Editorials

Thiazolidinediones for type 2 diabetes

BMJ 2000; 321 doi: https://doi.org/10.1136/bmj.321.7256.252 (Published 29 July 2000) Cite this as: BMJ 2000;321:252

New agents reduce insulin resistance but need long term clinical trials

  1. Andrew J Krentz (a.j.krentz@soton.ac.uk), consultant in diabetes and endocrinology,
  2. Clifford J Bailey (c.j.bailey@aston.ac.uk), head of diabetes research,
  3. Arne Melander (arne.melander@nepi.net), head of NEPI Foundation
  1. Southampton General Hospital, Southampton SO16 6YD
  2. Department of Pharmaceutical Sciences, University of Aston, Birmingham B4 7ET
  3. Medical Research Centre, Malmö University Hospital SE-205 02, Sweden

    Insulin resistance, or more appropriately the reduced action of insulin, is a prominent defect in type 2 diabetes.1 It is commonly present in people before diabetes has developed and has even been observed in euglycaemic relatives of patients with type 2 diabetes.2 It has been proposed that the reduced action of insulin is fundamental to the cardiovascular risk factors that are part of the syndrome of insulin resistance.3 Avoidance of obesity and adequate levels of physical activity are non-pharmacological cornerstones of the fight against insulin resistance. Before the introduction of troglitazone in 1997 metformin was the only drug able to sensitise target tissues (skeletal muscle, adipose tissue, and the liver) to insulin. Troglitazone was the first of a new class of drugs with direct insulin sensitising actions—the thiazolidinediones (also known as glitazones).4 Troglitazone has now been superseded by more potent agents, rosiglitazone and pioglitazone.

    Thiazolidinediones activate nuclear peroxisome proliferator activated receptor γ (PPAR-γ), which is expressed predominantly in adipose tissue. 4 5 Insulin action is improved through the increased transcription of …

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