新生儿姜黄素摄入量对脂质和葡萄糖代谢关键分子标记物的影响

IF 5.3 2区 医学 Q1 PHYSIOLOGY Physiology Pub Date : 2024-05-01 DOI:10.1152/physiol.2024.39.s1.1144
M. Matumba, Emmanuel Mukwevho
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引用次数: 0

摘要

肥胖症的高发病率源于富含果糖的饮食摄入量增加,这对全球儿童的公共健康构成了严重威胁。肥胖与多种代谢紊乱有关,包括胰岛素抵抗和 2 型糖尿病。此外,2 型糖尿病的特点是脂质和葡萄糖代谢受损。本研究调查了新生儿摄入姜黄素对与肝脏脂质代谢有关的关键分子标志物表达的影响[肝激酶 B-1 (LKB-1)、AMP 激活蛋白激酶 (AMPK)、肉碱棕榈酰化酶 (Carnitine palmitoyll)]、肉碱棕榈酰基转移酶-1 (CPT-1) 和乙酰辅酶 A 羧化酶-1 (ACC-1)]和葡萄糖代谢[丝氨酸/苏氨酸蛋白激酶 (AKT-1)、葡萄糖转运体-2 (GLUT-2)、糖原磷酸化酶 (GP) 和磷酸葡萄糖转氨酶 (PGM)]相关的关键分子标记。姜黄素是从姜黄中提取的一种多酚化合物,目前正在对其在各种疾病中的潜在治疗应用进行广泛研究。本研究通过给 Sprague Dawley 大鼠喂食高果糖饮食诱导代谢综合征模型,并以姜黄素作为治疗药物。基因表达通过实时定量 PCR 技术进行评估,蛋白质表达则通过 Western 印迹技术进行分析。研究发现,高果糖饮食会导致肝组织中与脂质代谢相关的基因和蛋白质(如 AMPK、LKB-1、ACC-1 和 CPT-1)上调。姜黄素治疗可逆转这些影响,恢复正常的脂质代谢。此外,高果糖饮食下调了肝脏胰岛素信号转导过程中 AKT-1 的表达,姜黄素则抵消了这一影响。此外,高果糖饮食增加了肝脏葡萄糖的产生,GP和PGM基因和蛋白表达的上调表明了这一点,而姜黄素治疗通过下调GP和PGM的表达抑制了肝脏葡萄糖的产生。这些发现增进了我们对姜黄素分子机制的了解,而我们对这些机制的了解尚不充分。它们进一步证明了姜黄素的积极作用。因此,新生儿早期摄入姜黄素可能是预防高果糖饮食引起的肥胖和相关代谢紊乱(包括胰岛素抵抗和 2 型糖尿病)的一种潜在策略。脂质和葡萄糖代谢。该项目由西北大学资助。本文是在 2024 年美国生理学峰会上发表的摘要全文,仅提供 HTML 格式。本摘要没有附加版本或附加内容。生理学》未参与同行评审过程。
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The Impact of Neonatal Curcumin Intake on Key Molecular Markers in Lipid and Glucose Metabolism
The high prevalence of obesity, resulting from the increased consumption of a fructose-rich diet, poses a serious global threat to children's public health. Obesity is linked to several metabolic disorders, including insulin resistance and type-2 diabetes. Furthermore, type-2 diabetes is characterized by impaired lipid and glucose metabolism. This study investigated the impact of neonatal curcumin intake on the expression of key molecular markers related to liver lipid metabolism [Liver kinase B-1 (LKB-1), AMP-activated protein kinase (AMPK), Carnitine palmitoyltransferase-1 (CPT-1), and Acetyl-coenzyme A carboxylase-1 (ACC-1)] and glucose metabolism [serine/threonine-protein kinase (AKT-1), Glucose transporter-2 (GLUT-2), glycogen phosphorylase (GP), and Phosphoglucomutase (PGM)]. Curcumin, a polyphenolic compound derived from turmeric, is currently under extensive research for its potential therapeutic applications in various diseases. In this study, a metabolic syndrome model was induced in Sprague Dawley rats by feeding them a high fructose diet, with curcumin administered as the treatment. Gene expression was assessed through Real-Time quantitative PCR, and protein expression was analyzed using the western blot technique. The study observed that a high fructose diet led to the upregulation of genes and proteins associated with lipid metabolism, such as AMPK, LKB-1, ACC-1, and CPT-1 in liver tissues. Curcumin treatment reversed these effects, restoring normal lipid metabolism. Additionally, the high fructose diet downregulated the expression of AKT-1 in hepatic insulin signaling, which was counteracted by curcumin. Moreover, the high fructose diet increased hepatic glucose production, as indicated by the upregulation of GP and PGM gene and protein expression, while curcumin treatment suppressed hepatic glucose production by downregulating GP and PGM expression. The findings improve our understanding of curcumin's molecular mechanisms, which are not yet fully understood. They offer further evidence of curcumin's positive effects. Thus, early neonatal consumption of curcumin could be a potential strategy to prevent high fructose diet-induced obesity and related metabolic disorders, including insulin resistance and type-2 diabetes. Lipid and Glucose Metabolism. This project was funded by the North-West University. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
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Physiology
Physiology 医学-生理学
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