Fibrosis Developmental Mechanisms in the Type 2 Diabetic Liver

Undergraduate #48
Discipline: Biological Sciences
Subcategory: Cell and Molecular Biology

Fabiola A. Juárez Jaramillo - California State University Los Angeles
Co-Author(s): Katrina Go Yamazaki, California State University Los Angeles

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Type 2 Diabetes (T2D) hepatic effects are macrovesicular lipid accumulation, inflammation, and injury leading to hepatic fibrosis [2]. Activated hepatic stellate cells (HSC) have been associated with an unbalanced synthesis of fibrillar collagens (I and III) and extracellular matrix (ECM) degradation by matrix metalloproteinase (MMPs) in particular, MMP-2 and MMP-9 [3]. Therefore, inflammatory cytokines identification and MMPs enzymatic activity levels on the onset of T2D-induced rat models is crucial. Thus, two specific aims: 1) to investigate MMP-2 and MMP-9 enzymatic activity levels and 2) to identify TNF-α inflammatory cytokine expression in liver tissue. In vivo Sprague Dawley rat models included controls and T2D-induced by High Energy Diet (HED). Results of western analysis showed no TNF-α expression and analysis of gelatin Zymography MMP-2 and MMP-9 showed no significant difference between control and diabetic liver tissue. Future studies: western analysis optimization, interleukin 1 (IL-1) cytokine analysis to further assess inflammation, liver tissue staining to assess hepatic lipid content, and TGF-β1 pro-fibrogenic cytokine analysis.

Funder Acknowledgement(s): Minority Biomedical Research Support Program-Research Initiative for Scientific Enhancement (MBRS-RISE) part of Minority Opportunities in Research (MORE). Grant Number: GM061331.

Faculty Advisor: Katrina Yamazaki,