Author

Yue Zheng

Date of Award

8-2009

Level of Access

Campus-Only Thesis

Degree Name

Master of Science (MS)

Department

Biochemistry

Advisor

Juergen Naggert

Second Committee Member

Mary Ann Handel

Third Committee Member

Sharon L. Ashworth

Abstract

Body weight is maintained through regulating food intake and energy expenditure by the brain. Defects in the neuronal control circuits in the presence of over-nutrition can lead to increased energy storage as fat in adipose tissue and development of obesity. Adipose tissue secretes the hormone leptin to signal fat storage reserves in the body to the central control circuits to mediate long-term appetitive controls and energy expenditure. We identified a new mouse model, Nmfl5, with primary leptin resistance and obesity. In chapter 1, a series of experiments demonstrated that the Nmfl5 mouse model can provide new insights into obesity and associated cardiomyopathy. When leptin binds to the leptin receptor, it eventually reduces appetite through a cascade signaling pathway. It has been suggested that the leptin receptor may be localized on the primary cilium. In chapter 2, using the Alms mouse, a model with cilia dysfunction and early onset obesity, we tested whether adipocytes receive signals through the primary cilium to develop into an effective storage tissue.

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