FGF21 receptor knock out; its role in lipid metabolism in the liver

Authors' Affiliations

Ummah Salma Nisar, MD, Dept. of Pathology, Quillen College of Medicine, East Tennessee State University, Johnson City, TN George Youngberg, MD, Dept. of Pathology, Quillen College of Medicine, East Tennessee State University, Johnson City, TN

Location

D.P. Culp Center Ballroom

Start Date

4-5-2024 9:00 AM

End Date

4-5-2024 11:30 AM

Poster Number

81

Name of Project's Faculty Sponsor

Allan Forsman

Faculty Sponsor's Department

Health Sciences

Classification of First Author

Undergraduate Student

Competition Type

Competitive

Type

Poster Presentation

Presentation Category

Health

Abstract or Artist's Statement

Fibroblast Growth Factor 21 (FGF21) has been shown to be a key player in the intricate pathway regulating lipid metabolism and lipid reduction in the liver. It is also known to regulate metabolic expenditure and insulin sensitivity. Transgenic fibroblast growth factor receptor knock out (Fgfr1 KO) mice are genetically altered to lack the receptor for FGF21. There have been no studies that have investigated the ramifications of interrupting the FGF21 pathway in the liver. This study analyzed liver tissues from 4 different treatment groups of mice: 1 - transgenic Fgfr1 KO mice fed a very high fat diet (VHFD), 2 - wild type (WT) mice fed a VHFD, 3 - transgenic Fgfr1 KO mice fed a low-fat (LF) diet, and 4 - WT mice fed a LF diet. Mice were approximately 4 weeks old at the onset of the experiment, and were fed their respective diets for 12 weeks. At the end of the feeding period the mice were sacrificed, the tissues harvested, and placed in 10% formalin for overnight fixation. The tissues were then transferred to 70% ETOH until paraffin embedding. Paraffin embedding was carried out using standard embedding techniques. Paraffin embedded tissues were sectioned at 4µm, and mounted on glass microscope slides. Three methods were employed to evaluate the histology/pathology of the liver tissue; 1 – H&E staining, 2 – Masson’s Trichrome staining, and 3 – immunohistochemical staining. We hypothesize that, since FGF21 plays a key role in the metabolism of lipids/lipid deposition in the liver, FgfrR1 KO mice fed a VHFD will have extensive lipid accumulation in their liver. Our observations indicate a gradation of lipid related pathologies across our treatment groups, thus supporting our hypothesis. WT mice fed a VHFD have more lipid related pathologies than WT mice fed a LF diet. Fgfr1 KO mice fed a LF diet have more lipid related pathologies than their WT counterparts. Fgfr1 KO mice fed a VHFD have the greatest amount of lipid related pathologies.

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Apr 5th, 9:00 AM Apr 5th, 11:30 AM

FGF21 receptor knock out; its role in lipid metabolism in the liver

D.P. Culp Center Ballroom

Fibroblast Growth Factor 21 (FGF21) has been shown to be a key player in the intricate pathway regulating lipid metabolism and lipid reduction in the liver. It is also known to regulate metabolic expenditure and insulin sensitivity. Transgenic fibroblast growth factor receptor knock out (Fgfr1 KO) mice are genetically altered to lack the receptor for FGF21. There have been no studies that have investigated the ramifications of interrupting the FGF21 pathway in the liver. This study analyzed liver tissues from 4 different treatment groups of mice: 1 - transgenic Fgfr1 KO mice fed a very high fat diet (VHFD), 2 - wild type (WT) mice fed a VHFD, 3 - transgenic Fgfr1 KO mice fed a low-fat (LF) diet, and 4 - WT mice fed a LF diet. Mice were approximately 4 weeks old at the onset of the experiment, and were fed their respective diets for 12 weeks. At the end of the feeding period the mice were sacrificed, the tissues harvested, and placed in 10% formalin for overnight fixation. The tissues were then transferred to 70% ETOH until paraffin embedding. Paraffin embedding was carried out using standard embedding techniques. Paraffin embedded tissues were sectioned at 4µm, and mounted on glass microscope slides. Three methods were employed to evaluate the histology/pathology of the liver tissue; 1 – H&E staining, 2 – Masson’s Trichrome staining, and 3 – immunohistochemical staining. We hypothesize that, since FGF21 plays a key role in the metabolism of lipids/lipid deposition in the liver, FgfrR1 KO mice fed a VHFD will have extensive lipid accumulation in their liver. Our observations indicate a gradation of lipid related pathologies across our treatment groups, thus supporting our hypothesis. WT mice fed a VHFD have more lipid related pathologies than WT mice fed a LF diet. Fgfr1 KO mice fed a LF diet have more lipid related pathologies than their WT counterparts. Fgfr1 KO mice fed a VHFD have the greatest amount of lipid related pathologies.