José Antonio Palma-Jacinto, Edgar López-López, José Luis Medina-Franco, Oreth Montero-Ruíz, Isela Santiago-Roque
{"title":"Putative mechanism of a multivitamin treatment against insulin resistance.","authors":"José Antonio Palma-Jacinto, Edgar López-López, José Luis Medina-Franco, Oreth Montero-Ruíz, Isela Santiago-Roque","doi":"10.1080/21623945.2024.2369777","DOIUrl":null,"url":null,"abstract":"<p><p>Insulin resistance is caused by the abnormal secretion of proinflammatory cytokines in adipose tissue, which is induced by an increase in lipid accumulation in adipocytes, hepatocytes, and myocytes. The inflammatory pathway involves multiple targets such as nuclear factor kappa B, inhibitor of nuclear factor κ-B kinase, and mitogen-activated protein kinase. Vitamins are micronutrients with anti-inflammatory activities that have unclear mechanisms. The present study aimed to describe the putative mechanisms of vitamins involved in the inflammatory pathway of insulin resistance. The strategy to achieve this goal was to integrate data mining and analysis, target prediction, and molecular docking simulation calculations to support our hypotheses. Our results suggest that the multitarget activity of vitamins A, B1, B2, B3, B5, B6, B7, B12, C, D3, and E inhibits nuclear factor kappa B and mitogen-activated protein kinase, in addition to vitamins A and B12 against inhibitor of nuclear factor κ-B kinase. The findings of this study highlight the pharmacological potential of using an anti-inflammatory and multitarget treatment based on vitamins and open new perspectives to evaluate the inhibitory activity of vitamins against nuclear factor kappa B, mitogen-activated protein kinase, and inhibitor of nuclear factor κ-B kinase in an insulin-resistant context.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":null,"pages":null},"PeriodicalIF":3.5000,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11216102/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Adipocyte","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1080/21623945.2024.2369777","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/6/27 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
引用次数: 0
Abstract
Insulin resistance is caused by the abnormal secretion of proinflammatory cytokines in adipose tissue, which is induced by an increase in lipid accumulation in adipocytes, hepatocytes, and myocytes. The inflammatory pathway involves multiple targets such as nuclear factor kappa B, inhibitor of nuclear factor κ-B kinase, and mitogen-activated protein kinase. Vitamins are micronutrients with anti-inflammatory activities that have unclear mechanisms. The present study aimed to describe the putative mechanisms of vitamins involved in the inflammatory pathway of insulin resistance. The strategy to achieve this goal was to integrate data mining and analysis, target prediction, and molecular docking simulation calculations to support our hypotheses. Our results suggest that the multitarget activity of vitamins A, B1, B2, B3, B5, B6, B7, B12, C, D3, and E inhibits nuclear factor kappa B and mitogen-activated protein kinase, in addition to vitamins A and B12 against inhibitor of nuclear factor κ-B kinase. The findings of this study highlight the pharmacological potential of using an anti-inflammatory and multitarget treatment based on vitamins and open new perspectives to evaluate the inhibitory activity of vitamins against nuclear factor kappa B, mitogen-activated protein kinase, and inhibitor of nuclear factor κ-B kinase in an insulin-resistant context.
胰岛素抵抗是由脂肪组织中促炎细胞因子的异常分泌引起的,而脂肪组织中促炎细胞因子的异常分泌是由脂肪细胞、肝细胞和肌细胞中脂质积累的增加诱发的。炎症途径涉及多个靶点,如核因子卡巴 B、核因子κ-B 激酶抑制剂和丝裂原活化蛋白激酶。维生素是具有抗炎活性的微量营养素,但其机制尚不清楚。本研究旨在描述维生素参与胰岛素抵抗炎症途径的假定机制。实现这一目标的策略是整合数据挖掘和分析、靶点预测和分子对接模拟计算,以支持我们的假设。我们的结果表明,维生素 A、B1、B2、B3、B5、B6、B7、B12、C、D3 和 E 的多靶点活性可抑制核因子卡巴 B 和丝裂原活化蛋白激酶,此外,维生素 A 和 B12 还可抑制核因子κ-B 激酶抑制因子。这项研究的结果凸显了利用维生素进行抗炎和多靶点治疗的药理潜力,并为评估维生素在胰岛素抵抗情况下对核因子卡巴B、丝裂原活化蛋白激酶和核因子κ-B激酶抑制剂的抑制活性开辟了新的前景。
期刊介绍:
Adipocyte recognizes that the adipose tissue is the largest endocrine organ in the body, and explores the link between dysfunctional adipose tissue and the growing number of chronic diseases including diabetes, hypertension, cardiovascular disease and cancer. Historically, the primary function of the adipose tissue was limited to energy storage and thermoregulation. However, a plethora of research over the past 3 decades has recognized the dynamic role of the adipose tissue and its contribution to a variety of physiological processes including reproduction, angiogenesis, apoptosis, inflammation, blood pressure, coagulation, fibrinolysis, immunity and general metabolic homeostasis. The field of Adipose Tissue research has grown tremendously, and Adipocyte is the first international peer-reviewed journal of its kind providing a multi-disciplinary forum for research focusing exclusively on all aspects of adipose tissue physiology and pathophysiology. Adipocyte accepts high-profile submissions in basic, translational and clinical research.