We have read the article ‘New onset diabetes mellitus induced by statins: current evidence’ by Chrysant SG with interest and found that the article has been framed after reviewing the previously published articles for risk of New Onset of Diabetes Mellitus (NODM) in subjects of randomized clinical trials and in population-based studies.
In abstract, it has been mentioned by the author that risk of NODM incidence with statins use is due to decrease in adiponectin levels and increase in insulin secretion. In contrary to this statement, the pathophysiological mechanisms of statin-induced NODM mentioned in Section 4 and in Table 4 of the review, it is mentioned as increased adiponectin level is one of the reasons for statin-induced NODM.
Various researchers and also the author himself in the context of his article have reported that, statins cause NODM by altering the insulin resistance leading to decrease in the secretion of insulin and decrease in adiponectin levels [Citation1–Citation5]. Other factors include inhibition of β-cell glucose transporters, pro-inflammatory and oxidative β-cell effects of plasma-derived cholesterol, β-cell apoptosis, delayed ATP production, etc. [Citation2,Citation6].
Hence, after contemplating the cited articles, it is buttressed that statin induces NODM by various mechanisms one of which is by decreasing adiponectin levels and not by increasing it. With great gratitude, we would like to request the author to relook into the review and confirm about statin-induced NODM mechanism in a more precise manner.
Note: Also, a typographical error in the conclusion of the article for the word statin as station requires rectification.
We would be highly obliged for your kind consideration of including the abovementioned rectifications into your article to avoid discrepancy and highlight a clear idea for statins being one of the causes for NODM.
Declaration of interest
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
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References
- Yada T, Nakata M, Shiraishi T, et al. Inhibition by simvastatin, but not pravastatin, of glucose-induced cytosolic Ca2+ signalling and insulin secretion due to blockade of L-type Ca2+ channels in rat islet beta-cells. Br J Pharmacol. 1999;126:1205–1213.
- Sampson UK, Linton MF, Fazio S. Are statins diabetogenic? Curr Opin Cardiol. 2011 Jul;26(4):342–347.
- Cederberg H, Stancakova A, Yaluri N, et al. Increased risk of diabetes with statin treatment is associated with impaired insulin sensitivity and insulin secretion: a 6 year follow-up study of the METSIM cohort. Diabetologia. 2015;58:1109–1117.
- Koh KK, Quon MJ, Han SH, et al. Differential metabolic effects of pravastatin and simvastatin in hypercholesterolemic patients. Atherosclerosis. 2009 Jun;204(2):483–490.
- Koh KK, Quon MJ, Sakuma I, et al. Differential metabolic effects of rosuvastatin and pravastatin in hypercholesterolemic patients. Int J Cardiol. 2013 Jun 20;166(2):509–515.
- Sattar N, Taskinen MR. Statins are diabetogenic – myth or reality? Atheroscler Suppl. 2012;13:1–10.