[1] |
中华医学会糖尿病分会. 中国2型糖尿病防治指南(2017年版)[J]. 中国实用内科杂志, 2018, 38(4): 292-344.
|
[2] |
Jiang F, Zhu H, Zheng X, et al. Duodenal-jejunal bypass for the treatment of type 2 diabetes in Chinese patients with an average body mass index<24 kg/m2 [J]. Surg Obes Relat Dis, 2014, 10(4): 641-646.
|
[3] |
Ruan X, Zhang W, Cai H, et al. Sleeve gastrectomy with duodenojejunal end-to-side anastomosis in the treatment of type 2 diabetes: the initial experiences in a Chinese population with a more than 4-year follow-up[J]. Surg Obes Relat Dis, 2017, 13(10): 1683-1691.
|
[4] |
Rubino F, Nathan DM, Eckel RH, et al. Metabolic surgery in the treatment algorithm for type 2 diabetes: a joint statement by international diabetes organizations [J]. Diabetes Care. 2016, 39(6): 861-877.
|
[5] |
Albaugh VL, Banan B, Antoun J, et al. Role of Bile Acids and GLP-1 in Mediating the Metabolic Improvements of Bariatric Surgery [J]. Gastroenterology, 2019, 156(4): 1041-1051.
|
[6] |
Angrisani L, Santonicola A, Iovino P, et al. Bariatric Surgery Worldwide 2013[J]. Obes Surg, 2015, 25(10): 1822-1832.
|
[7] |
Lee JH, Nguyen QN, Le QA. Comparative effectiveness of 3 bariatric surgery procedures: Roux-en-Y gastric bypass, laparoscopic adjustable gastric band, and sleeve gastrectomy[J]. Surg Obes Relat Dis, 2016, 12(5): 997-1002.
|
[8] |
朱恒梁, 蒋飞照, 郑晓风, 等. 2型糖尿病外科治疗临床路径及其探讨[J]. 温州医学院学报, 2012, 42(5): 424-431.
|
[9] |
Müller T, Finan B, Bloom S, et al. Glucagon-like peptide 1 (GLP-1)[J]. Mol Metab, 2019, 30: 72-130.
|
[10] |
Zhu H, Wang H, Zheng Z, et al. Ileal transposition rapidly improves glucose tolerance and gradually improves insulin resistance in non-obese type 2 diabetic rats[J]. Gastroenterol Rep, 2018, 6(4): 291-297.
|
[11] |
朱恒梁,蒋飞照.胃肠道钠-葡萄糖共转运体1可能介导代谢减重手术改善血糖[J]. 中华肥胖与代谢病电子杂志, 2016, 2(2): 80-84.
|
[12] |
Mithieux G. A synergy between incretin effect and intestinal gluconeogenesis accounting for the rapid metabolic benefits of gastric bypass surgery [J]. Curr Diab Rep, 2012, 12(2): 167-171.
|
[13] |
Mingrone G, Castagneto-Gissey L. Mechanisms of early improvement/resolution of type 2 diabetes after bariatric surgery [J]. Diabetes Metab, 2009, 35(6 Pt2):518-523.
|
[14] |
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 [J]. Ann Surg, 2006, 244(5):741-749.
|
[15] |
Chiang J, Ferrell J. Bile Acids as Metabolic Regulators and Nutrient Sensors[J]. Annu Rev Nutr, 2019, 39: 175-200.
|
[16] |
Düfer M, Hörth K, Wagner R, et al. Bile acids acutely stimulate insulin secretion of mouse β-cells via farnesoid X receptor activation and K(ATP) channel inhibition[J]. Diabetes, 2012, 61(6): 1479-1489.
|
[17] |
Werling M, Fandriks L, Olbers T, et al. Biliopancreatic diversion is associated with greater increases in energy expenditure than Roux-en-Y gastric bypass[J]. PLoS One, 2018, 13(4):e0194538.
|
[18] |
Kohil R, Setchell KD, Kirby M, et al. A surgical model in male obese rats uncovers protective effects of bile acids post-bariatric surgery[J]. Endocrinology, 2013, 154(7): 2341-2351.
|
[19] |
Albaugh VL, Flynn CR, Cai S, et al. Early increases in bile acids post Roux-en-Y gastric bypass are driven by insulin sensitizing secondary bile acids [J]. J Clin Endocrinol Metab, 2015, 100(9): E1225-1233.
|
[20] |
Kaska L, Sledzinski T, Chomiczewska A, et al. Improved glucose metabolism following bariatric surgery is associated with increased circulating bile acid concentrations and remodeling of the gut microbiome [J]. World J Gastroenterol, 2016, 22(39): 8698-8719.
|
[21] |
Kübeck R, Bonet-Ripoll C, Hoffmann C, et al. Dietary fat and gut microbiota interactions determine diet-induced obesity in mice [J]. Mol Metab, 2016, 5(12):1162-1174.
|
[22] |
Patti ME, Houten SM, Bianco AC, et al. Serum bile acids are higher in humans with prior gastric bypass: potential contribution to improved glucose and lipid metabolism[J]. Obesity (Silver Spring, Md), 2009, 17(9):1671-1677.
|
[23] |
Cummings DE, Rubino F. Metabolic surgery for the treatment of type 2 diabetes in obese individuals[J]. Diabetologia, 2018, 61(2):257-264.
|
[24] |
Chavez-Talavera O, Tailleux A, Lefebvre P, et al. Bile acid control of metabolism and inflammation in obesity, type 2 diabetes, dyslipidemia, and nonalcoholic fatty liver disease[J]. Gastroenterology, 2017, 152(7):1679-1694e3.
|
[25] |
Stofan M, Guo GL. Bile Acids and FXR: Novel Targets for Liver Diseases[J]. Front Med (Lausanne), 2020, 7: 544.
|
[26] |
Kir S, Beddow SA, Samuel VT, et al. FGF19 as a Postprandial, Insulin-Independent Activator of Hepatic Protein and Glycogen Synthesis[J]. Science, 2011, 331(6024): 1621-1624.
|
[27] |
Escalera LMdl, Kyrou I, Vrbikova J, et al. Impact of gut hormone FGF-19 on type-2 diabetes and mitochondrial recovery in a prospective study of obese diabetic women undergoing bariatric surgery[J]. BMC Med, 2017, 15(34): 1-9.
|
[28] |
Taoka H, Yokoyama Y, Morimoto K, et al. Role of bile acids in the regulation of the metabolic pathways[J]. World Journal of Diabetes, 2016, 7(13): 260-270.
|
[29] |
Ji S, Liu Q, Zhang S, et al. FGF15 Activates Hippo Signaling to Suppress Bile Acid Metabolism and Liver Tumorigenesis[J]. Dev Cell, 2019, 48(4): 460-474.e469.
|
[30] |
Trabelsi MS, Daoudi M, Prawitt J, et al. Farnesoid X receptor inhibits glucagon-like peptide-1 production by enteroendocrine L cells[J]. Nat Commun, 2015, 6:7629.
|
[31] |
Pathak P, Xie C, Nichols RG, et al. Intestine farnesoid X receptor agonist and the gut microbiota activate G-protein bile acid receptor-1 signaling to improve metabolism [J]. Hepatology, 2018, 68(4):1574-1588.
|
[32] |
Parker HE, Wallis K, le Roux CW, et al. Molecular mechanisms underlying bile acid-stimulated glucagon-like peptide-1 secretion[J]. Br J Pharmacol, 2012, 165(2): 414-423.
|
[33] |
Pols TW, Noriega LG, Nomura M, et al. The bile acid membrane receptor TGR5 as an emerging target in metabolism and inflammation[J]. J Hepatol, 2011, 54(6): 1263-1272.
|
[34] |
Bayer CC, Jack TSA, Jacob WAN, et al. Bile acids drive colonic secretion of glucagon-like-peptide 1 and peptide-YY in rodents[J]. Am J Physiol Gastrointest Liver Physiol, 2019, 316(5): G574-584.
|
[35] |
Katsuma S, Hirasawa A, Tsujimoto G. Bile acids promote glucagon-like peptide-1 secretion through TGR5 in a murine enteroendocrine cell line STC-1[J]. Biochem Biophys Res Commun, 2005, 329(1): 386-390.
|
[36] |
Watanabe M, Houten SM, Mataki C, et al. Bile acids induce energy expenditure by promoting intracellular thyroid hormone activation[J]. Nature, 2006, 439 (7075): 484-489.
|
[37] |
Baggio LL, Ussher JR, McLean BA, et al. The autonomic nervous system and cardiac GLP-1 receptors control heart rate in mice[J]. Mol Metab, 2017, 6(11):1339-1349.
|
[38] |
Werling M, Olbers T, Fändriks L, et al. Increased Postprandial Energy Expenditure May Explain Superior Long Term Weight Loss after Roux-en-Y Gastric Bypass Compared to Vertical Banded Gastroplasty[J]. PLoS One, 2013, 8(4):e60280.
|