There have been concerns about the risk of lactic acidosis with metformin but the risk is probably much less than had been thought. 8 Metformin may also increase peripheral insulin sensitivity by enhancing glucose uptake in the muscle. Metformin increases insulin sensitivity in the liver by inhibiting hepatic gluconeogenesis and thereby reducing hepatic glucose production. The balance of actions on different tissues is different between the glitazones and metformin, and they are sometimes used in combination. A newer group called the thiazolidinediones (TZDs), or glitazones, includes rosiglitazone and pioglitazone. they reduce the insulin resistance) The commonest one in the UK is metformin, from the group of drugs called the biguanides. Insulin sensitizers, which make tissues such as the liver and the muscles more sensitive to insulin (i.e. 7 They are shorter acting, and have been suggested for controlling postprandial hyperglycaemia, perhaps in combination with a long-acting insulin. They bind to the same receptor but are less potent than the sulfonylureas. A newer group of secretagogues is the meglitinide analogues, including nateglinide and repaglinide, but these are used far less than the sulfonylureas.
The ones most used in the UK are gliclazide, glipizide, glimepiride and glibenclamide (glyburide). There are seven of these in the British National Formulary (BNF), but older ones such as chlorpropamide are now little used. Insulin secretagogues, which stimulate the pancreas to release more insulin, by binding to a sulfonylurea receptor The main group is the sulfonylureas.
6 Several classes of oral agents are available. Type 2 diabetes has traditionally been treated in a stepwise manner, starting with lifestyle modifications and encouragement of physical activity and, when necessary, pharmacotherapy with oral agents. The difficulty in maintaining metabolic control over time may be related to several behavioural factors (for example, difficulties with healthy eating, exercise, medication regimens) but primarily reflects the underlying progressive decline in beta-cell function, 4 so that control deteriorated over a 9-year follow-up period. Individuals with type 2 diabetes may have few or none of the classic clinical symptoms (such as thirst, passing abnormally large amounts of urine) of hyperglycaemia, and may be diagnosed incidentally as seen in the UKPDS, 3 where 33% were found by incidental means (for example, urine testing for an insurance medical) and 53% via symptoms. 1 In the United Kingdom Prospective Diabetes Study (UKPDS), 2 beta-cell function was found to be impaired at diagnosis, especially in patients who were not overweight. However, in most patients who may develop type 2 diabetes, the pancreatic beta-cell function progressively declines, leading to hyperglycaemia and clinical diabetes. The higher than usual level of insulin is known as hyperinsulinaemia. The pancreatic beta cell is initially able to compensate for insulin resistance, by increasing production, thereby maintaining normal blood glucose levels. They are usually insulin resistant, and therefore require higher levels of insulin in order to keep blood glucose within the normal range. Type 2 diabetes is usually seen in people who are overweight or obese, particularly if inactive.
The cause, or causes, of type 1 diabetes are not known. In type 1 diabetes, the beta cells are lost because of an autoimmune process, little or no insulin is produced, and insulin treatment is required for survival. Insulin lowers blood glucose and glucagon raises it. In non-diabetic people, the level of glucose in the blood is controlled by a balance of hormonal actions, principally insulin and glucagon, both of which are produced by specific types of cell in the pancreas, beta cells producing insulin and alpha cells producing glucagon. Diabetes mellitus is characterised by raised blood glucose levels.
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