[1] Shyangdan DS, Uthman OA, Waugh N. SGLT-2 receptor inhibitors for treating patients with type 2 diabetes mellitus: a systematic review and network meta-analysis. BMJ Open. 2016;6:e009417.
[2] Storgaard H, Gluud LL, Bennett C, Grøndahl MF, Christensen MB, Knop FK, et al.Benefits and Harms of Sodium-Glucose Co-Transporter 2 Inhibitors in Patients with Type 2 Diabetes: A Systematic Review and Meta-Analysis. PLoS One. 2016;11:e0166125.
[3] Vasilakou D, Karagiannis T, Athanasiadou E, Mainou M, Liakos A, Bekiari E, et al.Sodium-glucose cotransporter 2 inhibitors for type 2 diabetes: a systematic review and meta- analysis. Ann Intern Med. 2013;159:262-74.
[4] Bolinder J, Ljunggren Ö, Kullberg J, Johansson L, Wilding J, Langkilde AM, et al. Effects of dapagliflozin on body weight, total fat mass, and regional adipose tissue distribution in patients with type 2 diabetes mellitus with inadequate glycemic control on metformin. J Clin Endocrinol Metab. 2012;97:1020-31.
[5] Ferrannini E, Ramos SJ, Salsali A, Tang W, List JF. Dapagliflozin monotherapy in type 2 diabetic patients with inadequate glycemic control by diet and exercise: a randomized, double-blind, placebo-controlled, phase 3 trial. Diabetes Care. 2010;33:2217-24.
[6] Daniele G, Xiong J, Solis-Herrera C, Merovci A, Eldor R, Tripathy D, et al. Dapagliflozin Enhances Fat Oxidation and Ketone Production in Patients With Type 2 Diabetes. Diabetes Care. 2016;39:2036-41.
[7] Szekeres Z, Toth K, Szabados E. The Effects of SGLT2 Inhibitors on Lipid Metabolism.Metabolites. 2021;11.
[8] Beylot M. Regulation of in vivo ketogenesis: role of free fatty acids and control by epinephrine, thyroid hormones, insulin and glucagon. Diabetes Metab. 1996;22:299-304.
[9] Osataphan S, Macchi C, Singhal G, Chimene-Weiss J, Sales V, Kozuka C, et al. SGLT2 inhibition reprograms systemic metabolism via FGF21-dependent and -independent mechanisms. JCI Insight. 2019;4.
[10] Inagaki T, Dutchak P, Zhao G, Ding X, Gautron L, Parameswara V, et al. Endocrine regulation of the fasting response by PPARalpha-mediated induction of fibroblast growth factor 21. Cell Metab. 2007;5:415-25.
[11] Ferrannini E, Baldi S, Frascerra S, Astiarraga B, Heise T, Bizzotto R, et al. Shift to Fatty Substrate Utilization in Response to Sodium-Glucose Cotransporter 2 Inhibition in Subjects Without Diabetes and Patients With Type 2 Diabetes. Diabetes. 2016;65:1190-5.
[12] Hazlehurst JM, Woods C, Marjot T, Cobbold JF, Tomlinson JW. Non-alcoholic fatty liver disease and diabetes. Metabolism. 2016;65:1096-108.
[13] Li B, Wang Y, Ye Z, Yang H, Cui X, Wang Z, et al. Effects of Canagliflozin on Fatty Liver Indexes in Patients with Type 2 Diabetes: A Meta-analysis of Randomized Controlled Trials. J Pharm Pharm Sci. 2018;21:222-35.
[14] Koike Y, Shirabe SI, Maeda H, Yoshimoto A, Arai K, Kumakura A, et al. Effect of canagliflozin on the overall clinical state including insulin resistance in Japanese patients with type 2 diabetes mellitus. Diabetes Res Clin Pract. 2019;149:140-6.
[15] Sasaki T, Sugawara M, Fukuda M. Sodium-glucose cotransporter 2 inhibitor-induced changes in body composition and simultaneous changes in metabolic profile: 52-week prospective LIGHT (Luseogliflozin: the Components of Weight Loss in Japanese Patients with Type 2 Diabetes Mellitus) Study. J Diabetes Investig. 2019;10:108-17.
[16] Kamei S, Iwamoto M, Kameyama M, Shimoda M, Kinoshita T, Obata A, et al. Effect of Tofogliflozin on Body Composition and Glycemic Control in Japanese Subjects with Type 2 Diabetes Mellitus. J Diabetes Res. 2018;2018:6470137.
[17] Sugiyama S, Jinnouchi H, Kurinami N, Hieshima K, Yoshida A, Jinnouchi K, et al.Dapagliflozin Reduces Fat Mass without Affecting Muscle Mass in Type 2 Diabetes. J Atheroscler Thromb. 2018;25:467-76.
[18] Inoue H, Morino K, Ugi S, Tanaka-Mizuno S, Fuse K, Miyazawa I, et al. Ipragliflozin, a sodium-glucose cotransporter 2 inhibitor, reduces bodyweight and fat mass, but not muscle mass, in Japanese type 2 diabetes patients treated with insulin: A randomized clinical trial. J Diabetes Investig. 2019;10:1012-21.
[19] Moszak M, Klupczyńska A, Kanikowska A, Kokot Z, Zawada A, Grzymisławska M, et al. The influence of a 3-week body mass reduction program on the metabolic parameters and free amino acid profiles in adult Polish people with obesity. Adv Clin Exp Med. 2018;27:749- 57.
[20] Williamson E, Moore DR. A Muscle-Centric Perspective on Intermittent Fasting: A Suboptimal Dietary Strategy for Supporting Muscle Protein Remodeling and Muscle Mass? Front Nutr. 2021;8:640621.
[21] Kappel BA, Lehrke M, Schütt K, Artati A, Adamski J, Lebherz C, et al. Effect of Empagliflozin on the Metabolic Signature of Patients With Type 2 Diabetes Mellitus and Cardiovascular Disease. Circulation. United States2017. p. 969-72.
[22] Ye Q, Danzer CF, Fuchs A, Wolfrum C, Rudin M. Hepatic lipid composition differs between ob/ob and ob/+ control mice as determined by using in vivo localized proton magnetic resonance spectroscopy. MAGMA. 2012;25:381-9.
[23] Bollard ME, Garrod S, Holmes E, Lindon JC, Humpfer E, Spraul M, et al. High- resolution (1)H and (1)H-(13)C magic angle spinning NMR spectroscopy of rat liver. Magn Reson Med. 2000;44:201-7.
[24] Bolinder J, Ljunggren Ö, Johansson L, Wilding J, Langkilde AM, Sjöström CD, et al.Dapagliflozin maintains glycaemic control while reducing weight and body fat mass over 2 years in patients with type 2 diabetes mellitus inadequately controlled on metformin.Diabetes Obes Metab. 2014;16:159-69.
[25] Inoue H, Morino K, Ugi S, Tanaka-Mizuno S, Fuse K, Miyazawa I, et al. Ipragliflozin, a sodium-glucose cotransporter 2 inhibitor, reduces bodyweight and fat mass, but not muscle mass, in Japanese type 2 diabetes patients treated with insulin: A randomized clinical trial. J Diabetes Investig. 2018.
[26] Finck BN. Targeting Metabolism, Insulin Resistance, and Diabetes to Treat Nonalcoholic Steatohepatitis. Diabetes. 2018;67:2485-93.
[27] Reeder SB, Cruite I, Hamilton G, Sirlin CB. Quantitative Assessment of Liver Fat with Magnetic Resonance Imaging and Spectroscopy. J Magn Reson Imaging. 2011;34:729-49.
[28] Szczepaniak LS, Nurenberg P, Leonard D, Browning JD, Reingold JS, Grundy S, et al.Magnetic resonance spectroscopy to measure hepatic triglyceride content: prevalence of hepatic steatosis in the general population. Am J Physiol Endocrinol Metab. 2005;288:E462- 8.
[29] Befroy DE, Shulman GI. Magnetic resonance spectroscopy studies of human metabolism. Diabetes. 2011;60:1361-9.
[30] Noureddin M, Lam J, Peterson MR, Middleton M, Hamilton G, Le TA, et al. Utility of magnetic resonance imaging versus histology for quantifying changes in liver fat in nonalcoholic fatty liver disease trials. Hepatology. 2013;58:1930-40.
[31] Shen W, Chen J, Gantz M, Velasquez G, Punyanitya M, Heymsfield SB. A single MRI slice does not accurately predict visceral and subcutaneous adipose tissue changes during weight loss. Obesity (Silver Spring). 2012;20:2458-63
[32] Blonde L, Stenlöfe K, Fung A, Xie J, Canovatchel W, Meininger G. Effects of canagliflozin on body weight and body composition in patients with type 2 diabetes over 104 weeks. Postgrad Med. 2016; 128:371-80.
[33] Giesecke K, Magnusson I, Ahlberg M, Hagenfeldt L, Wahren J. Protein and amino acid metabolism during early starvation as reflected by excretion of urea and methylhistidines.Metabolism. 1989;38:1196-200.
[34] Ross BD, Hems R, Krebs HA. The rate of gluconeogenesis from various precursors in the perfused rat liver. Biochem J. 1967;102:942-51.
[35] Merovci A, Solis-Herrera C, Daniele G, Eldor R, Fiorentino TV, Tripathy D, et al.Dapagliflozin improves muscle insulin sensitivity but enhances endogenous glucose production. J Clin Invest. 2014;124:509-14.
[36] Felig P, Marliss E, Cahill GF, Jr. Plasma amino acid levels and insulin secretion in obesity. N Engl J Med. 1969;281:811-6.
[37] Suhre K, Meisinger C, Döring A, Altmaier E, Belcredi P, Gieger C, et al. Metabolic footprint of diabetes: a multiplatform metabolomics study in an epidemiological setting. PLoS One. 2010;5:e13953.
[38] Wang TJ, Larson MG, Vasan RS, Cheng S, Rhee EP, McCabe E, et al. Metabolite profiles and the risk of developing diabetes. Nat Med. 2011;17:448-53.
[39] Würtz P, Tiainen M, Mäkinen VP, Kangas AJ, Soininen P, Saltevo J, et al. Circulating metabolite predictors of glycemia in middle-aged men and women. Diabetes Care. 2012;35:1749-56.
[40] Nair KS, Garrow JS, Ford C, Mahler RF, Halliday D. Effect of poor diabetic control and obesity on whole body protein metabolism in man. Diabetologia. 1983;25:400-3.
[41] She P, Olson KC, Kadota Y, Inukai A, Shimomura Y, Hoppel CL, et al. Leucine and protein metabolism in obese Zucker rats. PLoS One. 2013;8:e59443.
[42] Herman MA, She P, Peroni OD, Lynch CJ, Kahn BB. Adipose tissue branched chain amino acid (BCAA) metabolism modulates circulating BCAA levels. J Biol Chem. 2010;285:11348-56.
[43] She P, Van Horn C, Reid T, Hutson SM, Cooney RN, Lynch CJ. Obesity-related elevations in plasma leucine are associated with alterations in enzymes involved in branched- chain amino acid metabolism. Am J Physiol Endocrinol Metab. 2007;293:E1552-63.
[44] Bletsa E, Filippas-Dekouan S, Kostara C, Dafopoulos P, Dimou A, Pappa E, et al. Effect of Dapagliflozin on Urine Metabolome in Patients with Type 2 Diabetes. J Clin Endocrinol Metab. 2021;106:1269-83.