The Role of Leptin in Modulating Alcohol-Associated Hepatic fibrosis: An in vitro study
This project will assess whether the hormone leptin, either directly and/or indirectly potentiates alcohol-induced liver injury and fibrosis.
The studies outlined we anticipate will elucidate the mechanisms whereby overweight and obesity makes the liver more susceptible to alcohol-associated liver disease. We will employ hepatic stellate cells (HSCs), Kupffer cells (KCs) and sinusoidal endothelial cells (SECs) isolated from both normal and Zucker rats (leptin receptor deficient) to determine whether combined treatment with leptin and alcohol (or acetaldehyde) directly and/or indirectly promotes alcohol-induced expression by HSCs of scar tissue components (Collagen I), or of mediators that are well known to drive the production of scar tissue. The relevant intracellular pathways involved in mediating these effects will be analyzed. Zucker rats will be used to clarify whether any observed effects are mediated by the leptin receptor.
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The opportunity ID for this research opportunity is: 202
Other opportunities with Professor Jacob George
- Identification and characterization of liver cancer stem cells from chemically induced liver cancer
- Characterization of ARL6IP5, PTPLB, and NIN in liver cancer
- Regulatory role of Notch signalling on hepatic stellate cells in the development of NASH and liver fibrosis
- Regulatory role of interleukin 6 (IL-6) on Notch signalling and impact on liver cancer