Hepatokines and Adipokines in Metabolic Syndrome

Alpana Mukhuty, S. Mondal, S. Mukhopadhyay
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Abstract

Abstract Hepatokines and adipokines are secretory proteins derived from hepatocytes and adipocytes, respectively. These proteins play a main role in the pathogenesis of metabolic syndrome (MetS), characterized by obesity, dysglycemia, insulin resistance, dyslipidemia, and hypertension. Adipose tissue and liver are important endocrine organs because they regulate metabolic homeostasis as well as inflammation because they secrete adipokines and hepatokines, respectively. These adipokines and hepatokines communicate their action through different autocrine, paracrine and endocrine pathways. Liver regulates systemic homeostasis and also glucose and lipid metabolism through hepatokines. Dysregulation of hepatokines can lead to progression toward MetS, type 2 diabetes (T2D), inflammation, hypertension, and other diseases. Obesity is now a worldwide epidemic. Increasing cases of obesity and obesity-associated metabolic syndrome has brought the focus on understanding the biology of adipocytes and the mechanisms occurring in adipose tissue of obese individuals. A lot of facts are now available on adipose tissue as well. Adipose tissue is now given the status of an endocrine organ. Recent evidence indicates that obesity contributes to systemic metabolic dysfunction. Adipose tissue plays a significant role in systemic metabolism by communicating with other central and peripheral organs via the production and secretion of a group of proteins known as adipokines. Adipokine levels regulate metabolic state of our body and are potent enough to have a direct impact upon energy homeostasis and systemic metabolism. Dysregulation of adipokines contribute to obesity, T2D, hypertension and several other pathological changes in various organs. This makes characterization of hepatokines and adipokines extremely important to understand the pathogenesis of MetS. Hepatokines such as fetuin-A and leukocyte cell-derived chemotaxin 2, and adipokines such as resistin, leptin, TNF-α, and adiponectin are some of the most studied proteins and they can modulate the manifestations of MetS. Detailed insight into the function and mechanism of these adipokines and hepatokines in the pathogenesis of MetS can show the path for devising better preventative and therapeutic strategies against this present-day pandemic.
代谢综合征中的肝因子和脂肪因子
摘要肝细胞因子和脂肪细胞因子分别是来源于肝细胞和脂肪细胞的分泌蛋白。这些蛋白质在代谢综合征(MetS)的发病机制中起主要作用,代谢综合征以肥胖、血糖异常、胰岛素抵抗、血脂异常和高血压为特征。脂肪组织和肝脏是重要的内分泌器官,因为它们分别调节代谢稳态和炎症,因为它们分泌脂肪因子和肝因子。这些脂肪细胞因子和肝细胞因子通过不同的自分泌、旁分泌和内分泌途径交流它们的作用。肝脏通过肝细胞因子调节系统稳态以及葡萄糖和脂质代谢。肝细胞因子的失调可导致MetS、2型糖尿病(T2D)、炎症、高血压和其他疾病的进展。肥胖现在是一种全球性的流行病。肥胖和肥胖相关代谢综合征病例的增加使人们关注脂肪细胞的生物学以及肥胖个体脂肪组织中发生的机制。关于脂肪组织,现在也有很多事实。脂肪组织现在被赋予内分泌器官的地位。最近的证据表明,肥胖会导致全身代谢功能障碍。脂肪组织通过产生和分泌一组被称为脂肪因子的蛋白质,与其他中枢和外周器官交流,在系统代谢中发挥着重要作用。脂肪因子水平调节我们身体的代谢状态,并足以对能量稳态和系统代谢产生直接影响。脂肪因子的失调会导致肥胖、T2D、高血压和其他各种器官的病理变化。这使得肝细胞因子和脂肪细胞因子的表征对于理解代谢综合征的发病机制极其重要。肝因子如胎球蛋白-A和白细胞衍生的趋化因子2,以及脂肪因子如抵抗素、瘦素、TNF-α和脂联素是研究最多的蛋白质,它们可以调节MetS的表现。深入了解这些脂肪因子和肝因子在代谢综合征发病机制中的作用和机制,可以为制定更好的预防和治疗策略提供途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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