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Faculty Detail    
Name MARTIN E YOUNG
 
Campus Address ZRB 308 Zip 0007
Phone 205-934-2328
E-mail meyoung@uab.edu
Other websites
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Medicine  Med - Cardiovascular Disease Associate Professor
Secondary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Associate Professor
Center  Medicine  Comprehensive Diabetes Ctr (Org Ret) Associate Professor
Center  Cell, Developmntl, & Integrative Biology  Ctr for Exercise Medicine Associate Professor
Center  Medicine  Ctr Cardiovasc Bio (Org Ret) Associate Professor
Center  Nutrition Sciences   Nutrition Obesity Res Ctr (NORC) Associate Professor

Graduate Biomedical Sciences Affiliations
Biochemistry and Structural Biology 

Biographical Sketch 
Training

University of Oxford, U.K.
1991 - 1995
M.Biochem. (BS and MS in Biochemistry)

University of Oxford, U.K.
1995 - 1998
Diabetes/Metabolism
D.Phil.

Boston University
1998 - 1999
Diabetes/Metabolism
Post-doctoral Fellowship

University of Texas-Houston (UT-Houston)
1999 - 2001
Heart/Metabolism
Post-doctoral Fellowship


Positions and Employment

1996-1998 Oriel College Metabolism Lecturer, University of Oxford, U.K.
1998-1999 NIH Post-Doctoral Fellowship, Boston University
1999-2001 NIH Post-Doctoral Fellowship, UT-Houston
2001-2002 Assistant Professor of Medicine (Research Track), Department of Internal Medicine, UT-Houston
2001-2005 Faculty Cross Appointment with the Department of Biochemistry and Molecular Biology, UT-Houston
2002-2005 Assistant Professor of Molecular Medicine, Institute of Molecular Medicine, UT-Houston
2005-2009 Assistant Professor of Pediatrics, Children’s Nutrition Research Center, Baylor College of Medicine
2009-Present Associate Professor of Medicine, Department of Medicine, University of Alabama at Birmingham


Other Experience and Professional Memberships

1996-1998 Tutoring of undergraduates (Biochemistry and Medical students) from Jesus, Oriel and St. Hughes Colleges, University of Oxford, U.K.
2001-2005 Conference Leader (Medical student teaching), Department of Biochemistry and Molecular Biology, UT-Houston
2003-2005 Biochemistry Lecturer, Medical School, UT-Houston
2002-2007 Member, American Diabetes Association
2001-Present Member, American Heart Association


Honors

1991-1995 Oriel College Scholar, University of Oxford, U.K.
2001 ISHR Best Poster Award
2001 ISHR Young Investigator Award 1st Runner-up
2009-Present Society for Heart and Vascular Metabolism, Treasurer/Secretary

Research/Clinical Interest
Title
Role of the Circadian Clock within the Heart
Description
Research in my laboratory is focused on identifying the role(s) of the circadian clock in both cardiac and skeletal muscle. Circadian clocks are intrinsically maintained molecular mechanisms that condition the cell to changes in its environment. These circadian clocks therefore confer a selective advantage by providing a mechanism for anticipation of change. We have recently characterized fully the circadian clock within both mammalian heart and skeletal muscle. The broad objective of my laboratory is therefore to test the hypothesis that the circadian clock within these muscle types synchronizes responsiveness of cardiac and skeletal muscle to diurnal variations in their environment. Impairment of this molecular mechanism would therefore result in an inability of these muscles to respond appropriately to the onset of such environmental influences (i.e. maladaptation). The primary humoral factors currently under investigation are nutrients, such as glucose and fatty acids. In the latter case, cardiac and skeletal muscle exhibit dramatic diurnal variations in their responsiveness to fatty acids. Failure to respond adequately to increased fatty acid availability will result in accumulation of intramyocellular fatty acid derivatives. The latter may play a significant role in the pathogenesis of insulin resistance, type II diabetes mellitus, and/or cardiomyopathy. To address this line of reasoning, we have recently generated two novel genetically manipulated mouse models in which the circadian clock is specifically impaired within cardiomyocytes or skeletal myocytes.