Neuroendocrine Regulation of Energy Metabolism by Brain- Derived Neurotrophic Factor
Qi Zhu 1, Xian Liu 2, Haifei Shi *1
1. Department of Biology, Miami University, Oxford, Ohio, USA.
2. Department of Bioengineering, Miami University, Oxford, Ohio, USA.
Millions of people suffer from obesity and related metabolic disorders. A key cause of obesity is increased food intake and decreased energy expenditure. The CNS receives information from the periphery relevant to an individual’s energy balance through metabolic, neural, and endocrine signals. Dysfunction of the sympathetic nervous system (SNS) is associated with a relatively high risk for development of obesity and metabolic diseases. Understanding how SNS regulates energy metabolism is crucial to developing better therapeutics for treatment and prevention of obesity. Brain-derived neurotrophic factor (BDNF) is a neurotrophin that plays essential roles in the regulation of energy balance by promoting decreased food intake and increased energy expenditure. There is increasing evidence that regulation of energy balance and body weight is not the same for both sexes. We reported sex differences in central Bdnf expression and the anorectic effects of BDNF, which were modulated by circulating levels of estradiol. Our recent data suggest that BDNF activates SNS, but the underlying neural mechanism for sex differences in energy metabolism regulated by BDNF is unclear. We are currently investigating neural mechanism of BDNF in regulating energy metabolism in male and female rats. Specifically, we examine if BDNF regulates energy metabolism by activating sympathetic outflow from the CNS to metabolic tissues, and if BDNF-induced SNS activation is tissue-specific and sex-different. Findings from our studies will elucidate and identify sex differences in the regulation of the BDNF signaling system with the long-term goal to generate data that will be useful in developing sex-specific therapeutics to treat or prevent obesity.
Acknowledgements: Supported by: Sigma Xi grant G2017031588446675 to QZ; Sigma Xi grant G20141015729643 to XL; NIH grant DK090823 to HS.
Key Words: central nervous system, sex difference, energy intake, energy expenditure, sympathetic activity, estrogen
Qi Zhu 1, Xian Liu 2, Haifei Shi *1
1. Department of Biology, Miami University, Oxford, Ohio, USA.
2. Department of Bioengineering, Miami University, Oxford, Ohio, USA.
Millions of people suffer from obesity and related metabolic disorders. A key cause of obesity is increased food intake and decreased energy expenditure. The CNS receives information from the periphery relevant to an individual’s energy balance through metabolic, neural, and endocrine signals. Dysfunction of the sympathetic nervous system (SNS) is associated with a relatively high risk for development of obesity and metabolic diseases. Understanding how SNS regulates energy metabolism is crucial to developing better therapeutics for treatment and prevention of obesity. Brain-derived neurotrophic factor (BDNF) is a neurotrophin that plays essential roles in the regulation of energy balance by promoting decreased food intake and increased energy expenditure. There is increasing evidence that regulation of energy balance and body weight is not the same for both sexes. We reported sex differences in central Bdnf expression and the anorectic effects of BDNF, which were modulated by circulating levels of estradiol. Our recent data suggest that BDNF activates SNS, but the underlying neural mechanism for sex differences in energy metabolism regulated by BDNF is unclear. We are currently investigating neural mechanism of BDNF in regulating energy metabolism in male and female rats. Specifically, we examine if BDNF regulates energy metabolism by activating sympathetic outflow from the CNS to metabolic tissues, and if BDNF-induced SNS activation is tissue-specific and sex-different. Findings from our studies will elucidate and identify sex differences in the regulation of the BDNF signaling system with the long-term goal to generate data that will be useful in developing sex-specific therapeutics to treat or prevent obesity.
Acknowledgements: Supported by: Sigma Xi grant G2017031588446675 to QZ; Sigma Xi grant G20141015729643 to XL; NIH grant DK090823 to HS.
Key Words: central nervous system, sex difference, energy intake, energy expenditure, sympathetic activity, estrogen