Influence on expression of MG53 protein in skeletal muscle tissue of non-obese type 2 diabetic mellitus rats after gastric bypass operation_CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY

Authors：

GONG Shuai ¹ , ZHANG Pengbo ¹ , ZHANG Chong ¹ , WU Nai ¹ , ZHANG Yi ¹ , ZHANG Xiuzhong ¹ , MENG Fanchao ² , QI Yanwei ² ,  REN Zeqiang ¹

1. Department of General Surgery, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221000, P. R. China;
2. Graduate School of Xuzhou Medical University, Xuzhou, Jiangsu 221002, P. R. China;

Corresponding?author：

REN Zeqiang, Email: rzq0805@163.com

Keywords：

type 2 diabetes mellitus; gastric bypass operation; mitsugumin53; insulin receptor substrate 1; E3 ubiquitin ligase; insulin resistance

DOI：

10.7507/1007-9424.201908050

Video：

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Objective To observe expressions of E3 ubiquitin ligase—mitsugmin53 (MG53) protein, MG53 mRNA, and insulin receptor substrate 1 (IRS-1) mRNA in skeletal muscle of non-obese type 2 diabetic mellitus (T2DM) rats after gastric bypass operation (GBP), and to investigate possible mechanism of GBP in improving insulin resistance.Methods Twenty-four healthy male GK rats were randomly divided into diabetic operation group, diabetic sham operation group, and diabetic control group, 8 rats in each group; besides, 8 male Wistar rats were served as normal control group. The expressions of MG53 protein in skeletal muscle tissue were detected by using Western blot method on week8 after operation. The mRNA levels of IRS-1 and MG53 in skeletal muscles tissue were measured by RT-PCR methods on week 8 after operation.Results ① The expressions of MG53 protein and MG53 mRNA in the diabetic sham operation group and diabetic control group were significantly higher than those in the diabetic operation group and the normal control group on week 8 after operation (P<0.05), respectively, which had no significant differences between the diabetic operation group and the normal control group (P>0.05), and between the diabetic sham operation group and the diabetic control group (P>0.05) on week 8 after surgery. ② Compared with the normal control group, the expression of IRS-1 mRNA was significantly decreased in the diabetic operation group, the diabetic sham operation group, and the diabetic control group (P<0.05), while there were no significant differences between the diabetic operation group, diabetic sham operation group, and the diabetic control group on week 8 after operation (P>0.05).Conclusion Expression of E3 ubiquitin ligase—MG53 protein in skeletal muscle tissue in T2DM rats following GBP is decreased, thus reduces the IRS-1 ubiquitin-degradation, increase the expression of IRS-1 protein in insulin signaling pathway of skeletal muscle tissue, and improve insulin resistance of skeletal muscle.

Citation： GONG Shuai, ZHANG Pengbo, ZHANG Chong, WU Nai, ZHANG Yi, ZHANG Xiuzhong, MENG Fanchao, QI Yanwei, REN Zeqiang. Influence on expression of MG53 protein in skeletal muscle tissue of non-obese type 2 diabetic mellitus rats after gastric bypass operation. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 2020, 27(4): 448-453. doi: 10.7507/1007-9424.201908050 Copy

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2.	Mingrone G, Panunzi S, De Gaetano A, et al. Bariatric surgery versus conventional medical therapy for type 2 diabetes. N Engl J Med, 2012, 366(17): 1577-1585.
3.	溫雨晴, 譚迎春, 張蓬波, 等. 胃轉流術對2型糖尿病大鼠脂肪組織胰島素抵抗的影響. 中華實驗外科雜志, 2013, 30(11): 2324-2326.
4.	張蓬波, 陳守坤, 張秀忠, 等. 胃轉流術對2型糖尿病大鼠肝組織胰島素受體底物-2、葡萄糖轉運體-2表達的影響. 中華實驗外科雜志, 2013, 30(12): 2587-2589.
5.	張秀忠, 任澤強, 張蓬波. 胃轉流術對2型糖尿病大鼠的降糖作用及對糖耐量和胰島素抵抗的影響. 中華實驗外科雜志, 2010, 27(12): 1892-1894.
6.	何勁松, 張井瀟, 李利發, 等. 空回腸旁路術對2型糖尿病大鼠骨骼肌蛋白酪氨酸磷酸酶1B表達的影響. 中國普外基礎與臨床雜志, 2016, 23(8): 910-914.
7.	Song R, Peng W, Zhang Y, et al. Central role of E3 ubiquitin ligase MG53 in insulin resistance and metabolic disorders. Nature, 2013, 494(7437): 375-379.
8.	Blaak EE. Metabolic fluxes in skeletal muscle in relation to obesity and insulin resistance. Best Pract Res Clin Endocrinol Metab, 2005, 19(3): 391-403.
9.	龔帥, 任澤強, 張蓬波, 等. 胃轉流術對非肥胖型2型糖尿病大鼠骨骼肌胰島素受體底物-1及泛素化蛋白表達的影響. 中國普外基礎與臨床雜志, 2016, 23(8): 915-921.
10.	Lima MM, Pareja JC, Alegre SM, et al. Acute effect of roux-en-y gastric bypass on whole-body insulin sensitivity: a study with the euglycemic-hyperinsulinemic clamp. J Clin Endocrinol Metab, 2010, 95(8): 3871-3875.
11.	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): 741-749.
12.	Ramos AC, Galv?o Neto MP, de Souza YM, et al. Laparoscopic duodenal-jejunal exclusion in the treatment of type 2 diabetes mellitus in patients with BMI <30 kg/m² (LBMI). Obes Surg, 2009, 19(3): 307-312.
13.	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.
14.	張新國, 楊學軍, 徐紅, 等. 胃旁路手術治療Ⅱ型糖尿病的體會. 中華普通外科雜志, 2005, 20(9): 599.
15.	王瑜, 王燕婷, 王烈. 胃轉流術對非肥胖型2型糖尿病的治療作用. 中國普通外科雜志, 2008, 17(10): 1003-1006.
16.	Han H, Wang L, Du H, et al. Expedited biliopancreatic juice flow to the distal gut benefits the diabetes control after duodenal-jejunal bypass. Obes Surg, 2015, 25(10): 1802-1809.
17.	李正才, 石志平, 莫濤, 等. 空回腸旁路術治療2型糖尿病24例療效觀察. 臨床外科雜志, 2018, 26(1): 45-46.
18.	萬鵬, 王瑜. 十二指腸空腸旁路術及迷走神經肝支對非肥胖2型糖尿病大鼠糖代謝的影響. 中國普外基礎與臨床雜志, 2015, 22(5): 565-570.
19.	洪智, 黃鶴, 張起維, 等. 不同Roux腸袢長度的十二指腸空腸旁路術對2型糖尿病模型大鼠糖代謝的影響. 沈陽醫學院學報, 2019, 21(4): 299-304.
20.	Gagliani N, Jofra T, Posgai AL, et al. Immune depletion in combination with allogeneic islets permanently restores tolerance to self-antigens in diabetic NOD mice. PLoS One, 2015, 10(11): e0142318.
21.	Bonfleur ML, Ribeiro RA, Pavanello A, et al. Duodenal-jejunal bypass restores insulin action and beta-cell function in hypothalamic-obese rats. Obes Surg, 2015, 25(4): 656-665.
22.	Dong X, Park S, Lin X, et al. Irs1 and Irs2 signaling is essential for hepatic glucose homeostasis and systemic growth. J Clin Invest, 2006, 116(1): 101-114.
23.	Grundy SM. Metabolic syndrome: connecting and reconciling cardiovascular and diabetes worlds. J Am Coll Cardiol, 2006, 47(6): 1093-1100.
24.	DeFronzo RA, Tripathy D. Skeletal muscle insulin resistance is the primary defect in type 2 diabetes. Diabetes Care, 2009, 32(Suppl 2): S157-S163.
25.	Goodyear LJ, Giorgino F, Sherman LA, et al. Insulin receptor phosphorylation, insulin receptor substrate-1 phosphorylation, and phosphatidylinositol 3-kinase activity are decreased in intact skeletal muscle strips from obese subjects. J Clin Invest, 1995, 95(5): 2195-2204.
26.	Caro JF, Ittoop O, Pories WJ, et al. Studies on the mechanism of insulin resistance in the liver from humans with noninsulin-dependent diabetes. Insulin action and binding in isolated hepatocytes, insulin receptor structure, and kinase activity. J Clin Invest, 1986, 78(1): 249-258.
27.	Rome S, Meugnier E, Vidal H. The ubiquitin-proteasome pathway is a new partner for the control of insulin signaling. Curr Opin Clin Nutr Metab Care, 2004, 7(3): 249-254.
28.	Laustsen PG, Russell SJ, Cui L, et al. Essential role of insulin and insulin-like growth factor 1 receptor signaling in cardiac development and function. Mol Cell Biol, 2007, 27(5): 1649-1664.

1. Schauer PR, Kashyap SR, Wolski K, et al. Bariatric surgery versus intensive medical therapy in obese patients with diabetes. N Engl J Med, 2012, 366(17): 1567-1576.
2. Mingrone G, Panunzi S, De Gaetano A, et al. Bariatric surgery versus conventional medical therapy for type 2 diabetes. N Engl J Med, 2012, 366(17): 1577-1585.
3. 溫雨晴, 譚迎春, 張蓬波, 等. 胃轉流術對2型糖尿病大鼠脂肪組織胰島素抵抗的影響. 中華實驗外科雜志, 2013, 30(11): 2324-2326.
4. 張蓬波, 陳守坤, 張秀忠, 等. 胃轉流術對2型糖尿病大鼠肝組織胰島素受體底物-2、葡萄糖轉運體-2表達的影響. 中華實驗外科雜志, 2013, 30(12): 2587-2589.
5. 張秀忠, 任澤強, 張蓬波. 胃轉流術對2型糖尿病大鼠的降糖作用及對糖耐量和胰島素抵抗的影響. 中華實驗外科雜志, 2010, 27(12): 1892-1894.
6. 何勁松, 張井瀟, 李利發, 等. 空回腸旁路術對2型糖尿病大鼠骨骼肌蛋白酪氨酸磷酸酶1B表達的影響. 中國普外基礎與臨床雜志, 2016, 23(8): 910-914.
7. Song R, Peng W, Zhang Y, et al. Central role of E3 ubiquitin ligase MG53 in insulin resistance and metabolic disorders. Nature, 2013, 494(7437): 375-379.
8. Blaak EE. Metabolic fluxes in skeletal muscle in relation to obesity and insulin resistance. Best Pract Res Clin Endocrinol Metab, 2005, 19(3): 391-403.
9. 龔帥, 任澤強, 張蓬波, 等. 胃轉流術對非肥胖型2型糖尿病大鼠骨骼肌胰島素受體底物-1及泛素化蛋白表達的影響. 中國普外基礎與臨床雜志, 2016, 23(8): 915-921.
10. Lima MM, Pareja JC, Alegre SM, et al. Acute effect of roux-en-y gastric bypass on whole-body insulin sensitivity: a study with the euglycemic-hyperinsulinemic clamp. J Clin Endocrinol Metab, 2010, 95(8): 3871-3875.
11. 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): 741-749.
12. Ramos AC, Galv?o Neto MP, de Souza YM, et al. Laparoscopic duodenal-jejunal exclusion in the treatment of type 2 diabetes mellitus in patients with BMI <30 kg/m² (LBMI). Obes Surg, 2009, 19(3): 307-312.
13. 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.
14. 張新國, 楊學軍, 徐紅, 等. 胃旁路手術治療Ⅱ型糖尿病的體會. 中華普通外科雜志, 2005, 20(9): 599.
15. 王瑜, 王燕婷, 王烈. 胃轉流術對非肥胖型2型糖尿病的治療作用. 中國普通外科雜志, 2008, 17(10): 1003-1006.
16. Han H, Wang L, Du H, et al. Expedited biliopancreatic juice flow to the distal gut benefits the diabetes control after duodenal-jejunal bypass. Obes Surg, 2015, 25(10): 1802-1809.
17. 李正才, 石志平, 莫濤, 等. 空回腸旁路術治療2型糖尿病24例療效觀察. 臨床外科雜志, 2018, 26(1): 45-46.
18. 萬鵬, 王瑜. 十二指腸空腸旁路術及迷走神經肝支對非肥胖2型糖尿病大鼠糖代謝的影響. 中國普外基礎與臨床雜志, 2015, 22(5): 565-570.
19. 洪智, 黃鶴, 張起維, 等. 不同Roux腸袢長度的十二指腸空腸旁路術對2型糖尿病模型大鼠糖代謝的影響. 沈陽醫學院學報, 2019, 21(4): 299-304.
20. Gagliani N, Jofra T, Posgai AL, et al. Immune depletion in combination with allogeneic islets permanently restores tolerance to self-antigens in diabetic NOD mice. PLoS One, 2015, 10(11): e0142318.
21. Bonfleur ML, Ribeiro RA, Pavanello A, et al. Duodenal-jejunal bypass restores insulin action and beta-cell function in hypothalamic-obese rats. Obes Surg, 2015, 25(4): 656-665.
22. Dong X, Park S, Lin X, et al. Irs1 and Irs2 signaling is essential for hepatic glucose homeostasis and systemic growth. J Clin Invest, 2006, 116(1): 101-114.
23. Grundy SM. Metabolic syndrome: connecting and reconciling cardiovascular and diabetes worlds. J Am Coll Cardiol, 2006, 47(6): 1093-1100.
24. DeFronzo RA, Tripathy D. Skeletal muscle insulin resistance is the primary defect in type 2 diabetes. Diabetes Care, 2009, 32(Suppl 2): S157-S163.
25. Goodyear LJ, Giorgino F, Sherman LA, et al. Insulin receptor phosphorylation, insulin receptor substrate-1 phosphorylation, and phosphatidylinositol 3-kinase activity are decreased in intact skeletal muscle strips from obese subjects. J Clin Invest, 1995, 95(5): 2195-2204.
26. Caro JF, Ittoop O, Pories WJ, et al. Studies on the mechanism of insulin resistance in the liver from humans with noninsulin-dependent diabetes. Insulin action and binding in isolated hepatocytes, insulin receptor structure, and kinase activity. J Clin Invest, 1986, 78(1): 249-258.
27. Rome S, Meugnier E, Vidal H. The ubiquitin-proteasome pathway is a new partner for the control of insulin signaling. Curr Opin Clin Nutr Metab Care, 2004, 7(3): 249-254.
28. Laustsen PG, Russell SJ, Cui L, et al. Essential role of insulin and insulin-like growth factor 1 receptor signaling in cardiac development and function. Mol Cell Biol, 2007, 27(5): 1649-1664.

CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY

Influence on expression of MG53 protein in skeletal muscle tissue of non-obese type 2 diabetic mellitus rats after gastric bypass operation

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