A recent study led by Maria Paula Macedo and Carlos Penha-Gonçalves of the Havana College of Medicine and the Gulben Kean Institute of Science found that the molecule CD26/DPP-4 is involved in the repair of acute liver injury and is a potential biomarker for liver disease. Related research was recently published in Hepatology Communications.
It was previously known that DPP-4 is responsible for regulating insulin secretion after eating. The method of regulating the sugar content in the blood of patients with type 2 diabetes is to inhibit the enzyme activity of CD26/DPP-4 by drugs. This method is closely related to the clinical. In addition, in addition to controlling blood sugar, DPP-4 is also associated with inflammatory responses in different situations.
In this study, the researchers explored the role of CD26/DPP-4 in liver tissue damage, which resulted in a significant reduction in the number of major liver immune cell populations (Kupffer cells). The results of the study showed that the level of CD26/DPP-4 increased when the number of hepatic immune cells decreased in a mouse model of acute or chronic liver injury. Conversely, during the recovery of these cells, the level of enzyme activity in the blood is reduced.
The authors also observed that specific clearance of Kupffer cells in the absence of liver damage also resulted in a significant increase in the enzymatic activity of CD26/DPP-4 in the blood. Therefore, these results indicate that Kupffer cell function changes are closely related to liver disease and CD26/DPP-4 molecules.
The relationship between hepatic immune cells and the enzymatic activity of CD26/DPP-4 in blood suggests that the level of enzymatic activity of CD26/DPP-4 in the blood may serve as a biomarker. In addition, it may be a non-invasive biochemical indicator for assessing liver damage, which has so far been done based on invasive means.
References: Nádia Duarte et al, Dipeptidyl Peptidase-4 Is a Pro-Recovery Mediator During Acute Hepatotoxic Damage and Mirrors Severe Shifts in Kupffer Cells, Hepatology Communications (2018). DOI: 10.1002/hep4.1225
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