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Statins and diabetes risk: how real is it and what are the mechanisms?

Robinson, Jennifer G.a,b,c

Current Opinion in Lipidology: June 2015 - Volume 26 - Issue 3 - p 228–235
doi: 10.1097/MOL.0000000000000172
LIPID METABOLISM: Edited by Kausik K. Ray and G. Kees Hovingh

Purpose of review In randomized trials and many observational studies, statins are associated with a modest excess of type 2 diabetes mellitus. High-intensity statins, such as atorvastatin 80 mg and rosuvastatin 20 mg, are associated with a higher excess risk of diabetes than moderate-intensity statins, such as atorvastatin 10 mg, simvastatin 20–40 mg, or pravastatin 40 mg.

Recent findings Multiple mechanisms have been proposed for statin-associated diabetes risk, primarily related to increased insulin resistance or impaired insulin secretion. Genetic polymorphisms with reduced HMG CoA reductase function are associated with weight gain, insulin resistance, and diabetes. Animal models have shown that HMG CoA inhibition has multiple downstream effects that may increase diabetes risk. Statin impairment of insulin signaling, decreased adipocyte differentiation, decreased pancreatic β-cell insulin secretion, and other effects have also been found. The excess risk of diabetes appears to be confined to those who are already at risk for developing diabetes. Diabetes is diagnosed only 2–4 months earlier in statin-treated patients and therefore is unlikely to have no long-term adverse consequences.

Summary The clinical impact of statin-associated diabetes is likely unimportant. The cardiovascular risk reduction benefit from statin far outweighs the potential for adverse effects in all but the very lowest risk individuals.

aDepartment of Epidemiology

bDepartment of Medicine

cPrevention Intervention Center, University of Iowa, Iowa City, Iowa, USA

Correspondence to Jennifer G. Robinson, MD, MPH, Department of Epidemiology, College of Public Health, University of Iowa, 145 North Riverside Drive, S455 CPHB, Iowa City, IA 52242-2007, USA. Tel: +1 319 384 1563, assistant +1 319 384 1540; fax: +1 319 384 4155; e-mail:

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