chohan, shaila2021-10-132021-10-132019-08https://hdl.handle.net/11299/224885University of Minnesota M.S. thesis. 2019. Major: Nutrition. Advisor: Xiaoli Chen. 1 computer file (PDF); 85 pages.Obesity is a major health issue faced by the present era. According to the CDC, obesity is not just a weight-gain problem; it can have serious deleterious effects on an individual’s physical, metabolic and psychological health. Dysfunctional adipose tissue is the major contributor to obesity and its associated metabolic syndrome. Brown adipose tissue (BAT) is a major thermogenic organ that regulates energy expenditure and is a potential target of drugs for combating obesity and type 2 diabetes. BAT is involved in non-shivering thermogenesis and is a site of glucose uptake and lipid oxidation. The mitochondrion plays a critical role in energy metabolism and it is a dynamic organelle that needs quality control while activated during thermogenesis. Exercise is a useful tool to activate brown adipose tissue. It helps stimulate the sympathetic nervous system to activate the mitochondrial oxidation of brown adipose tissue. When exercise activates adipose tissue, mitochondrial turnover is increased in BAT but decreased in beige adipose tissue. Lipocalin-2 is an adipokine that has a role in energy metabolism via activating BAT and white adipose tissue beiging. Our previous studies have demonstrated that Lcn-2 plays a key role in cold-induced thermogenesis. Herein, we sought to discover if Lcn-2 plays a role in exercise-induced thermogenesis and mitochondrial metabolism. We used a Lcn-2 KO mouse model to investigate the expression of thermogenic and mitochondrial genes. We showed that the expression levels of Ucp-1 were not significantly changed in BAT of Lcn-2 KO mice, i.e. Ucp-1 expression can be induced by exercise when Lcn-2 is not present. We also determined if Lcn-2 had any effects on mitophagy involving PINK-1/Parkin/P-62 system in BAT and iWAT in response to exercise. Interestingly, we found that Lcn-2 deficiency does seem to affect mitochondrial quality control as Lcn-2 KO does not show exercise-induced mitochondrial biogenesis but shows increased mitophagy in white adipose tissue, indicating that the beiging process is defective. We conclude that Lcn2 plays an important role in exercise-induced mitochondrial turnover and metabolism in brown and beige adipose tissue.enBrown Adipose TissueLipocalin-2MitochondriaMitophagyPINK-1/Parkinp-62Uncoupling Protein 1Thesis or Dissertation