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The pharmacotherapy of Type 2 Diabetes Mellitus (T2DM) has, in the past 60 years, been developing in unison with the advances in our understanding of diabetes pathophysiology. As our knowledge developed and changed, so did appear new drugs which better and in more targeted fashion rectified the pathological processes leading to the development of diabetes. If we look into the history of T2DM treatment, the first antidiabetic medicine was insulin – a hormone. Insulin is without a doubt the most important hormone in regulation of glycaemia. The secretion of insulin in response to increasing glucose levels in the bloodstream postprandially is influenced by several mechanisms in three stages: Neuronal (cephalic) phase Gastro-enteral phase (in response to gastrointestinal hormones) Nutritional phase (beta cell stimulation in response to nutrients – glucose, aminoacids, FFA) The gastro-enteral phase has been described many years ago as entero-insular axis. This description has been based on observation that the same glucose load administered orally stimulates higher insulin response than when administered intravenously. The difference has been described as an ‘incretin effect’. However, for decades to come, oral antidiabetics have never been able to capitalise on this mechanisms and took the route of influencing glucose homeostasis via peripheral insulin resistance, endogenous hepatic glucose production, or direct stimulation of beta cells. Currently, it is understood that glucose homeostasis is governed by complex interaction of several hormones: Insulin, amylin, incretins (GLP-1, GIP and possibly others) in balance with the contraregulatory hormones that include glucagon, cortisol, catecholamines and GH with IGF-1. Our understanding of diabetes pathophysiology has developed from dual basis of insulin resistance (IR) and insulin deficiency (ID), via trio of IR in skeletal muscle, ID in beta cell and increased hepatic gluconeogensis, all the way to DeFronzo’s (2009) ‘Ominous Octet’ of muscle, liver, and ┚-cell dysfunction, and additionally, fat cell pathology (accelerated lipolysis), gastrointestinal tract (incretin deficiency/resistance), ┙-cell (hyperglucagonemia), kidney (increased glucose reabsorption), and brain (insulin resistance) disorders.

Incretin-Based Treatment Strategy - GLP-1 Receptor Agonists (GLP-1R) or So-Called Incretin Mimetics