- BS, Biology, University of Maine at Machias,1998
- BA, Environmental Science, University of Maine at Machias,1998
- MS, Biochemistry, University of Maine, 2010
Prior to joining MMCRI in January of 2010, I worked for 10 years at The Jackson Laboratory; the initial 5 years were spent working in the Mutant Mouse Resource Lab (MMR) learning all aspects of mouse colony maintenance, from genetics to mouse phenotyping for bone and body composition, and eventually into molecular phenotyping. In 2005 I moved to the lab of Drs. Clifford Rosen and Wesley Beamer where, in addition to utilizing all the skills listed above, I gained further skills in metabolic phenotyping, specifically the running of metabolic cages including data interpretation and analysis, insulin tolerance tests, glucose tolerance tests and serum EIA and RIA techniques for metabolic markers. During this time my in vitro cell culture skills also flourished, as I assisted in the phenotyping and publication of numerous mouse models within our lab. In 2012 utilizing my metabolic background I helped create and currently manage the Physiology Core at MMCRI providing low cost high quality phenotyping for investigators both with in and outside of the institute.
My thesis research is centered around the role of tissue-nonspecific alkaline phosphatase a pro-mineralizing enzyme and its role in adipogenesis and mitochondrial function. Hypophosphatasia (HPP), a rare bone disease, is caused by loss-of-function mutations in the tissue-nonspecific alkaline phosphatase (TNAP) gene (ALPL) resulting in rickets, bone fragility, muscle weakness and lean body mass when severe in children. During the course of my studies I have become increasingly interested in Adult HPP phenotypes beyond known mineralization defects. Adult HPP has broad expressivity ranging from simple dental abnormalities to fractures, osteomalacia, chronic muscle weakness/pain as well as chronic fatigue with an estimated carrier prevalence estimated to be 1/300. We hypothesize that mitochondrial dysfunction with TNAP deficiency is causative of the chronic fatigue noted in Adult HPP populations.
- Guntur AR, Gerencser AA, Le PT, DeMambro VE, Bornstein SA, Mookerjee SA, Maridas DE, Clemmons DE, Brand MD, Rosen CJ. 2018. Osteoblast-like MC3T3-E1 Cells Prefer Glycolysis for ATP Production but Adipocyte-like 3T3-L1 Cells Prefer Oxidative Phosphorylation. J Bone Miner Res. 33(6):1052-1065.
- Liu P, Ji Y, Yuen T, Rendina-Ruedy E, DeMambro VE, Dhawan S, Abu-Amer W, Izadmehr S, Zhou B, Shin AC, Latif R, Thangeswaran P, Gupta A, Li J, Shnayder V, Robinson ST, Yu YE, Zhang X, Yang F, Lu P, Zhou Y, Zhu LL, Oberlin DJ, Davies TF, Reagan MR, Brown A, Kumar TR, Epstein S, Iqbal J, Avadhani NG, New MI, Molina H, van Klinken JB, Guo EX, Buettner C, Haider S, Bian Z, Sun L, Rosen CJ, Zaidi M. 2017. Blocking FSH induces thermogenic adipose tissue and reduces body fat. Nature. 546(7656):107-112.
- DeMambro VE, Le PT, Guntur, AR, Maridas DE, Canalis E, Nagano K, Baron R, Clemmons DR, Rosen CJ. 2015. Igfbp2 deletion in ovariectomized mice enhances energy expenditure but accelerates bone loss. Endocrinology. 156(11):4129-40.
- DeMambro VE, Kawai M, Clemens TL, Fulzele K, Maynard JA, Marín de Evsikova C, Johnson KR, Canalis E, Beamer WG, Rosen CJ, Donahue LR. 2010. A novel spontaneous mutation of Irs1 in mice results in hyperinsulinemia, reduced growth, low bone mass and impaired adipogenesis. J Endocrinol. 204(3):241-53.
To follow the full list with publications, press here.