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Publication Date

2024-05-13

First Advisor

Sharon Owino

Document Type

Honors Project

Degree Name

Bachelor of Arts

Department

Neuroscience

Keywords

GPR37, glucose metabolism, insulin signaling, heptocytes, liver, brain

Abstract

Diabetes mellitus (DM) represents a global health challenge, affecting approximately 422 million individuals worldwide (Safiri et al., 2022). Type II Diabetes is the most prevalent form; it is characterized by elevated blood glucose levels due to insulin resistance or inadequate insulin production. Under normal physiological conditions, glucose metabolism is a complex series of processes that uses simple sugars, specifically glucose, to produce energy. Glucose metabolism involves intricate pathways regulated by insulin, including glycogenesis, gluconeogenesis, glycolysis, and glycogenolysis. Insulin, a peptide hormone secreted by pancreatic β-cells, plays a central role in facilitating glucose uptake into cells through the activation of glucose transporters, like GLUT4 (Satoh et al., 2014). Insulin resistance, a characterization of T2DM, disrupts normal glucose metabolism, leading to chronically elevated blood glucose levels. The brain and the periphery both require glucose metabolism. G protein-coupled receptors (GPCRs), a diverse family of seven transmembrane proteins, play pivotal roles in cellular signaling cascades. Among them, G protein-coupled receptor 37 (GPR37) is an orphan receptor that is predominantly expressed in the brain, particularly in oligodendrocytes. GPR37 has been shown to be expressed in the liver. To date, nothing is known about GPR37’s role in regulating glucose metabolism, however its expression in the liver may suggest that it modulates metabolic parameters. The goal of this thesis is to characterize the metabolic profile of wild type mice (GPR37+/+), heterozygous mice (GPR37+/-), and knockout mice (GPR37-/-) in young, old, female, and male mice. The present study demonstrates that the loss of GPR37 decreases weights in young (6 month) and old (8-12 month) male mice. The loss of GPR37 induces lower blood glucose levels after 6 hr fast compared to baseline blood glucose levels in female and male mice; this effect is consistent with age. Loss of GPR37 increases insulin sensitivity in young (6 month) male mice.

Rights

©2024 Mariam Ahmed. Access limited to the Smith College community and other researchers while on campus. Smith College community members also may access from off-campus using a Smith College log-in. Other off-campus researchers may request a copy through Interlibrary Loan for personal use.

Language

English

Comments

57 pages; color illustrations. Includes bibliographical references (pages 45-57).

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