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New, Novel Lipid-Lowering Agents for Reducing Cardiovascular Risk: Beyond Statins
Kyuho Kim, Henry N. Ginsberg, Sung Hee Choi
Diabetes Metab J. 2022;46(4):517-532.   Published online July 27, 2022
DOI: https://doi.org/10.4093/dmj.2022.0198
Correction in: Diabetes Metab J 2022;46(5):817
  • 11,483 View
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  • 30 Web of Science
  • 32 Crossref
AbstractAbstract PDFPubReader   ePub   
Statins are the cornerstone of the prevention and treatment of atherosclerotic cardiovascular disease (ASCVD). However, even under optimal statin therapy, a significant residual ASCVD risk remains. Therefore, there has been an unmet clinical need for novel lipid-lowering agents that can target low-density lipoprotein cholesterol (LDL-C) and other atherogenic particles. During the past decade, several drugs have been developed for the treatment of dyslipidemia. Inclisiran, a small interfering RNA that targets proprotein convertase subtilisin/kexin type 9 (PCSK9), shows comparable effects to that of PCSK9 monoclonal antibodies. Bempedoic acid, an ATP citrate lyase inhibitor, is a valuable treatment option for the patients with statin intolerance. Pemafibrate, the first selective peroxisome proliferator-activated receptor alpha modulator, showed a favorable benefit-risk balance in phase 2 trial, but the large clinical phase 3 trial (PROMINENT) was recently stopped for futility based on a late interim analysis. High dose icosapent ethyl, a modified eicosapentaenoic acid preparation, shows cardiovascular benefits. Evinacumab, an angiopoietin-like 3 (ANGPTL3) monoclonal antibody, reduces plasma LDL-C levels in patients with refractory hypercholesterolemia. Novel antisense oligonucleotides targeting apolipoprotein C3 (apoC3), ANGPTL3, and lipoprotein(a) have significantly attenuated the levels of their target molecules with beneficial effects on associated dyslipidemias. Apolipoprotein A1 (apoA1) is considered as a potential treatment to exploit the athero-protective effects of high-density lipoprotein cholesterol (HDL-C), but solid clinical evidence is necessary. In this review, we discuss the mode of action and clinical outcomes of these novel lipid-lowering agents beyond statins.

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Original Article
Obesity and Metabolic Syndrome
Statins Increase Mitochondrial and Peroxisomal Fatty Acid Oxidation in the Liver and Prevent Non-Alcoholic Steatohepatitis in Mice
Han-Sol Park, Jung Eun Jang, Myoung Seok Ko, Sung Hoon Woo, Bum Joong Kim, Hyun Sik Kim, Hye Sun Park, In-Sun Park, Eun Hee Koh, Ki-Up Lee
Diabetes Metab J. 2016;40(5):376-385.   Published online April 5, 2016
DOI: https://doi.org/10.4093/dmj.2016.40.5.376
  • 6,707 View
  • 86 Download
  • 66 Web of Science
  • 127 Crossref
AbstractAbstract PDFPubReader   
Background

Non-alcoholic fatty liver disease is the most common form of chronic liver disease in industrialized countries. Recent studies have highlighted the association between peroxisomal dysfunction and hepatic steatosis. Peroxisomes are intracellular organelles that contribute to several crucial metabolic processes, such as facilitation of mitochondrial fatty acid oxidation (FAO) and removal of reactive oxygen species through catalase or plasmalogen synthesis. Statins are known to prevent hepatic steatosis and non-alcoholic steatohepatitis (NASH), but underlying mechanisms of this prevention are largely unknown.

Methods

Seven-week-old C57BL/6J mice were given normal chow or a methionine- and choline-deficient diet (MCDD) with or without various statins, fluvastatin, pravastatin, simvastatin, atorvastatin, and rosuvastatin (15 mg/kg/day), for 6 weeks. Histological lesions were analyzed by grading and staging systems of NASH. We also measured mitochondrial and peroxisomal FAO in the liver.

Results

Statin treatment prevented the development of MCDD-induced NASH. Both steatosis and inflammation or fibrosis grades were significantly improved by statins compared with MCDD-fed mice. Gene expression levels of peroxisomal proliferator-activated receptor α (PPARα) were decreased by MCDD and recovered by statin treatment. MCDD-induced suppression of mitochondrial and peroxisomal FAO was restored by statins. Each statin's effect on increasing FAO and improving NASH was independent on its effect of decreasing cholesterol levels.

Conclusion

Statins prevented NASH and increased mitochondrial and peroxisomal FAO via induction of PPARα. The ability to increase hepatic FAO is likely the major determinant of NASH prevention by statins. Improvement of peroxisomal function by statins may contribute to the prevention of NASH.

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Reviews
Diabetogenic Effect of Statins: A Double-Edged Sword?
Ji Sung Yoon, Hyoung Woo Lee
Diabetes Metab J. 2013;37(6):415-422.   Published online December 12, 2013
DOI: https://doi.org/10.4093/dmj.2013.37.6.415
  • 3,858 View
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AbstractAbstract PDFPubReader   

Statins are widely prescribed cholesterol-lowering agents, which have been demonstrated to significantly reduce cardiovascular morbidity and mortality. However, recent trials have reported that statins cause worsening of hyperglycemia and increase the risk of new-onset diabetes. The association between the diabetogenic effect of statins with intensive dose and accompanying major risk factors for diabetes has been demonstrated. However, statins do not appear to have a class effect on insulin sensitivity in non-diabetic patients. Numerous mechanisms have been suggested to explain how statins cause β-cell insulin secretory dysfunction and peripheral insulin resistance leading to incident diabetes. According to findings from an aggregate of large clinical trials, the benefits of statin treatment appear to outweigh the risk of new-onset diabetes. Therefore, it would be inappropriate to discontinue the use of statins for prevention of cardiovascular events because of its potential risk for development of incident diabetes. This review addresses the currently available evidence related to statin use and new-onset diabetes from a clinical perspective.

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Regulation of Muscle Pyruvate Dehydrogenase Complex in Insulin Resistance: Effects of Exercise and Dichloroacetate
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Diabetes Metab J. 2013;37(5):301-314.   Published online October 17, 2013
DOI: https://doi.org/10.4093/dmj.2013.37.5.301
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AbstractAbstract PDFPubReader   

Since the mitochondrial pyruvate dehydrogenase complex (PDC) controls the rate of carbohydrate oxidation, impairment of PDC activity mediated by high-fat intake has been advocated as a causative factor for the skeletal muscle insulin resistance, metabolic syndrome, and the onset of type 2 diabetes (T2D). There are also situations where muscle insulin resistance can occur independently from high-fat dietary intake such as sepsis, inflammation, or drug administration though they all may share the same underlying mechanism, i.e., via activation of forkhead box family of transcription factors, and to a lower extent via peroxisome proliferator-activated receptors. The main feature of T2D is a chronic elevation in blood glucose levels. Chronic systemic hyperglycaemia is toxic and can lead to cellular dysfunction that may become irreversible over time due to deterioration of the pericyte cell's ability to provide vascular stability and control to endothelial proliferation. Therefore, it may not be surprising that T2D's complications are mainly macrovascular and microvascular related, i.e., neuropathy, retinopathy, nephropathy, coronary artery, and peripheral vascular diseases. However, life style intervention such as exercise, which is the most potent physiological activator of muscle PDC, along with pharmacological intervention such as administration of dichloroacetate or L-carnitine can prove to be viable strategies for treating muscle insulin resistance in obesity and T2D as they can potentially restore whole body glucose disposal.

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Original Article
Effects of Lovastatin on Free Fatty Acid Oxidation in Cultured L6 Rat Skeletal Muscle Cells.
Dong Lim Kim, Kee Ho Song, Hae Rim Kim, Suk Kyeong Kim
Korean Diabetes J. 2007;31(3):230-235.   Published online May 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.3.230
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AbstractAbstract PDF
BACKGROUND
Recent clinical studies suggest that statins improve insulin resistance and glucose metabolism in patients with metabolic syndrome and type 2 diabetes. To evaluate the possible mechanism of this action, we measured free fatty acid oxidation in cultured L6 rat skeletal muscle cell line. METHODS: Cultured L6 myotubes were treated with or without lovastatin (1, 5, 20 micrometer) for 24 hours or 48 hours and palmitate oxidation was measured. We also measured protein concentration of the cells. RESULTS: Lovastain increased palmitate oxidation in dose and time dependent manner in L6 myotubes (24 hr; 1 micrometer 119.2 +/- 11.9% of control, 5 micrometer 140.9 +/- 8.1%, 20 micrometer 150 +/- 5%, P = 0.05 vs control, respectively, 48 hr 1 micrometer 120.9 +/- 14.5%, 5 micrometer 176.6 +/- 28.2%, 20 micrometer 196.0 +/- 19.9%, P < 0.01 vs control, respectively). However, lovastatin decreased total cellular protein (24 hr: 1 micrometer 89.2 +/- 6.1% of control, 5 micrometer 79.3 +/- 7.6%, 20 micrometer 65.4 +/- 4.2%, P = 0.05 vs control, respectively, 48 hr: 1 micrometer 81.7 +/- 5.1%, 5 micrometer 58.6 +/- 11.9%, 20 micrometer 48.1 +/- 6.9%, P < 0.01 vs control, respectively). CONCLUSION: Lovastatin increased skeletal muscle free fatty acid oxidation in L6 rat skeletal muscle cells. This would be one of the mechanisms which lovastatin improves insulin resistance.

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