Victoria Vieira-Potter

Victoria Vieira-Potter


Associate Professor of Nutrition & Exercise Physiology

Division of Food, Nutrition & Exercise Sciences (FNES)

Research at a glance

Area(s) of Expertise

Research Summary

The PhIT FAT laboratory, led by Dr. Vieira-Potter, studies how age-related shifts in sex hormones (e.g., menopause in women) cause weight gain and increase metabolic disease risk by directly and indirectly affecting fat cells. They study how estrogen and exercise positively affect fat cells so that these mechanisms can be targeted therapeutically to reduce obesity and its associated diseases, such as type 2 diabetes.

The Vieira-Potter laboratory studies sex differences in adipose tissue metabolism, and how sex hormones (namely, estrogen) and exercise affect fat cell metabolism. This is done via use of a variety of animal models and state-of-the-art molecular tools. Our goal is to determine adipose (i.e., fat) tissue-specific mechanisms by which hormone shifts and obesity affect cardiometabolic disease risk, and to discover novel interventions to mitigate this risk by specifically targeting adipose tissue. Our work has demonstrated that female hormone loss adversely affects adipose tissue both directly, via loss of the protective effects of estrogen receptor signaling, and indirectly, via brain-specific mechanisms that result in sedentary behavior. Our work has shown that exercise is an effective approach to improve adipose tissue metabolism in states of hormone loss, and that the mechanism may involve exercise-mediated improvements in adipocyte mitochondrial activity. Mechanistically, an overarching hypothesis is that the estrogen receptor critically regulates the mitochondrial protein, uncoupling protein (UCP1), which is also induced with exercise training. Estrogen’s role in UCP1 regulation may help explain the now well-established age-dependent sex difference, where females are protected against metabolic diseases compared to age-matched males, until they reach menopause (i.e., the natural state of estrogen depletion which associates with an abrupt increase in metabolic disease risk). Exercise, via its stimulation of catecholamines, activates beta 3 adrenergic receptors on adipocytes, which induces UCP1. A recent finding from our laboratory indicates that estrogen receptor is necessary for exercise-mediated UCP1 responses in adipose tissue, yet the alpha (i.e., feminizing and cancer-promoting) sub-type is dispensable. A striking discovery has been the consistent/statistically significant, strong, species-independent, and sex-independent relationship between estrogen receptor subtype beta (ERb) and UCP1 in adipose tissue. Current studies are investigating the synergistic potential of novel ERb ligands and beta 3 adrenergic receptor agonists (i.e., adipocyte specific exercise mimetics) to mitigate obesity and improve systemic metabolism.
In addition to directly affecting adipose tissue metabolism, our group has also shown that estrogen deprivation may suppress voluntary physical activity via modulation of dopamine signaling in the reward region of the brain, the nucleus accumbens. Our published data suggest that estrogen positively affects dopamine production in this brain region, potentially explaining estrogen’s positive effect on motivated behaviors such as wheel running in rodents. This discovery led to a current NIH/NIDA-funded project investigating the role of estrogen signaling in the nucleus accumbens on motivation both for wheel running and drug seeking in rats. Our newest preliminary findings suggest that ERb-mediated actions in the nucleus accumbens, in addition to potentially affecting motivated running behavior, may directly affect fat cell metabolism by stimulating adipocyte mitochondrial activity and UCP1.
Our lab is also interested in nutritional approaches to improving adipose tissue metabolism. Prior work has shown that a soy phytoestrogen-rich diet improves adipose tissue and systemic metabolism, and reduces obesity in both rats and mice via a mechanism that appears to involve phytoestrogen activation of estrogen receptors. Additional mechanistic and translation studies in humans are in the planning stages. In collaboration with Dr. Jaapna Dhillon, we are conducting studies funded by the California Almond Board to determine if almond consumption improves adipose tissue metabolism and immune health among obese adults. Finally, in collaboration with Dr. Jill Kanaley, we are conducting human studies to determine how sleep restriction adversely affects adipose tissue metabolism to test the hypothesis that this may explain how chronic sleep deprivation leads to obesity and increases cardiometabolic disease risk.

Educational background

  • Ph.D., University of Illinois, 2009
  • M.S., University of New Hampshire, 2004
  • B.A., Wheaton College (Norton, MA), 2001

Courses taught

  • Human Nutrition II (4340/7340)
  • Nutrition in Human Health (8340)
  • Sports Nutrition (4970/7970)
  • Nutrition Science Communication (WI) (4951)
  • Etiology of Obesity (8030)