Background: Insulin resistance is common in polycystic ovary syndrome (PCOS), especially in obese patients. Hepassocin is a peptid marker which increases in obesity and insulin resistance.
Objective: We aimed to investigate hepassocin levels in patients with PCOS in this study.
Methods: This prospective case-control study was conducted with a total of 60 patients with PCOS and age-matched 30 healthy women with body mass index < 30. Patients with PCOS were classified as obese PCOS and non-obese PCOS according to their BMI. Hepassocin levels were measured by using a commercially available enzyme-linked immunosorbent assay (ELISA) kit. A multivariate linear regression analysis was used to determine independent factors related to hepassocin levels.
Results: Hepassocin levels of the obese-PCOS group were found significantly higher than non-obese PCOS and control group (6.95 ± 3.59, 2.69 ± 2.51, 2.66 ± 2.22, respectively, p < 0.001). There was no significant difference in hepassocin levels between control and non-obese PCOS group (p = 0.99). Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) was independently associated with hepassocin concentrations after adjusting for age, low density lipoprotein C (LDL-C), high density lipoprotein C (HDL-C), triglyceride (TG), total testosterone, dehydroepiandrosterone sulfate (DHEA-S), and C reactive protein (CRP).
Conclusion: Obese patients with PCOS exhibited high serum levels of hepassocin. HOMA-IR index was found as the independent variable associated with high levels of hepassocin. Hepassocin can be used as a simple and easy way of detecting insulin resistance in obese patients with PCOS.
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http://dx.doi.org/10.1016/j.ejogrb.2021.10.034 | DOI Listing |
Naunyn Schmiedebergs Arch Pharmacol
October 2024
Biochemistry Department, Faculty of Pharmacy, Mansoura University, Mansoura, 35516, Egypt.
Hypoxia and tumor cell immunological escape greatly hinder the hepatocellular carcinoma (HCC) treatment efficiency. This study is designed to investigate the capability of carvacrol (CVR) to enhance sorafenib (SOR) anti-cancer efficacy and modulate anti-HCC immunity. CVR target and biological activities were predicted using Swiss Target Prediction website and PASS web server.
View Article and Find Full Text PDFEur Rev Med Pharmacol Sci
August 2023
Department of Pharmacy Practice, College of Pharmacy, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia.
Objective: Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver metabolic disease affecting millions globally. This study aimed to assess the safety and efficacy of a high oral loading dose of cholecalciferol supplement on NAFLD patients and to investigate its potential role on serum inflammatory biomarkers.
Patients And Methods: One hundred patients with NAFLD and type 2 diabetes mellitus were involved in the study.
Biomedicines
July 2023
Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan.
Hepatic dysfunction is commonly observed in subjects with hyperthyroidism. Hepassocin is a hepatokine playing an important role in metabolic diseases and exhibiting a hepatic protective effect. Nevertheless, the relationship between hepassocin and hyperthyroidism was still unknown.
View Article and Find Full Text PDFTransl Res
October 2023
Biochemistry department, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt. Electronic address:
In hepatocellular carcinoma (HCC), sorafenib (Sora) efficacy is limited by primary and/or acquired resistance. Emerging evidence shows that the inflammatory factor interleukin 6 (IL-6) plays a role in Sora resistance. Norcantharidin (NCTD), a derivative of cantharidine, was identified as a potent IL-6 inhibitor.
View Article and Find Full Text PDFFEBS J
September 2022
State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Institute of Lifeomics, Beijing, China.
Hepassocin (HPS) is a hepatokine associated with metabolic regulation and development of non-alcoholic steatohepatitis (NASH). However, previous reports on HPS are controversial and its true function is not yet understood. Here, we demonstrated that hepatic HPS expression levels were upregulated in short-term feeding and downregulated in long-term feeding in high-fat diet (HFD)- and methionine- and choline-deficient (MCD) diet-fed mice, as well as in genetically obese (ob/ob) mice.
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