 1. PMID: 7678183.PubMedCrossRef Hotamisligil GS, Shargill NS, Spiegelman BM. Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance. Science. 1993;259(5091):87–91. Epub 1993 Jan 1. PMID: 7678183.PubMedCrossRef
10.
Zurück zum Zitat Fasshauer M, Klein J, Neumann S, et al. Adiponectin gene expression is inhibited by beta-adrenergic stimulation via protein kinase A in 3T3-L1 adipocytes. FEBS Lett. 2001;507(2):142–6. Epub 2001 Oct 26. PMID: 11684087.PubMedCrossRef Fasshauer M, Klein J, Neumann S, et al. Adiponectin gene expression is inhibited by beta-adrenergic stimulation via protein kinase A in 3T3-L1 adipocytes. FEBS Lett. 2001;507(2):142–6. Epub 2001 Oct 26. PMID: 11684087.PubMedCrossRef
11.
Zurück zum Zitat Buchwald H, Avidor Y, Braunwald E, et al. Bariatric surgery: a systematic review and meta-analysis. JAMA. 2004;292(14):1724–37. Epub 2004 Oct 13. PMID: 15479938.PubMedCrossRef Buchwald H, Avidor Y, Braunwald E, et al. Bariatric surgery: a systematic review and meta-analysis. JAMA. 2004;292(14):1724–37. Epub 2004 Oct 13. PMID: 15479938.PubMedCrossRef
12.
Zurück zum Zitat Pories WJ, Swanson MS, MacDonald KG, et al. Who would have thought it? An operation proves to be the most effective therapy for adult-onset diabetes mellitus. Ann Surg. 1995;222(3):339–50. discussion 50-2. Epub 1995 Oct 13. PMID: 7677463.PubMedCrossRef Pories WJ, Swanson MS, MacDonald KG, et al. Who would have thought it? An operation proves to be the most effective therapy for adult-onset diabetes mellitus. Ann Surg. 1995;222(3):339–50. discussion 50-2. Epub 1995 Oct 13. PMID: 7677463.PubMedCrossRef
13.
Zurück zum Zitat Habib P, Scrocco JD, Terek M, et al. Effects of bariatric surgery on inflammatory, functional and structural markers of coronary atherosclerosis. Am J Cardiol. 2009;104(9):1251–5. Epub 2009 Nov 1. PMID: 19840571.PubMedCrossRef Habib P, Scrocco JD, Terek M, et al. Effects of bariatric surgery on inflammatory, functional and structural markers of coronary atherosclerosis. Am J Cardiol. 2009;104(9):1251–5. Epub 2009 Nov 1. PMID: 19840571.PubMedCrossRef
14.
Zurück zum Zitat Moschen AR, Molnar C, Geiger S, et al. 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. Epub 2010 Sep 01. PMID: 20660075.PubMedCrossRef Moschen AR, Molnar C, Geiger S, et al. 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. Epub 2010 Sep 01. PMID: 20660075.PubMedCrossRef
15.
Zurück zum Zitat Garcia de la Torre N, Rubio MA, Bordiu E, et al. Effects of weight loss after bariatric surgery for morbid obesity on vascular endothelial growth factor-A, adipocytokines, and insulin. J Clin Endocrinol Metab. 2008;93(11):4276–81. Epub 2008 Aug 21. PMID: 18713823.PubMedCrossRef Garcia de la Torre N, Rubio MA, Bordiu E, et al. Effects of weight loss after bariatric surgery for morbid obesity on vascular endothelial growth factor-A, adipocytokines, and insulin. J Clin Endocrinol Metab. 2008;93(11):4276–81. Epub 2008 Aug 21. PMID: 18713823.PubMedCrossRef
16.
Zurück zum Zitat Cancello R, Henegar C, Viguerie N, et al. Reduction of macrophage infiltration and chemoattractant gene expression changes in white adipose tissue of morbidly obese subjects after surgery-induced weight loss. Diabetes. 2005;54(8):2277–86. Epub 2005 Jul 28. PMID: 16046292.PubMedCrossRef Cancello R, Henegar C, Viguerie N, et al. Reduction of macrophage infiltration and chemoattractant gene expression changes in white adipose tissue of morbidly obese subjects after surgery-induced weight loss. Diabetes. 2005;54(8):2277–86. Epub 2005 Jul 28. PMID: 16046292.PubMedCrossRef
17.
Zurück zum Zitat Miller GD, Nicklas BJ, Fernandez A. Serial changes in inflammatory biomarkers after Roux-en-Y gastric bypass surgery. Surg Obes Relat Dis. 2011;7(5):618–24. Epub 2011 May 07. PMID: 21546319.PubMedCrossRef Miller GD, Nicklas BJ, Fernandez A. Serial changes in inflammatory biomarkers after Roux-en-Y gastric bypass surgery. Surg Obes Relat Dis. 2011;7(5):618–24. Epub 2011 May 07. PMID: 21546319.PubMedCrossRef
18.
Zurück zum Zitat Speck M, Cho YM, Asadi A, et al. Duodenal–jejunal bypass protects GK rats from {beta}-cell loss and aggravation of hyperglycemia and increases enteroendocrine cells coexpressing GIP and GLP-1. Am J Physiol Endocrinol Metab. 2011;300(5):E923–32. Epub 2011 Feb 10. PMID: 21304061.PubMedCrossRef Speck M, Cho YM, Asadi A, et al. Duodenal–jejunal bypass protects GK rats from {beta}-cell loss and aggravation of hyperglycemia and increases enteroendocrine cells coexpressing GIP and GLP-1. Am J Physiol Endocrinol Metab. 2011;300(5):E923–32. Epub 2011 Feb 10. PMID: 21304061.PubMedCrossRef
19.
Zurück zum Zitat Araujo AC, Bonfleur ML, Balbo SL, et al. Duodenal–jejunal bypass surgery enhances glucose tolerance and beta-cell function in Western diet obese rats. Obes Surg. 2012;22(5):819–26. Epub 2012 Mar 14. PMID: 22411572.PubMedCrossRef Araujo AC, Bonfleur ML, Balbo SL, et al. Duodenal–jejunal bypass surgery enhances glucose tolerance and beta-cell function in Western diet obese rats. Obes Surg. 2012;22(5):819–26. Epub 2012 Mar 14. PMID: 22411572.PubMedCrossRef
20.
Zurück zum Zitat Rubino F, Marescaux J. Effect of duodenal–jejunal exclusion in a non-obese animal model of type 2 diabetes: a new perspective for an old disease. Ann Surg. 2004;239(1):1–11. Epub 2003 Dec 20. PMID: 14685093.PubMedCrossRef Rubino F, Marescaux J. Effect of duodenal–jejunal exclusion in a non-obese animal model of type 2 diabetes: a new perspective for an old disease. Ann Surg. 2004;239(1):1–11. Epub 2003 Dec 20. PMID: 14685093.PubMedCrossRef
21.
Zurück zum Zitat Wang TT, Hu SY, Gao HD, et al. Ileal transposition controls diabetes as well as modified duodenal jejunal bypass with better lipid lowering in a nonobese rat model of type II diabetes by increasing GLP-1. Ann Surg. 2008;247(6):968–75. Epub 2008 Jun 04. PMID: 18520224.PubMedCrossRef Wang TT, Hu SY, Gao HD, et al. Ileal transposition controls diabetes as well as modified duodenal jejunal bypass with better lipid lowering in a nonobese rat model of type II diabetes by increasing GLP-1. Ann Surg. 2008;247(6):968–75. Epub 2008 Jun 04. PMID: 18520224.PubMedCrossRef
22.
Zurück zum Zitat Geloneze B, Geloneze SR, Chaim E, et al. Metabolic surgery for non-obese type 2 diabetes incretins, adipocytokines, and insulin secretion/resistance changes in a 1-year interventional clinical controlled study. Ann Surg. 2012;256(1):72–8. Epub 2012 Jul. PMID: 22664560.PubMedCrossRef Geloneze B, Geloneze SR, Chaim E, et al. Metabolic surgery for non-obese type 2 diabetes incretins, adipocytokines, and insulin secretion/resistance changes in a 1-year interventional clinical controlled study. Ann Surg. 2012;256(1):72–8. Epub 2012 Jul. PMID: 22664560.PubMedCrossRef
23.
Zurück zum Zitat Liu SZ, Sun D, Zhang GY, et al. A high-fat diet reverses improvement in glucose tolerance induced by duodenal–jejunal bypass in type 2 diabetic rats. Chin Med J (Engl). 2012;125(5):912–9. Epub 2012 Apr 12. PMID: 22490596. Liu SZ, Sun D, Zhang GY, et al. A high-fat diet reverses improvement in glucose tolerance induced by duodenal–jejunal bypass in type 2 diabetic rats. Chin Med J (Engl). 2012;125(5):912–9. Epub 2012 Apr 12. PMID: 22490596.
24.
Zurück zum Zitat Pacheco D, de Luis DA, Romero A, et al. The effects of duodenal–jejunal exclusion on hormonal regulation of glucose metabolism in Goto–Kakizaki rats. Am J Surg. 2007;194(2):221–4. Epub 2007 Jul 10. PMID: 17618808.PubMedCrossRef Pacheco D, de Luis DA, Romero A, et al. The effects of duodenal–jejunal exclusion on hormonal regulation of glucose metabolism in Goto–Kakizaki rats. Am J Surg. 2007;194(2):221–4. Epub 2007 Jul 10. PMID: 17618808.PubMedCrossRef
25.
Zurück zum Zitat Rubino F, Zizzari P, Tomasetto C, et al. The role of the small bowel in the regulation of circulating ghrelin levels and food intake in the obese Zucker rat. Endocrinology. 2005;146(4):1745–51. Epub 2004 Dec 31. PMID: 15625244.PubMedCrossRef Rubino F, Zizzari P, Tomasetto C, et al. The role of the small bowel in the regulation of circulating ghrelin levels and food intake in the obese Zucker rat. Endocrinology. 2005;146(4):1745–51. Epub 2004 Dec 31. PMID: 15625244.PubMedCrossRef
26.
Zurück zum Zitat Fried M, Ribaric G, Buchwald JN, et al. Metabolic surgery for the treatment of type 2 diabetes in patients with BMI < 35 kg/m(2): an integrative review of early studies. Obes Surg. 2010;20(6):776–90. Epub 2010 May 21. PMID: 20333558.PubMedCrossRef Fried M, Ribaric G, Buchwald JN, et al. Metabolic surgery for the treatment of type 2 diabetes in patients with BMI < 35 kg/m(2): an integrative review of early studies. Obes Surg. 2010;20(6):776–90. Epub 2010 May 21. PMID: 20333558.PubMedCrossRef
27.
Zurück zum Zitat Geloneze B, Geloneze SR, Fiori C, et al. Surgery for nonobese type 2 diabetic patients: an interventional study with duodenal–jejunal exclusion. Obes Surg. 2009;19(8):1077–83. Epub 2009 Jul 17. PMID: 15475464.PubMedCrossRef Geloneze B, Geloneze SR, Fiori C, et al. Surgery for nonobese type 2 diabetic patients: an interventional study with duodenal–jejunal exclusion. Obes Surg. 2009;19(8):1077–83. Epub 2009 Jul 17. PMID: 15475464.PubMedCrossRef
28.
Zurück zum Zitat Reis CEG, Alvarez-Leite JI, Bressan J, et al. Role of bariatric-metabolic surgery in the treatment of obese type 2 diabetes with body mass index < 35 kg/m(2): a literature review. Diabetes Technol The. 2012;14(4):365–72. Epub 2012 Apr 02. PMID: 22126155.CrossRef Reis CEG, Alvarez-Leite JI, Bressan J, et al. Role of bariatric-metabolic surgery in the treatment of obese type 2 diabetes with body mass index < 35 kg/m(2): a literature review. Diabetes Technol The. 2012;14(4):365–72. Epub 2012 Apr 02. PMID: 22126155.CrossRef
29.
Zurück zum Zitat Swarbrick MM, Stanhope KL, Austrheim-Smith IT, et al. Longitudinal changes in pancreatic and adipocyte hormones following Roux-en-Y gastric bypass surgery. Diabetologia. 2008;51(10):1901–11. Epub 2008 Aug 16. PMID: 18704364.PubMedCrossRef Swarbrick MM, Stanhope KL, Austrheim-Smith IT, et al. Longitudinal changes in pancreatic and adipocyte hormones following Roux-en-Y gastric bypass surgery. Diabetologia. 2008;51(10):1901–11. Epub 2008 Aug 16. PMID: 18704364.PubMedCrossRef
30.
Zurück zum Zitat Cummings BP, Strader AD, Stanhope KL, et al. Ileal interposition surgery improves glucose and lipid metabolism and delays diabetes onset in the UCD-T2DM rat. Gastroenterology. 2010;138(7):2437–46. 46 e1. Epub 2010 Mar 17. PMID: 20226188.PubMedCrossRef Cummings BP, Strader AD, Stanhope KL, et al. Ileal interposition surgery improves glucose and lipid metabolism and delays diabetes onset in the UCD-T2DM rat. Gastroenterology. 2010;138(7):2437–46. 46 e1. Epub 2010 Mar 17. PMID: 20226188.PubMedCrossRef
31.
Zurück zum Zitat Evans JL, Goldfine ID, Maddux BA, et al. Oxidative stress and stress-activated signaling pathways: a unifying hypothesis of type 2 diabetes. Endocr Rev. 2002;23(5):599–622. Epub 2002 Oct 10. PMID: 12372842.PubMedCrossRef Evans JL, Goldfine ID, Maddux BA, et al. Oxidative stress and stress-activated signaling pathways: a unifying hypothesis of type 2 diabetes. Endocr Rev. 2002;23(5):599–622. Epub 2002 Oct 10. PMID: 12372842.PubMedCrossRef
32.
Zurück zum Zitat Boden G. Role of fatty acids in the pathogenesis of insulin resistance and NIDDM. Diabetes. 1997;46(1):3–10. Epub 1997 Jan 01. PMID: 8971073.PubMedCrossRef Boden G. Role of fatty acids in the pathogenesis of insulin resistance and NIDDM. Diabetes. 1997;46(1):3–10. Epub 1997 Jan 01. PMID: 8971073.PubMedCrossRef
33.
Zurück zum Zitat Rubino F, Forgione A, Cummings DE, et al. The mechanism of diabetes control after gastrointestinal bypass surgery reveals a role of the proximal small intestine in the pathophysiology of type 2 diabetes. Ann Surg. 2006;244(5):741–9. Epub 2006 Oct 25. PMID: 17060767.PubMedCrossRef Rubino F, Forgione A, Cummings DE, et al. The mechanism of diabetes control after gastrointestinal bypass surgery reveals a role of the proximal small intestine in the pathophysiology of type 2 diabetes. Ann Surg. 2006;244(5):741–9. Epub 2006 Oct 25. PMID: 17060767.PubMedCrossRef
34.
Zurück zum Zitat Lee YS, Shin S, Shigihara T, et al. Glucagon-like peptide-1 gene therapy in obese diabetic mice results in long-term cure of diabetes by improving insulin sensitivity and reducing hepatic gluconeogenesis. Diabetes. 2007;56(6):1671–9. Epub 2007 Mar 21. PMID: 17369525.PubMedCrossRef Lee YS, Shin S, Shigihara T, et al. Glucagon-like peptide-1 gene therapy in obese diabetic mice results in long-term cure of diabetes by improving insulin sensitivity and reducing hepatic gluconeogenesis. Diabetes. 2007;56(6):1671–9. Epub 2007 Mar 21. PMID: 17369525.PubMedCrossRef
35.
Zurück zum Zitat Cases JA, Gabriely I, Ma XH, et al. Physiological increase in plasma leptin markedly inhibits insulin secretion in vivo. Diabetes. 2001;50(2):348–52. Epub 2001 Mar 29. PMID: 11272146.PubMedCrossRef Cases JA, Gabriely I, Ma XH, et al. Physiological increase in plasma leptin markedly inhibits insulin secretion in vivo. Diabetes. 2001;50(2):348–52. Epub 2001 Mar 29. PMID: 11272146.PubMedCrossRef
36.
Zurück zum Zitat Considine RV, Sinha MK, Heiman ML, et al. Serum immunoreactive-leptin concentrations in normal-weight and obese humans. N Engl J Med. 1996;334(5):292–5. Epub 1996 Feb 01. PMID: 8532024.PubMedCrossRef Considine RV, Sinha MK, Heiman ML, et al. Serum immunoreactive-leptin concentrations in normal-weight and obese humans. N Engl J Med. 1996;334(5):292–5. Epub 1996 Feb 01. PMID: 8532024.PubMedCrossRef
37.
Zurück zum Zitat Weyer C, Funahashi T, Tanaka S, et al. Hypoadiponectinemia in obesity and type 2 diabetes: close association with insulin resistance and hyperinsulinemia. J Clin Endocrinol Metab. 2001;5(86):1930–5. Epub 2001 May 10. PMID: 11344187.CrossRef Weyer C, Funahashi T, Tanaka S, et al. Hypoadiponectinemia in obesity and type 2 diabetes: close association with insulin resistance and hyperinsulinemia. J Clin Endocrinol Metab. 2001;5(86):1930–5. Epub 2001 May 10. PMID: 11344187.CrossRef
38.
Zurück zum Zitat Yokota T, Oritani K, Takahashi I, et al. Adiponectin, a new member of the family of soluble defense collagens, negatively regulates the growth of myelomonocytic progenitors and the functions of macrophages. Blood. 2000;96(5):1723–32. Epub 2000 Sep 01. PMID: 10961870.PubMed Yokota T, Oritani K, Takahashi I, et al. Adiponectin, a new member of the family of soluble defense collagens, negatively regulates the growth of myelomonocytic progenitors and the functions of macrophages. Blood. 2000;96(5):1723–32. Epub 2000 Sep 01. PMID: 10961870.PubMed
39.
Zurück zum Zitat Degawa-Yamauchi M, Moss KA, Bovenkerk JE, et al. Regulation of adiponectin expression in human adipocytes: effects of adiposity, glucocorticoids, and tumor necrosis factor alpha. Obes Res. 2005;13(4):662–9. Epub 2005 Apr. PMID: 15897474.PubMedCrossRef Degawa-Yamauchi M, Moss KA, Bovenkerk JE, et al. Regulation of adiponectin expression in human adipocytes: effects of adiposity, glucocorticoids, and tumor necrosis factor alpha. Obes Res. 2005;13(4):662–9. Epub 2005 Apr. PMID: 15897474.PubMedCrossRef
40.
Zurück zum Zitat Mohamed-Ali V, Goodrick S, Rawesh A, et al. Subcutaneous adipose tissue releases interleukin-6, but not tumor necrosis factor-alpha, in vivo. J Clin Endocrinol Metab. 1997;82(12):4196–200. Epub 1997 Dec. PMID: 9398739.PubMedCrossRef Mohamed-Ali V, Goodrick S, Rawesh A, et al. Subcutaneous adipose tissue releases interleukin-6, but not tumor necrosis factor-alpha, in vivo. J Clin Endocrinol Metab. 1997;82(12):4196–200. Epub 1997 Dec. PMID: 9398739.PubMedCrossRef
41.
Zurück zum Zitat Rotter V, Nagaev I, Smith U. Interleukin-6 (IL-6) induces insulin resistance in 3T3-L1 adipocytes and is, like IL-8 and tumor necrosis factor-alpha, overexpressed in human fat cells from insulin-resistant subjects. J Biol Chem. 2003;278(46):45777–84. Epub 2003 Nov 14. PMID: 12952969.PubMedCrossRef Rotter V, Nagaev I, Smith U. Interleukin-6 (IL-6) induces insulin resistance in 3T3-L1 adipocytes and is, like IL-8 and tumor necrosis factor-alpha, overexpressed in human fat cells from insulin-resistant subjects. J Biol Chem. 2003;278(46):45777–84. Epub 2003 Nov 14. PMID: 12952969.PubMedCrossRef
42.
Zurück zum Zitat Hirosumi J, Tuncman G, Chang L, et al. A central role for JNK in obesity and insulin resistance. Nature. 2002;420(6913):333–6. Epub 2002 Nov 21. PMID: 12447443.PubMedCrossRef Hirosumi J, Tuncman G, Chang L, et al. A central role for JNK in obesity and insulin resistance. Nature. 2002;420(6913):333–6. Epub 2002 Nov 21. PMID: 12447443.PubMedCrossRef
43.
Zurück zum Zitat Zhang H, Wang Y, Zhang J, et al. Bariatric surgery reduces visceral adipose inflammation and improves endothelial function in type 2 diabetic mice. Arterioscler Thromb Vasc Biol. 2011;31(9):2063–9. Epub 2011 Sep. PMID: 21680898.PubMedCrossRef Zhang H, Wang Y, Zhang J, et al. Bariatric surgery reduces visceral adipose inflammation and improves endothelial function in type 2 diabetic mice. Arterioscler Thromb Vasc Biol. 2011;31(9):2063–9. Epub 2011 Sep. PMID: 21680898.PubMedCrossRef
44.
Zurück zum Zitat Illan-Gomez F, Gonzalvez-Ortega M, Orea-Soler I, et al. Obesity and inflammation: change in adiponectin, C-reactive protein, tumour necrosis factor-alpha and interleukin-6 after bariatric surgery. Obes Surg. 2012;22(6):950–5. Epub 2012 Apr 25. PMID: 22527592.PubMedCrossRef Illan-Gomez F, Gonzalvez-Ortega M, Orea-Soler I, et al. Obesity and inflammation: change in adiponectin, C-reactive protein, tumour necrosis factor-alpha and interleukin-6 after bariatric surgery. Obes Surg. 2012;22(6):950–5. Epub 2012 Apr 25. PMID: 22527592.PubMedCrossRef
45.
Zurück zum Zitat Curat CA, Miranville A, Sengenes C, et al. From blood monocytes to adipose tissue-resident macrophages: induction of diapedesis by human mature adipocytes. Diabetes. 2004;53(5):1285–92. Epub 2004 May. PMID: 15111498.PubMedCrossRef Curat CA, Miranville A, Sengenes C, et al. From blood monocytes to adipose tissue-resident macrophages: induction of diapedesis by human mature adipocytes. Diabetes. 2004;53(5):1285–92. Epub 2004 May. PMID: 15111498.PubMedCrossRef
46.
Zurück zum Zitat Lee HC, Kim MK, Kwon HS, et al. Early changes in incretin secretion after laparoscopic duodenal–jejunal bypass surgery in type 2 diabetic patients. Obes Surg. 2010;20(11):1530–5. Epub 2010 Aug 31. PMID: 20803098.PubMedCrossRef Lee HC, Kim MK, Kwon HS, et al. Early changes in incretin secretion after laparoscopic duodenal–jejunal bypass surgery in type 2 diabetic patients. Obes Surg. 2010;20(11):1530–5. Epub 2010 Aug 31. PMID: 20803098.PubMedCrossRef
47.
Zurück zum Zitat Lee YS, Park MS, Choung JS, et al. Glucagon-like peptide-1 inhibits adipose tissue macrophage infiltration and inflammation in an obese mouse model of diabetes. Diabetologia. 2012;55(9):2456–68. Epub 2012 Jun 23. PMID: 22722451.PubMedCrossRef Lee YS, Park MS, Choung JS, et al. Glucagon-like peptide-1 inhibits adipose tissue macrophage infiltration and inflammation in an obese mouse model of diabetes. Diabetologia. 2012;55(9):2456–68. Epub 2012 Jun 23. PMID: 22722451.PubMedCrossRef
48.
Zurück zum Zitat Bruun JM, Lihn AS, Verdich C, et al. Regulation of adiponectin by adipose tissue-derived cytokines: in vivo and in vitro investigations in humans. Am J Physiol Endocrinol Metab. 2003;285(3):E527–33. Epub 2003 May 09. PMID: 12736161.PubMed Bruun JM, Lihn AS, Verdich C, et al. Regulation of adiponectin by adipose tissue-derived cytokines: in vivo and in vitro investigations in humans. Am J Physiol Endocrinol Metab. 2003;285(3):E527–33. Epub 2003 May 09. PMID: 12736161.PubMed
49.
Zurück zum Zitat Feldstein AE, Werneburg NW, Canbay A, et al. Free fatty acids promote hepatic lipotoxicity by stimulating TNF-alpha expression via a lysosomal pathway. Hepatology. 2004;40(1):185–94. Epub 2004 Jul 09. PMID: 15239102.PubMedCrossRef Feldstein AE, Werneburg NW, Canbay A, et al. Free fatty acids promote hepatic lipotoxicity by stimulating TNF-alpha expression via a lysosomal pathway. Hepatology. 2004;40(1):185–94. Epub 2004 Jul 09. PMID: 15239102.PubMedCrossRef
50.
Zurück zum Zitat Gastaldelli A. Abdominal fat: does it predict the development of type 2 diabetes? Am J Clin Nutr. 2008;87(5):1118–9. Epub 2008 May 13.PMID: 18469227.PubMed Gastaldelli A. Abdominal fat: does it predict the development of type 2 diabetes? Am J Clin Nutr. 2008;87(5):1118–9. Epub 2008 May 13.PMID: 18469227.PubMed
Metadaten
Titel
Duodenal–Jejunal Bypass Improves Glucose Metabolism and Adipokine Expression Independently of Weight Loss in a Diabetic Rat Model
verfasst von
Chunxiao Hu
Guangyong Zhang
Dong Sun
Haifeng Han
Sanyuan Hu
Publikationsdatum
01.09.2013
Verlag
Springer US
Erschienen in
Obesity Surgery / Ausgabe 9/2013
Print ISSN: 0960-8923
Elektronische ISSN: 1708-0428
DOI
https://doi.org/10.1007/s11695-013-0976-1

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Update Chirurgie

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S3-Leitlinie „Diagnostik und Therapie des Karpaltunnelsyndroms“

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“

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“

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.