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- W638945176 abstract "Author(s): Falkenhagen, Katherine M. | Abstract: Members of the corticotropin-releasing factor (CRF) family of peptides are powerful modulators of numerous metabolic pathways including mechanisms of insulin secretion and glucose homeostasis. Drugs targeted to modulate the CRF system may be relevant treatments for human metabolic disorders. However, a more integrated understanding of the CRF system is needed before such drugs can be developed. The general aims of this dissertation were to investigate the influence of the CRF family of peptides on energy metabolism with a focus on the most newly discovered members of this family, Urocortin 2 (Ucn 2) and Urocortin 3 (Ucn 3). Ucn 2 inhibits insulin signaling in skeletal muscle and Ucn 3 enhances glucose-induced insulin secretion from the pancreas. We generated a mouse deficient in both peptides to investigate how these urocortins physiologically contribute to energy homeostasis parameters such as body weight and glucose homeostasis. Additionally, we further characterized the role of endogenous Ucn 2 in skeletal muscle by analyzing metabolic properties, such as fiber type composition, mitochondrial density and fatigue of skeletal muscle from Ucn 2 KO mice. Lastly, we sought to determine if Ucn 2 is regulated in skeletal muscle by metabolic status. Our three main findings were that (1) the loss of both Ucn 2 and Ucn 3 in the dKO mouse model contributes abnormal metabolic phenotypes such as increased body weight and higher concentrations of blood lipids, (2) endogenous Ucn 2 is not involved in mitochondrial pathways, but may be involved in muscle fatigue, and (3) Ucn 2 mRNA expression levels in skeletal muscle may be influenced by energy availability status with overnight fasting decreasing Ucn 2 mRNA expression and high fat feeding trending towards an increase of Ucn 2 mRNA expression. Overall, our studies suggest a complex role of Ucn 2 and Ucn 3 in energy metabolism and specifically show that endogenous Ucn 2 may contribute to muscle fatigue with mechanisms that do not involve mitochondrial density or activity. These findings support the continued investigation of CRF system as potential targets for the treatment of metabolic disorders" @default.
- W638945176 created "2016-06-24" @default.
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- W638945176 date "2012-01-01" @default.
- W638945176 modified "2023-09-27" @default.
- W638945176 title "Exploring the role of Urocortin 2 and Urocortin 3 in energy metabolism" @default.
- W638945176 hasPublicationYear "2012" @default.
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