The prevalence of the metabolic syndrome is increasing at alarming rates in the United States, even in the pediatric population. In this proposal, Dr. Biddinger, focusing on the liver, will examine the molecular links between insulin resistance, dyslipidemia and gallstones, three features of the metabolic syndrome, and how they are modified by dietary factors. These studies build on Dr. Biddinger's prior work examining the effects of diet and genetic background on hepatic lipid metabolism and gene expression, and the development of the metabolic syndrome. The primary goal of this mentored career development award is to provide a mechanism for Dr. Biddinger, a trained pediatric endocrinologist, to achieve scientific independence. By developing an expertise in lipid metabolism and microarray analysis, she will distinguish herself from her mentor, Dr. C. Ronald Kahn, and be well positioned to make significant scientific and medical contributions to the understanding of insulin resistance in children and adolescents.

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Clinical Investigator Award (CIA) (K08)
Project #
7K08DK073358-03
Application #
7671492
Study Section
Diabetes, Endocrinology and Metabolic Diseases B Subcommittee (DDK)
Program Officer
Hyde, James F
Project Start
2007-09-01
Project End
2011-08-31
Budget Start
2009-09-01
Budget End
2011-08-31
Support Year
3
Fiscal Year
2009
Total Cost
$127,233
Indirect Cost
Name
Children's Hospital Boston
Department
Type
DUNS #
076593722
City
Boston
State
MA
Country
United States
Zip Code
02115
Haas, Joel T; Biddinger, Sudha B (2009) Dissecting the role of insulin resistance in the metabolic syndrome. Curr Opin Lipidol 20:206-10
Biddinger, Sudha B; Haas, Joel T; Yu, Bian B et al. (2008) Hepatic insulin resistance directly promotes formation of cholesterol gallstones. Nat Med 14:778-82
Biddinger, Sudha B; Hernandez-Ono, Antonio; Rask-Madsen, Christian et al. (2008) Hepatic insulin resistance is sufficient to produce dyslipidemia and susceptibility to atherosclerosis. Cell Metab 7:125-34