April Binder (Biological Sciences)
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. The metabolic rates of the mice were measured before and after cold exposure using respirometry. Quantitative real-time PCR has also been done to measure expression of genes associated with thermogenesis in adipose tissue. Changes in expression levels can indicate the upregulation or downregulation of thermogenesis. The data from these analyses will help to inform whether NAG-1 acts synergistically with the B3-adrenergic stimulated response or not. Further downstream targets of NAG-1 in conjunction with cold exposure can be identified for possible therapeutics to treat obesity.
Keywords: METABOLISM, OBESITY, COLD EXPOSURE