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Mechanisms of statin-induced new-onset diabetes
Maryam Paseban1, Alexandra E Butler2, Amirhossein Sahebkar3,4,5
1Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Abstract:
Statins, with their lipid-lowering properties, are a first-line therapy for the prevention of cardiovascular diseases. Recent evidence, however, suggests that statins can increase the risk of new-onset diabetes (NOD). The molecular mechanisms of statin-induced NOD are not precisely known, although some pathophysiologic mechanisms have been suggested. Specific to the beta cell, these mechanisms include alterations in insulin secretion, changes in ion channels, modulation of signaling pathways, and inflammation/oxidative stress. Outwith the beta cell, other suggested mechanisms involve adipocytes, including alterations in adipocyte differentiation and modulation of leptin and adiponectin, and genetic and epigenetic mechanisms, including alterations in microRNA. The evidence supporting these and other mechanisms will be discussed. Greater understanding of the underlying mechanisms linking the onset of diabetes to statin therapy is essential and clinically relevant, as it may enable novel preventative or therapeutic approaches to be instituted and guide the production of a new generation of statins lacking this side effect.
Insights
Statins, used for cardiovascular disease prevention, may increase the risk of new-onset diabetes (NOD). Research is exploring the molecular mechanisms behind this side effect to develop safer alternatives.
Area of Science:
- Biochemistry
- Endocrinology
- Pharmacology
Background:
- Statins are primary treatments for cardiovascular disease due to their lipid-lowering effects.
- Emerging research indicates a potential link between statin use and an increased risk of new-onset diabetes (NOD).
Purpose of the Study:
- To review and discuss the proposed molecular and pathophysiological mechanisms underlying statin-induced new-onset diabetes.
- To highlight the clinical relevance of understanding these mechanisms for future therapeutic strategies.
Main Methods:
- Literature review and synthesis of existing evidence on statin-induced diabetes.
- Discussion of proposed mechanisms involving pancreatic beta cells, adipocytes, and genetic/epigenetic factors.
Main Results:
- Statin-induced NOD may involve alterations in beta-cell function, including insulin secretion and signaling pathways.
- Mechanisms outside the beta cell include effects on adipocytes and modulation of adipokines like leptin and adiponectin.
- Genetic and epigenetic factors, such as microRNA alterations, are also implicated.
Conclusions:
- Understanding the mechanisms of statin-induced NOD is crucial for clinical practice.
- This knowledge may lead to the development of preventative strategies or novel statin generations with reduced diabetic side effects.
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