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Developmental influences on brown adipose tissue maturation and function

Grant number: 16/22867-4
Support type:Scholarships abroad - Research Internship - Doctorate
Effective date (Start): February 01, 2017
Effective date (End): June 30, 2017
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal researcher:Jose Donato Junior
Grantee:Angela Maria Ramos Lobo
Supervisor abroad: Lori Zeltser
Home Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Research place: Columbia University in the City of New York, United States  
Associated to the scholarship:14/11752-6 - Study of leptin functions during intrauterine and childhood stages in mice, BP.DR


Approximately 17% of U.S. children and adolescents are obese, and are thus at high risk of developing further complications in adulthood. Animal models recapitulate epidemiological observations in humans that rapid early growth rates (1-3 weeks in rodents and 1-2 years of age in children) are associated with later obesity risk, independent of birth weight. Using the mouse model system, the Zeltser lab demonstrated that early-onset adiposity is associated with a structural impairment in the mitochondria of brown adipose tissue (BAT), which reduces basal metabolic rate and further exacerbates obesity. Conversely, they found that reducing body weight gain and adiposity in young mice (<5 weeks of age) improves BAT mitochondrial capacity, and produces long-lasting increases in basal metabolism and reductions in adiposity. The central hypothesis of this project is that rapid early growth suppresses BAT function. BAT is one of the largest consumers of glucose in the body, thus, reducing its activity would allow glucose to be re-directed to energetically-costly processes related to growth. Our objective is to explore how interactions between diet and growth influence BAT development and function, by establishing a detailed timeline for the development of the BAT depot (size, morphology, expression profile and activity) together with physiological endpoints (growth, adiposity, food intake and glucose homeostasis) in C57BL6/J mice from birth to 5 weeks of age. Then we will begin to determine how these are impacted by changes in the postnatal growth trajectory due to maternal high fat diet-feeding by assessing impacts on BAT mitochondrial biogenesis, capacity and activity. Understanding the relationship between BAT activity, growth and adiposity is critical to improve strategies to fight childhood obesity. (AU)

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