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Erschienen in: Obesity Surgery 2/2011

01.02.2011 | Physiology Research

Duodenal–Jejunal Bypass Surgery Does Not Increase Skeletal Muscle Insulin Signal Transduction or Glucose Disposal in Goto–Kakizaki Type 2 Diabetic Rats

verfasst von: Timothy P. Gavin, Ruben C. Sloan III, Eric Z. Lukosius, Melissa A. Reed, John R. Pender, Van Boghossian, Jacqueline J. Carter, Robert D. McKernie, Kushal Parikh, J. William Price, Edward B. Tapscott, Walter J. Pories, G. Lynis Dohm

Erschienen in: Obesity Surgery | Ausgabe 2/2011

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Abstract

Background

Duodenal–jejunal bypass (DJB) has been shown to reverse type 2 diabetes (T2DM) in Goto–Kakizaki (GK) rats, a rodent model of non-obese T2DM. Skeletal muscle insulin resistance is a hallmark decrement in T2DM. The aim of the current work was to investigate the effects of DJB on skeletal muscle insulin signal transduction and glucose disposal. It was hypothesized that DJB would increase skeletal muscle insulin signal transduction and glucose disposal in GK rats.

Methods

DJB was performed in GK rats. Sham operations were performed in GK and nondiabetic Wistar–Kyoto (WKY) rats. At 2 weeks post-DJB, oral glucose tolerance (OGTT) was measured. At 3 weeks post-DJB, insulin-induced signal transduction and glucose disposal were measured in skeletal muscle.

Results

In GK rats and compared to sham operation, DJB did not (1) improve fasting glucose or insulin, (2) improve OGTT, or (3) increase skeletal muscle insulin signal transduction or glucose disposal. Interestingly, skeletal muscle glucose disposal was similar between WKY-Sham, GK-Sham, and GK-DJB.

Conclusions

Bypassing of the proximal small intestine does not increase skeletal muscle glucose disposal. The lack of skeletal muscle insulin resistance in GK rats questions whether this animal model is adequate to investigate the etiology and treatments for T2DM. Additionally, bypassing of the foregut may lead to different findings in other animal models of T2DM as well as in T2DM patients.
Literatur
1.
Zurück zum Zitat American Diabetes Association. Economic costs of diabetes in the U.S. in 2002. Diabetes Care. 2003;26:917–32. American Diabetes Association. Economic costs of diabetes in the U.S. in 2002. Diabetes Care. 2003;26:917–32.
2.
Zurück zum Zitat Brozinick Jr JT, Roberts BR, Dohm GL. Defective signaling through Akt-2 and -3 but not Akt-1 in insulin-resistant human skeletal muscle: potential role in insulin resistance. Diabetes. 2003;52:935–41.CrossRefPubMed Brozinick Jr JT, Roberts BR, Dohm GL. Defective signaling through Akt-2 and -3 but not Akt-1 in insulin-resistant human skeletal muscle: potential role in insulin resistance. Diabetes. 2003;52:935–41.CrossRefPubMed
3.
Zurück zum Zitat Buchwald H, Avidor Y, Braunwald E, et al. Bariatric surgery: a systematic review and meta-analysis. JAMA. 2004;292:1724–37.CrossRefPubMed Buchwald H, Avidor Y, Braunwald E, et al. Bariatric surgery: a systematic review and meta-analysis. JAMA. 2004;292:1724–37.CrossRefPubMed
4.
Zurück zum Zitat 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;122:248–56. e245.CrossRefPubMed 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;122:248–56. e245.CrossRefPubMed
5.
Zurück zum Zitat Cani PD, Bibiloni R, Knauf C, et al. Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice. Diabetes. 2008;57:1470–81.CrossRefPubMed Cani PD, Bibiloni R, Knauf C, et al. Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice. Diabetes. 2008;57:1470–81.CrossRefPubMed
6.
Zurück zum Zitat Chou CJ, Membrez M, Blancher F. Gut decontamination with norfloxacin and ampicillin enhances insulin sensitivity in mice. Nestle Nutr Workshop Ser Pediatr Program. 2008;62:127–37. discussion 137–140.CrossRefPubMed Chou CJ, Membrez M, Blancher F. Gut decontamination with norfloxacin and ampicillin enhances insulin sensitivity in mice. Nestle Nutr Workshop Ser Pediatr Program. 2008;62:127–37. discussion 137–140.CrossRefPubMed
7.
Zurück zum Zitat Cohen RV, Schiavon CA, Pinheiro JS, et al. Duodenal–jejunal bypass for the treatment of type 2 diabetes in patients with body mass index of 22–34 kg/m(2): a report of 2 cases. Surg Obes Relat Dis. 2007;3:195–7.CrossRefPubMed Cohen RV, Schiavon CA, Pinheiro JS, et al. Duodenal–jejunal bypass for the treatment of type 2 diabetes in patients with body mass index of 22–34 kg/m(2): a report of 2 cases. Surg Obes Relat Dis. 2007;3:195–7.CrossRefPubMed
8.
Zurück zum Zitat Corcoran MP, Lamon-Fava S, Fielding RA. Skeletal muscle lipid deposition and insulin resistance: effect of dietary fatty acids and exercise. Am J Clin Nutr. 2007;85:662–77.PubMed Corcoran MP, Lamon-Fava S, Fielding RA. Skeletal muscle lipid deposition and insulin resistance: effect of dietary fatty acids and exercise. Am J Clin Nutr. 2007;85:662–77.PubMed
9.
Zurück zum Zitat Dadke S, Kusari J, Chernoff J. Down-regulation of insulin signaling by protein-tyrosine phosphatase 1B is mediated by an N-terminal binding region. J Biol Chem. 2000;275:23642–7.CrossRefPubMed Dadke S, Kusari J, Chernoff J. Down-regulation of insulin signaling by protein-tyrosine phosphatase 1B is mediated by an N-terminal binding region. J Biol Chem. 2000;275:23642–7.CrossRefPubMed
10.
Zurück zum Zitat DeFronzo RA, Ferrannini E, Simonson DC. Fasting hyperglycemia in non-insulin-dependent diabetes mellitus: contributions of excessive hepatic glucose production and impaired tissue glucose uptake. Metabolism. 1989;38:387–95.CrossRefPubMed DeFronzo RA, Ferrannini E, Simonson DC. Fasting hyperglycemia in non-insulin-dependent diabetes mellitus: contributions of excessive hepatic glucose production and impaired tissue glucose uptake. Metabolism. 1989;38:387–95.CrossRefPubMed
11.
Zurück zum Zitat DeFronzo RA, Jacot E, Jequier E, et al. The effect of insulin on the disposal of glucose: results from indirect calorimetry and hepatic and femoral venous catheterization. Diabetes. 1981;30:1000–7.PubMed DeFronzo RA, Jacot E, Jequier E, et al. The effect of insulin on the disposal of glucose: results from indirect calorimetry and hepatic and femoral venous catheterization. Diabetes. 1981;30:1000–7.PubMed
12.
Zurück zum Zitat Dohm GL, Kasperek GJ, Tapscott EB, et al. Effect of exercise on synthesis and degradation of muscle protein. Biochem J. 1980;188:255–62.PubMed Dohm GL, Kasperek GJ, Tapscott EB, et al. Effect of exercise on synthesis and degradation of muscle protein. Biochem J. 1980;188:255–62.PubMed
13.
Zurück zum Zitat Dolan PL, Tapscott EB, Dorton PJ, et al. Contractile activity restores insulin responsiveness in skeletal muscle of obese Zucker rats. Biochem J. 1993;289(Pt 2):423–6.PubMed Dolan PL, Tapscott EB, Dorton PJ, et al. Contractile activity restores insulin responsiveness in skeletal muscle of obese Zucker rats. Biochem J. 1993;289(Pt 2):423–6.PubMed
14.
Zurück zum Zitat Ferzli GS, Dominique E, Ciaglia M, et al. Clinical improvement after duodenojejunal bypass for nonobese type 2 diabetes despite minimal improvement in glycemic homeostasis. World J Surg. 2009;33:972–9.CrossRefPubMed Ferzli GS, Dominique E, Ciaglia M, et al. Clinical improvement after duodenojejunal bypass for nonobese type 2 diabetes despite minimal improvement in glycemic homeostasis. World J Surg. 2009;33:972–9.CrossRefPubMed
15.
Zurück zum Zitat Friedman JE, Dohm GL, Leggett-Frazier N, et al. Restoration of insulin responsiveness in skeletal muscle of morbidly obese patients after weight loss. Effect on muscle glucose transport and glucose transporter GLUT4. J Clin Invest. 1992;89:701–5.CrossRefPubMed Friedman JE, Dohm GL, Leggett-Frazier N, et al. Restoration of insulin responsiveness in skeletal muscle of morbidly obese patients after weight loss. Effect on muscle glucose transport and glucose transporter GLUT4. J Clin Invest. 1992;89:701–5.CrossRefPubMed
16.
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;19:1077–83.CrossRefPubMed 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;19:1077–83.CrossRefPubMed
17.
Zurück zum Zitat Krein SL, Funnell MM, Piette JD. Economics of diabetes mellitus. Nurs Clin North Am. 2006;41:499–511. v–vi.CrossRefPubMed Krein SL, Funnell MM, Piette JD. Economics of diabetes mellitus. Nurs Clin North Am. 2006;41:499–511. v–vi.CrossRefPubMed
18.
Zurück zum Zitat Krook A, Kawano Y, Song XM, et al. Improved glucose tolerance restores insulin-stimulated Akt kinase activity and glucose transport in skeletal muscle from diabetic Goto–Kakizaki rats. Diabetes. 1997;46:2110–4.CrossRefPubMed Krook A, Kawano Y, Song XM, et al. Improved glucose tolerance restores insulin-stimulated Akt kinase activity and glucose transport in skeletal muscle from diabetic Goto–Kakizaki rats. Diabetes. 1997;46:2110–4.CrossRefPubMed
19.
Zurück zum Zitat Matthews DR, Hosker JP, Rudenski AS, et al. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28:412–9.CrossRefPubMed Matthews DR, Hosker JP, Rudenski AS, et al. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28:412–9.CrossRefPubMed
20.
Zurück zum Zitat Membrez M, Blancher F, Jaquet M, et al. Gut microbiota modulation with norfloxacin and ampicillin enhances glucose tolerance in mice. FASEB J. 2008;22:2416–26.CrossRefPubMed Membrez M, Blancher F, Jaquet M, et al. Gut microbiota modulation with norfloxacin and ampicillin enhances glucose tolerance in mice. FASEB J. 2008;22:2416–26.CrossRefPubMed
21.
Zurück zum Zitat Movassat J, Bailbe D, Lubrano-Berthelier C, et al. Follow-up of GK rats during prediabetes highlights increased insulin action and fat deposition despite low insulin secretion. Am J Physiol Endocrinol Metab. 2008;294:E168–75.CrossRefPubMed Movassat J, Bailbe D, Lubrano-Berthelier C, et al. Follow-up of GK rats during prediabetes highlights increased insulin action and fat deposition despite low insulin secretion. Am J Physiol Endocrinol Metab. 2008;294:E168–75.CrossRefPubMed
22.
23.
Zurück zum Zitat Pories WJ, Caro JF, Flickinger EG, et al. The control of diabetes mellitus (NIDDM) in the morbidly obese with the Greenville gastric bypass. Ann Surg. 1987;206:316–23.CrossRefPubMed Pories WJ, Caro JF, Flickinger EG, et al. The control of diabetes mellitus (NIDDM) in the morbidly obese with the Greenville gastric bypass. Ann Surg. 1987;206:316–23.CrossRefPubMed
24.
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;222:339–50. discussion 350–332.CrossRefPubMed 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;222:339–50. discussion 350–332.CrossRefPubMed
25.
Zurück zum Zitat Portha B, Serradas P, Bailbe D, et al. Beta-cell insensitivity to glucose in the GK rat, a spontaneous nonobese model for type II diabetes. Diabetes. 1991;40:486–91.CrossRefPubMed Portha B, Serradas P, Bailbe D, et al. Beta-cell insensitivity to glucose in the GK rat, a spontaneous nonobese model for type II diabetes. Diabetes. 1991;40:486–91.CrossRefPubMed
26.
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;244:741–9.CrossRefPubMed 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;244:741–9.CrossRefPubMed
27.
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;239:1–11.CrossRefPubMed 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;239:1–11.CrossRefPubMed
Metadaten
Titel
Duodenal–Jejunal Bypass Surgery Does Not Increase Skeletal Muscle Insulin Signal Transduction or Glucose Disposal in Goto–Kakizaki Type 2 Diabetic Rats
verfasst von
Timothy P. Gavin
Ruben C. Sloan III
Eric Z. Lukosius
Melissa A. Reed
John R. Pender
Van Boghossian
Jacqueline J. Carter
Robert D. McKernie
Kushal Parikh
J. William Price
Edward B. Tapscott
Walter J. Pories
G. Lynis Dohm
Publikationsdatum
01.02.2011
Verlag
Springer-Verlag
Erschienen in
Obesity Surgery / Ausgabe 2/2011
Print ISSN: 0960-8923
Elektronische ISSN: 1708-0428
DOI
https://doi.org/10.1007/s11695-010-0304-y

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