Acyl ghrelin, desacyl ghrelin and their ratio affect hepatic steatosis via PPARγ signaling pathway.

Background and Study Aims: Ghrelin is an appetite hormone-containing 28-amino acid and has 4 different forms in the body. Ghrelin forms have different physiological functions in the body. This study aims to analyze the effect of acyl and desacyl ghrelin hormone on hepatic steatosis and biochemical findings in 36 male Wistar rats.
Materials and Methods: Rats were split into 6 equal groups, consisting of control, acyl ghrelin, desacyl ghrelin, acyl/desacyl 3:1, acyl/desacyl 1:1, and acyl/desacyl 1:3 groups, and administered placebo or 200 ng/kg hormone subcutaneous twice a day for 14 days. Oral Glucose Tolerance Test (OGTT) was performed on Day 15, Insulin Tolerance Test (ITT) on Day 16, and scarification procedure on Day 17. Certain biochemical data and liver diacylglycerol (DAG), glycogen, protein kinase C and PPAR-γ levels were detected in the blood. Histological analyses were also conducted on the liver tissues.
Results: The highest plasma total cholesterol and VLDL-K levels were found in the acyl/desacyl 1:3 group, and lower insulin, and HOMA-IR levels were found in groups where acyl and desacyl were administered together (p < 0.05). PPAR-γ gene expression level increased in acyl ghrelin and acyl/desacyl 1:3 groups compared to the control group. Protein kinase C gene expression was highest in the acyl/desacyl 1:3 group. The most severe degenerative findings compliant with steatosis in the liver were observed in the acyl ghrelin group (p < 0.05).
Conclusion: It was determined that administering rats acyl alone and acyl/desacyl by 1:3 caused the highest PPAR-γ gene expression, serum total cholesterol, HDL-K, and VLDL-K levels in the body. Besides, it is shown that desacyl ghrelin effectively regulates the blood glucose level when administered alone.
Competing Interests: Declaration of competing interests Authors state no conflict of interest.
(Copyright © 2023 Pan-Arab Association of Gastroenterology. Published by Elsevier B.V. All rights reserved.)