Document Type

Thesis

Date of Degree Completion

Spring 2021

Degree Name

Master of Science (MS)

Department

Biology

Committee Chair

April Binder

Second Committee Member

David Darda

Third Committee Member

Jason Irwin

Abstract

Obesity is a multifaceted metabolic disorder with severe worldwide public health consequences. While obesity can often be treated using diet and exercise, there are complex genetic interactions driving obesity that don’t always respond to such changes. One important research focus for addressing genetic factors is activating brown adipose tissue which increases thermogenesis, the process of burning stored fats to generate heat. Cold exposure is a known way to activate brown adipose tissue through b3-adrenergic signaling. This signaling pathway causes an upregulation of thermogenesis in brown adipocytes and beige adipocytes, which is white adipose tissue that “browns” and becomes metabolically active. In this study, transgenic mice that constitutively express the human non-steroidal anti-inflammatory gene 1 (NAG-1) were used as a model to further understand the mechanisms of increasing metabolism. At room temperature, NAG-1 mice have less adipose tissue, higher metabolic rates, and longer lifespans than their wildtype littermates. Wildtype and NAG-1 mice were subjected to a prolonged cold exposure at 10ºC for seven days. NAG-1 mice had lower body weights throughout the study compared to wildtype mice. NAG-1 mice had higher metabolic rates before and after cold exposure. Adipocyte size analysis indicated adult wildtype male mice have significantly larger white adipocytes after cold exposure than NAG-1 males. Quantitative real-time PCR indicated higher expression of Glut4 and Atgl in wildtype mice, indicating that NAG-1 does not upregulate expression of thermogenic genes in response to cold exposure. The data from these analyses suggest that NAG-1 does not act synergistically with the b-3 adrenergic stimulated pathway in cold response.

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