title: Statin therapy and new-onset diabetes: molecular mechanisms and clinical relevance.
abstract: Despite positive effects on the plasma lipid profile and vascular events, statin use is associated with various side effects. Among these, statins might cause a disruption of a number of regulatory pathways including insulin signaling. This may affect insulin sensitivity, pancreatic beta-cell function and adipokine secretion. The statin-associated risk of new-onset diabetes (NOD) appears to be a dose-dependent class effect. It still remains unclear whether statin treatment is associated with increased risk of NOD in the general population or if there are groups of individuals at particular risk. However, according to the available data it seems that cardiovascular (CV) benefits in high-risk individuals strongly favor statin therapy since it outweighs other risks. Whether statins should be used for primary prevention among patients with a relatively low baseline CV risk is still questionable, however the results of primary prevention trials have shown reductions in mortality in this population. Thus, there is a need for randomized, placebo-controlled statin studies with carefully selected groups of patients and NOD as a key end point in order to resolve queries concerning this issue.
authors.affiliation: Department of Hypertension, Chair of Nephrology and Hypertension, Medical University of Lodz, Lodz, Poland. maciejbanach@aol.co.uk
authors.forename: Maciej
authors.initials: M
authors.lastname: Banach
authors.forename: Malgorzata
authors.initials: M
authors.lastname: Malodobra-Mazur
authors.forename: Anna
authors.initials: A
authors.lastname: Gluba
authors.forename: Niki
authors.initials: N
authors.lastname: Katsiki
authors.forename: Jacek
authors.initials: J
authors.lastname: Rysz
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Dobrzyn
mesh_terms: D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism; D054392:Adipokines / Q000378:metabolism; D000818:Animals; D003924:Diabetes Mellitus, Type 2 / Q000139:chemically induced* / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism; D050171:Dyslipidemias / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D019317:Evidence-Based Medicine; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000009:adverse effects* / Q000494:pharmacology / Q000627:therapeutic use; D007004:Hypoglycemic Agents / Q000494:pharmacology / Q000627:therapeutic use; D007328:Insulin / Q000378:metabolism / Q000494:pharmacology / Q000627:therapeutic use; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000187:drug effects / Q000378:metabolism; D011972:Receptor, Insulin / Q000819:agonists / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D054392:Adipokines; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007004:Hypoglycemic Agents; D007328:Insulin; D011972:Receptor, Insulin