The metabolic hormone adiponectin could serve as a predictive biomarker for type 2 diabetes (T2D), according to a study published online in Clinical Pharmacology & Therapeutics. The research may help doctors prescribe better therapies with fewer side effects to the 24 million Americans who suffer from type 2 diabetes.
Adiponectin is a hormone that regulates a number of metabolic processes, such as glucose regulation and the metabolism of fat for energy production. Numerous studies have shown a link between adiponectin and insulin sensitivity but the study from John A. Wagner and colleagues re-affirms that levels of the hormone in T2D patients could also predict how they will respond to certain anti-diabetes drugs. A group of receptors known as PPARs play an important role in regulating metabolism genes that help cells respond to insulin. Compiling data from patients involved in several different clinical trials, the team showed that levels of adiponectin in the blood are a robust predictor of PPAR activation and subsequent response to insulin. The findings support the possible use of adiponectin as a biomarker to monitor glucose tolerance. The authors also propose that adiponectin could serve as a diagnostic biomarker to predict how patients will respond to thiazolidinediones, a commonly used drug in the treatment to T2D. This study was conducted by the Metabolic Disorders Steering Committee of the Biomarkers Consortium which is managed by the Foundation for the National Institutes of Health. The committee, comprised of government, industry and non-profit partners, used blinded data from four pharmaceutical companies that had conducted separate clinical trials with PPAR targeting and non-PPAR targeting drugs. This process of pooling data may ultimately lead to reduced research and development costs and improved patient care. Author contact: John A. Wagner (Merck Research Laboratories, Rahway, New Jersey, USA) E-mail: wagner@merck.com Abstract available online. (C) Clinical Pharmacology & Therapeutics press release.
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