Cardiovascular Prevention and Pharmacotherapy

Review Articles

The crosstalk between insulin resistance and nonalcoholic fatty liver disease/metabolic dysfunction-associated fatty liver disease: a culprit or a consequence?: Dae-Jeong Koo, Won-Young Lee; Cardiovasc Prev Pharmacother. 2022;4(4):132-141. Published online October 20, 2022; DOI: https://doi.org/10.36011/cpp.2022.4.e17

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Nonalcoholic fatty liver disease (NAFLD), which has recently undergone a change in its definition and acronym to “metabolic dysfunction associated fatty liver disease (MAFLD),” is clinically significant as an increasingly prevalent independent risk factor for cardiovascular diseases. Insulin resistance is considered to be a key mechanism in the development and progression of NAFLD/MAFLD, and fatty liver disease itself may exacerbate insulin resistance. In this review, we describe the mechanisms underlying the interaction between insulin resistance and fatty liver, and we summarize the therapeutic attempts based on those mechanisms.

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Insulin Resistance, Non-Alcoholic Fatty Liver Disease and Type 2 Diabetes Mellitus: Clinical and Experimental Perspective
Inha Jung, Dae-Jeong Koo, Won-Young Lee
Diabetes & Metabolism Journal.2024; 48(3): 327. CrossRef

Targets for rescue from fatty acid-induced lipotoxicity in pancreatic beta cells: Seok-Woo Hong, Won-Young Lee; Cardiovasc Prev Pharmacother. 2022;4(2):57-62. Published online April 26, 2022; DOI: https://doi.org/10.36011/cpp.2022.4.e9

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A persistent intake of excess calories increases plasma levels of free fatty acids, particularly the saturated form that has been shown to exert toxic effects on pancreatic beta cells by inducing dysfunction and apoptosis (i.e., lipotoxicity). An insufficient supply of insulin due to beta cell failure is a major factor in the onset and progression of type 2 diabetes; therefore, it is crucial to understand the cellular mechanisms of lipotoxicity to prevent beta cell failure. Many studies on the effects of lipotoxicity have demonstrated the various factors responsible for beta cell impairment, but the mechanisms of dysfunction and apoptosis resulting from lipotoxicity have not been fully described. This review discusses lipotoxicity-induced alterations of cellular mechanisms, and assesses drugs such as incretin mimetics, thiazolidinedione, and clusterin. Understanding the molecular mechanisms of lipotoxicity-induced beta cell failure is useful in guiding the development of new therapeutic targets for diabetes treatment.

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ВПЛИВ ПОЛІВІТАМІННОГО КОМПЛЕКСУ НА СТАН ПІДШЛУНКОВОЇ ЗАЛОЗИ ХОМ’ЯКІВ ЗА УМОВ ЕКСПЕРИМЕНТАЛЬНОГО МЕТАБОЛІЧНОГО СИНДРОМУ
Н. Ю. Духніч, К. О. Калько, О. Я. Міщенко
Medical and Clinical Chemistry.2023; (3): 72. CrossRef

Anti-inflammatory effects of colchicine on coronary artery disease: Hun-Jun Park; Cardiovasc Prev Pharmacother. 2022;4(1):7-12. Published online January 20, 2022; DOI: https://doi.org/10.36011/cpp.2022.4.e5

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Inflammation plays a crucial role in the pathophysiology of coronary artery disease (CAD). Several types of sterile inflammation are mediated through the nucleotide-binding oligomerization domain-like receptor pyrin domain containing 3 (NLRP3) inflammasome. Colchicine has recently been shown to effectively block NLRP3 inflammasome assembly in addition to several other actions on inflammatory cells. Recent evidence also points to favorable effects of colchicine in patients with CAD, including lower levels of inflammatory markers, coronary plaque stabilization, and more favorable cardiac recovery after injury. This review focuses on the role of colchicine in the process of atherosclerosis and discusses its potential as a therapeutic option for the prevention and treatment of CAD.

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The Action of Colchicine in Patients with Metabolic Syndrome and Obesity: Perspectives and Challenges
Fábio Vieira de Bulhões, Gabriele Eliza Assis, Ana Beatriz Cazé, Jackson Pedro Barros-Pereira, Gabriela Garcia de Carvalho Laguna, Alex Cleber Improta-Caria, Roque Aras-Júnior
Metabolites.2024; 14(11): 629. CrossRef

Special Article

Inflammation in Metabolic Diseases and Insulin Resistance: Won-Young Lee; Cardiovasc Prev Pharmacother. 2021;3(2):31-37. Published online April 30, 2021; DOI: https://doi.org/10.36011/cpp.2021.3.e5

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Increased inflammation and insulin resistance are commonly observed in obesity and diabetes. Inflammatory mediators secreted by the adipose tissue contribute to the pathogenesis of diabetes and cardiovascular diseases. Free fatty acids and pro-inflammatory cytokines from adipose tissue inhibit the intracellular insulin signaling pathway, further contributing to the progression of diabetes. Meta-analysis studies show that high sensitivity C-reactive protein can be used as a predictor of future all-cause mortality, including cardiovascular and cancer mortality. In addition to the discovery of novel therapeutic methods targeting inflammatory mediators, basic lifestyle interventions, such as regular exercise, healthy eating, and proper weight control, are absolutely crucial for reducing inflammation and preventing mortality.

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Links between oral microbiome and insulin resistance: Involvement of MAP kinase signaling pathway
Yi-Ru Chang, Wen-Chi Cheng, Ya-Chun Hsiao, Guan-Wei Su, Shan-Jen Lin, Yu-Shan Wei, Hsiu-Chuan Chou, Hsiu-Ping Lin, Guan-Yu Lin, Hong-Lin Chan
Biochimie.2023; 214: 134. CrossRef

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