Department of Histology and Cytophysiology, Medical University of Białystok, Mickiewicza 2C Street, 15-222, Białystok, Poland.
BMC Gastroenterol. 2022 May 12;22(1):233. doi: 10.1186/s12876-022-02299-6.
Adipokines such as leptin, visfatin and chemerin play a pivotal role not only in the pathogenesis of excessive weight gain but also impact on hepatic metabolism. However, alterations in the production of these peptides in the liver of overweight individuals have not been fully elucidated yet. The aim of the study was to evaluate changes in leptin, visfatin and chemerin biosynthesis in the liver of men with different BMI.
Fourteen adult men without symptoms from the digestive system were recruited. Research material consisted of liver samples. Study participants were divided into two groups: lean (BMI ≤ 25 kg/m) and overweight subjects (BMI > 25 kg/m). Paraffin liver sections were processed by immunohistochemistry for detection of leptin, visfatin and chemerin. Hepatic expression of leptin, visfatin and chemerin genes was determined by qRT-PCR method.
Increased immunoreactivity for leptin and chemerin, and decreased immunoreaction for visfatin were observed in the liver of overweight men in comparison to lean subjects. Overweight subjects with hepatic steatosis displayed increased immunoreactivity for leptin and weaker immunoreaction against visfatin and chemerin in the liver, compared to individuals with normal organ structure. Expression of leptin and chemerin was enhanced in the liver of overweight individuals, with the highest expression observed in subjects with hepatic steatosis. Conversely, expression of visfatin in the male liver was decreased in overweight subjects and those with and liver steatosis.
The present study proves that the expression of leptin, visfatin and chemerin in the male liver is altered in overweight individuals. Our report also indicates the potential importance of these peptides in hepatic steatosis associated with overweight.
脂肪因子，如瘦素、内脂素和趋化素，不仅在体重过度增加的发病机制中起着关键作用，而且还影响肝脏代谢。然而，超重个体肝脏中这些肽的产生变化尚未完全阐明。本研究旨在评估不同 BMI 男性肝脏中瘦素、内脂素和趋化素生物合成的变化。
招募了 14 名无消化系统症状的成年男性。研究材料包括肝组织样本。研究对象分为两组：瘦组（BMI≤25kg/m）和超重组（BMI>25kg/m）。通过免疫组织化学法检测肝组织中瘦素、内脂素和趋化素的表达。采用 qRT-PCR 方法检测肝组织中瘦素、内脂素和趋化素基因的表达。
与瘦组相比，超重组男性肝脏中瘦素和趋化素的免疫反应性增强，而内脂素的免疫反应性减弱。与肝组织结构正常的个体相比，伴有肝脂肪变性的超重组患者肝脏中瘦素的免疫反应性增强，而对内脂素和趋化素的免疫反应性减弱。超重个体的肝组织中瘦素和趋化素的表达增强，其中肝脂肪变性患者的表达最强。相反，超重患者和伴有肝脂肪变性的患者的肝组织中内脂素的表达降低。
本研究证明了男性肝脏中瘦素、内脂素和趋化素的表达在超重个体中发生了改变。我们的报告还表明，这些肽类在与超重相关的肝脂肪变性中具有潜在的重要性。
