Carbohydrate absorption inhibitors α-glucosidose inhibitors Acarbose: Dose Adverse events

Determinants of PPG Relatively complex network controlling PPG: Pre-prandial glycaemic level Insulin secretion and insulin sensitivity Glucagon and other counter-regulatory hormones PPG Meal size and meal content Gastric emptying and incretin hormones FPG, fasting plasma glucose; PPG, postprandial plasma glucose 1. Ceriello. Int J Clin Pract 2010;64:1705–11; 2. Alsahli & Gerich. Ref Mod Biomed Res 2014;doi:10.1016/B978-0-12-801238-3.03827-7

Prandial insulin secretion Cephalic phase of insulin secretion1 Evoked by the sight, smell and taste of food (before gut absorption) Postprandial biphasic insulin secretion2: First phase/early phase, transitory: Critical role in PPG homeostasis (targeting the liver) Can prevent chronic postprandial hyperglycaemia (glucotoxicity) and chronic hyperinsulinaemia (beta-cell exhaustion) Second phase, more gradually: Related to the degree and duration of the stimulus β-cell insulin content3: 2–3% released during first phase 20% released during second phase First- and second-phase insulin secretion in the β-cell4 240 Insulin secretion Time (min) 5 Second-phase insulin secretion Glucose stimulation First-phase insulin secretion PPG, postprandial plasma glucose Bruce et al. Metabolism 1987;36:721–5; 1. Caumo & Luzi. Am J Physiol Endocrinol Metab 2004;287:E371–85; 2. DelPrato. Diabetologia 2003;46(Suppl. 1):2–8; 3. Cheng et al. Curr Molec Med 2013;13:126–39

Acarbose 300 mg Acarbose = 1500 mg Metformin

Acarbose Initially 25 mg po with first bite of meals. Can increase 50-100 mg q8h at 4-8 w, base on: PPG – HbA1C- tolerance.

Prandial insulin secretion 240 Insulin secretion Time (min) 5 Second-phase insulin secretion Glucose stimulation First-phase insulin secretion

Maximum Dose: < 60 kg 50 mg q8h > 60 kg 100 mg q8h

Efficacy and safety of combination therapy with an alpha-glucosidase inhibitor and a dipeptidyl peptidase-4 inhibitor in patients with type 2 diabetes mellitus: A systematic review with meta-analysis AGI increases GLP-1 secretion. Because DPP4 inhibitor protects GLP-1 and GIP from enzymatic degradation, combination of DPP4 inhibitor and AGI may synergistically increase active GLP-1 levels.

In conclusion, addition of a DPP4 inhibitor to patients with inadequately controlled T2DM with AGI therapy achieved a clinically significant improvement in glycemic control without increasing the risk of weight gain and hypoglycemia. Therefore, this combination should be a viable option in the pharmacological therapy for T2DM.