Phone
(608) 262-1372Website
View WebsiteOffice Location
543A HF DeLuca Biochemistry Laboratories
433 Babcock Drive
Madison, WI 53706-1544

B.S., University of Wisconsin-Madison
Ph.D., University of California-San Diego
- Transcripts with high distal heritability mediate genetic effects on complex metabolic traits
- VDAC1 is a target for pharmacologically induced insulin hypersecretion in β cells
- Systems genetics uncovers associations among host amylase locus, gut microbiome, and metabolic traits in mice
- Haem biosynthesis regulates BCAA catabolism and thermogenesis in brown adipose tissue
- Target deconvolution of an insulin hypersecretion-inducer acting through VDAC1 with a distinct transcriptomic signature in beta-cells
- Transcripts with high distal heritability mediate genetic effects on complex metabolic traits
- Multiple promoter and enhancer differences likely contribute to augmented G6PC2 expression in human versus mouse pancreatic islet alpha cells
- Systems genetics approach uncovers associations between host amylase locus, gut microbiome and metabolic traits in hyperlipidemic mice
- D2H2: diabetes data and hypothesis hub
- Heme biosynthesis regulates BCAA catabolism and thermogenesis in brown adipose tissue
Genetic Pipeline
Our projects come from genes we identify in our screens using mouse genetics. We then study these genes in transgenic mice and in cell lines.
Gene causal networks and diabetes
By combining global gene expression profiling and genetics, we are able to construct causal networks linking specific genes with diabetes phenotypes. One of those genes is the transcription factor NFATc2. We are studying its regulation in relation to β-cell function and diabetes.
Genetics of metabolic outcome
There is tremendous variability in the response of individuals to different diets. Likewise, mouse strains vary in their response to diet. These responses are due to differences in the control of metabolic pathways. We are conducting a genetic screen using stable isotope tracers to measure metabolic outcome through many pathways in mice subjected to two extreme diets. We will map the genetic drivers responsible for strain differences in diet responsiveness
grow magazine article, Spring 2015, about Attie’s Diabetes research click here.