References
- Ward WK, Bolgiano DC, McKnight B, et al. Diminished B cell secretory capacity in patients with noninsulin-dependent diabetes mellitus. J Clin Invest. 1984;74:1318–1328.
- Leahy JL, Bonner-Weir S, Weir GC. Beta-cell dysfunction induced by chronic hyperglycemia. Current ideas on mechanism of impaired glucose-induced insulin secretion. Diabetes Care. 1992;15:442–455.
- Rossetti L, Giaccari A, DeFronzo RA. Glucose toxicity. Diabetes Care. 1990;13:610–630.
- Rossetti L, Shulman GI, Zawalich W, et al. Effect of chronic hyperglycemia on in vivo insulin secretion in partially pancreatectomized rats. J Clin Invest. 1987;80:1037–1044.
- Ilkova H, Glaser B, Tunckale A, et al. Induction of long-term glycemic control in newly diagnosed type 2 diabetic patients by transient intensive insulin treatment. Diabetes Care. 1997;20:1353–1356.
- Weng J, Li Y, Xu W, et al. Effect of intensive insulin therapy on beta-cell function and glycaemic control in patients with newly diagnosed type 2 diabetes: a multicentre randomised parallel group trial. Lancet. 2008;371:1753–1760.
- Ohta A, Kato H, Murayama K, et al. Effect of insulin glargine on endogenous insulin secretion and beta-cell function in Japanese type 2 diabetic patients using oral antidiabetic drugs. Endocr J. 2014;61:13–18.
- Asai S, Ohta A, Kato H, et al. Effect of sitagliptin on glycemic control and beta cell function in Japanese patients given basal-supported oral therapy for type 2 diabetes. Endocr J. 2014;61:1213–1220.
- Gerich JE. Role of the kidney in normal glucose homeostasis and in the hyperglycaemia of diabetes mellitus: therapeutic implications. Diabet Med. 2010;27:136–142.
- Merovci A, Mari A, Solis C, et al. Dapagliflozin lowers plasma glucose concentration and improves β-cell function. J Clin Endocrinol Metab. 2015;100:1927–1932.
- Ferrannini E, Muscelli E, Frascerra S, et al. Metabolic response to sodium-glucose cotransporter 2 inhibition in type 2 diabetic patients. J Clin Invest. 2014;124:499–508.
- Takahara M, Shiraiwa T, Matsuoka TA, et al. Ameliorated pancreatic β cell dysfunction in type 2 diabetic patients treated with a sodium-glucose cotransporter 2 inhibitor ipragliflozin. Endocr J. 2015;62:77–86.
- Bonora E, Zavaroni I, Coscelli C, et al. Decreased hepatic insulin extraction in subjects with mild glucose intolerance. Metabolism. 1983;32:438–446.
- Bolinder J, Ljunggren Ö, Kullberg J, 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;97:1020–1031.
- Seufert J. SGLT2 inhibitors - an insulin-independent therapeutic approach for treatment of type 2 diabetes: focus on canagliflozin. Diabetes Metab Syndr Obes. 2015;8:543–554.
- Ohkura T. Ipragliflozin: A novel sodium-glucose cotransporter 2 inhibitor developed in Japan. World J Diabetes. 2015;6:136–144.
- Komiya C, Tsuchiya K, Shiba K, et al. Ipragliflozin Improves Hepatic Steatosis in Obese Mice and Liver Dysfunction in Type 2 Diabetic Patients Irrespective of Body Weight Reduction. PLoS One. 2016;11:e0151511.
- Polidori D, Sha S, Heise T, et al. Effect of canagliflozin, a sodium glucose co-transporter 2 inhibitor, on C-peptide kinetics. Clinical Pharm in Drug Dev. 2015;4:12–17.
- Vauhkonen IK, Niskanen LK, Mykkänen L, et al. Hyperproinsulinemia is not a characteristic feature in the offspring of patients with different phenotypes of type II diabetes. Eur J Endocrinol. 2000;143:251–260.
- Loopstra-Masters RC, Haffner SM, Lorenzo C, et al. Proinsulin-to-C-peptide ratio versus proinsulin-to-insulin ratio in the prediction of incident diabetes: the Insulin Resistance Atherosclerosis Study (IRAS). Diabetologia. 2011;54:3047–3054.
- Unger RH. Lipotoxicity in the pathogenesis of obesity-dependent NIDDM. Genetic and clinical implications. Diabetes. 1995;44:863–870.