Research Staff
Candace A. Gename Junior Scientist   I was born and raised in Racine, Wisconsin (home to the Racine Belles and Danish Kringle).  I received my B.S. in Biology at the University of Minnesota-Twin Cities in 2008. In addition to science and research, I enjoy spending time with family and friends, swimming, shopping, learning how to golf, living in big cities/visiting small ones, and plotting future travels.
I am a Junior Scientist within the Obesity and Energy Metabolism Core of the Minnesota Obesity Center (MNOC). The MNOC is established to foster obesity center research and education while providing its members with a cost-effective option for access to core facilities and services used in obesity research. These facilities and services include: viral production, microarray analysis, real-time PCR, and small animal indirect calorimetry.
Jessica M. Curtis, B.A. PhD Candidate Research Assistant
I am originally from Lake Jackson, Texas, but moved here with my family in 2000. In 2006, I obtained my bachelors degree from the College of St. Catherine in St. Paul, MN with a major in Biology and a minor in Chemistry. I was also a member of the St. Kate's swim team. In my free time I enjoy live music, gardening, traveling, and playing with my dogs.  My research project focuses on the role adipocyte mitochondrial dysfunction in the pathogenesis of insulin resistance and Type II Diabetes. The antioxidant enzyme Glutathione S-Transferase A4, or GSTA4, is critical for the removal of 4-HNE, a small aldehyde generated from lipid peroxidation under conditions of elevated oxidative stress. 4-HNE can covalently modify proteins, in a reaction termed protein carbonylation, leading to protein degradation and altered protein function. The incidence of such modifications in adipose tissue are significantly elevated with obesity, most likely due to the selective down regulation of GSTA4. My current aim is to identify carbonylated residues of ATP Synthase with mass spectrometry in adipocyte mitochondria from GSTA4 null mice and cell culture models. Carbonylation of ATP Synthase may cause the diminished activity I observe in GSTA4 silenced adipocytes.
Ann V. Hertzel, PhD Research Assistant Professor I am a native Minnesotan and attended Mankato State University (Mankato, MN), receiving a B.S. degree in Biochemistry in 1987. After working a year as a technician, I entered the Biochemistry graduate program at the University of Minnesota and obtained a Ph.D in 1994. I have two children, ages 3 and 1. I enjoy the outdoors and am a cycling enthusiast. I also enjoy hiking, camping, reading and I spend considerable time with birders.
Fatty acid binding proteins (FABP) provide intracellular solubilization and trafficking of fatty acids. This intracellular function results in changes in overall energy storage and utilization. The adipocyte FABPs (A-FABP and E-FABP) play a role in overall body glucose/insulin homeostasis. Knockout mice for the adipocyte FABP (A-FABP) have increased insulin sensitivity whereas the epithelial FABP (E-FABP) over expressing transgenic mice have reduced insulin sensitivity as assessed by fasting glucose, fasting insulin, glucose and insulin tolerance tests. We are currently utilizing these animal models to decipher the role of adipocyte FABPs in lipid and glucose homeostasis.
Wendy Hahn, BS Scientist I was born and raised in Minnesota. After receiving a BS in Microbiology from the University of Michigan, I worked for several years at the University of Michigan Medical School in the Physiology Department. It was there that I received my initial training into mouse models and the intriguing world of adipocyte biology.  I returned to Minnesota and joined the Bernlohr lab in July of 2005.  I currently reside in Hastings with my husband Justin and our dog Kota.
While I enjoy the title of lab safety officer and mouse colony manager for the Bernlohr lab, I’m also part of an exciting research team focused on metabolic consequence of accumulation of reactive aldehyde 4-HNE.  Oxidative stress results in formation of several species of reactive aldehydes via lipid peroxidation which can modify proteins and alter function. One of these reactive aldehydes, 4-HNE, can be conjugated to glutathione and exported by Glutathione S Transferase A4. The selective down regulation of GSTA4 in adipose tissue in obese insulin resistant mice and humans was recently discovered in our lab. GSTA4 Knock-down or null mouse models reveal several interesting metabolic phenotypes including mitochondrial dysfunction.  I am currently developing cell lines and a transgenic mouse that express GSTA4 from an adipocytes-specific promoter to rescue the expression of GSTA4 in obese mice. These models will enable us to discern the contribution of GSTA4 and 4-HNE levels to insulin resistance and mitochondrial dysfunction associated with obesity.
Kristina Hellberg Graduate Research Assistant I was born in Karlskoga, a small town in the middle of Sweden. I graduated with a master of science from Linköping University, Sweden, in 2007 in chemical biology with biomolecular techniques as my branch of studies. In the fall of 2006 I came to University of Minnesota as an exchange student for a semester. I liked the university and Minnesota so I joined the BMBB graduate program in 2007. My hobbies include traveling, working out and reading.
Fatty acid binding proteins (FABP) are proteins that help solubilize and transport fatty acids in cells. The adipocyte isoform of FABP (AFABP) is mainly expressed in adipocytes and macrophages and, interestingly, AFABP knock out mice are more insulin sensitive and protected from atherogenesis compared to wild type mice. AFABP can interact with other proteins such as hormone sensitive lipase (HSL), janus kinase 2 (JAK2) and the nuclear receptor peroxisome proliferator-activated receptor γ, (PPARγ). My research project is to further characterize how AFABP can interact with other proteins.
Marissa Lee Undergraduate Associate
I am an undergraduate student here at the University of Minnesota. I am a sophomore and am thinking about a major in the arts. I am interested in all different kinds of art, from painting to drawing to sculpture. Besides art, I love to be outdoors, especially in the summer, and enjoy hiking, rock climbing, and going to my family’s cabin. I am currently living off-campus with my boyfriend and our hamster, Doris. We also like spending time with friends and family and going to see movies. Although I am not a student of biology, I really enjoy working in the lab. I am basically a lab attendant, washing bottles for cell culture, keeping important tools and solutions stocked, and cleaning and organizing the lab. I also help the researchers with cell culture on the weekends, which I have found to be very interesting. I try to keep the lab running as smoothly as possible to allow the people who do research to do so easily and efficiently.
Anne J. Smith, MS Scientist I was born in Minnesota, grew up in Wisconsin, and have moved back and forth over the state line a few times in my life.  I received a BS degree from UW-RF and an MS degree from Marquette University.  After receiving my MS degree I worked for my advisor at the Medical College of Wisconsin for 3 years, following which I stayed home with my children for 10 years. We moved to the Twin Cities in 1984 and I have worked for Dave Bernlohr since 1985.  I have 2 grown daughters and 3 grandchildren.  I finished 4 years of training in Classical Homeopathy in 2002 and have a growing practice out of my home.  I enjoy studying homeopathy and have completed 6 years of post-grad homeopathy work since finishing my initial program.  I also enjoy spending time with family, reading, going to plays, concerts and movies, being out in nature, cooking, and playing French Horn with various amateur groups.
Lipocalin-2 (LCN2) is a member of the lipocalin superfamily, characterized by a b-barrel calyx that binds and transports small hydrophobic molecules such as arachidonic acid, various steroids, iron, and retinoids.  LCN2 has been shown to have a key role in the acute-phase response to infection.  Gene  and protein expression of LCN2 in liver and adipose tissue as well as circulating concentrations are increased in db/db obese mice compared with lean littermates, and mRNA and protein expression levels of LCN2 are upregulated in visceral adipose tissue in human obesity. LCN 2 has been identified as an adipokine that potentially connects obesity and its related adipose inflammation. Retinoic acid treatment of obese mice has been found to induce expression of PPARbeta/delta and RAR target genes involved in regulation of lipid homeostasis, leading to weight loss and improved insulin responsiveness. The data indicate that suppression of obesity and insulin resistance by retinoic acid is largely mediated by PPARbeta/delta and is further enhanced by activation of RARs.  Currently I have made several Flag-tagged LCN2 mutants in the area of the retinoic acid binding site. I will be expressing these mutants in mammalian cells and be looking for a mutant(s) protein that no longer binds retinoic acid to use in investigating  possible mechanisms by which LCN2 may play a role in connecting obesity and inflammation.
Federico J Serrot, MD
I was born and raised in Argentina (home of the best steak and barbecues in the world). I finished medical school in Buenos Aires in 2007. During the following year I took the medical board exams and stayed as an observer at the Department of Surgery for 3 months. I am planning to do my residency in Surgery as soon as I finish my two years of research fellowship. Apart from working, I enjoy outdoor sports, specially soccer and tennis (now only during summer). I will enjoy cold (really cold) winters learning how to ski. Wish me luck! I am working as a research fellow at the Department of Surgery with Dr. Sayeed Ikramuddin (Bariatric Surgeon). My research project is focused on the effect of weight loss surgery on type 2 diabetes mellitus. We are looking at adipocyte changes regarding oxidative stress and mitochondrial function before and after the surgical intervention in both human and animal models. We would also like to study the effects of incretins on adipose tissue and insulin resistance. This will hopefully help to better understand the improvement of diabetes mellitus after bariatric surgery.