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Faculty Detail    
Name BARBARA GOWER
 
Campus Address WEBB 616A Zip 3360
Phone 205-934-4087
E-mail bgower@uab.edu
Other websites
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Nutrition Sciences   Nutrition Sciences Chair Office Professor
Secondary  Physiology & Biophysics   Physiology & Biophysics Assistant Professor
Center  Center for Aging  COMPREHENSIVE CTR FOR HEALTHY AGING Professor
Center  Medicine  Comprehensive Diabetes Ctr Professor
Center  General Clinical Research Center  Ctr for Clinical & Translational Sci Professor
Center  Cell, Developmntl, & Integrative Biology  Ctr for Exercise Medicine Professor
Center  Medicine  Ctr Cardiovasc Bio Professor
Center  Nutrition Sciences   Clin Nutrition Res Professor
Center  Nutrition Sciences   Nutrition Obesity Res Ctr (NORC) Professor

Graduate Biomedical Sciences Affiliations
Integrative Biomedical Sciences 
Medical Scientist Training Program 

Biographical Sketch 
Dr. Gower is an Associate Professor in the Department of Nutrition Sciences, Division of Physiology and Metabolism. She also is Director of core laboratories for both the Clinical Nutrition Research Center (Energy Metabolism/Body Composition Core) and General Clinical Research Center (Physiology and Metabolism Core Laboratory). Dr. Gower’s research includes both basic and clinical investigations into aspects of obesity and energy metabolism, with an emphasis on insulin secretion/action and the role of the endocrine system in the regulation of metabolism.

Research/Clinical Interest
Title
Gonadal steroid hormones
Description
The NIDDK R01-funded project, “Ethnic Differences in Insulin Sensitivity” is directed toward understanding the physiological basis for the greater prevalence of type 2 diabetes among African Americans. Dr. Gower’s earlier work showed that insulin sensitivity is lower in African-American vs Caucasian prepubertal children, independent of body composition and fat distribution; in contrast, insulin secretion is higher in African-Americans, even after controlling for lower insulin sensitivity. This cross-sectional study tests the hypothesis that hyperinsulinemia resulting from reduced hepatic insulin clearance is the primary preexisting difference. To begin to probe the etiology of ethnic differences in insulin sensitivity, secretion, and clearance, three groups of subjects, ranging from prepubertal through older adult, are being examined. Both obese and normal-weight individuals are being studied to examine obesity-ethnicity interactions. Free fatty acid concentrations will be measured throughout a glucose tolerance test to begin to address the potential physiological ramifications of chronic hyperinsulinemia among African-Americans. Stable isotopic and mathematical modeling techniques are used to measure glucose production, insulin secretion, and insulin sensitivity. Another major emphasis of Dr. Gower’s research involves investigating the metabolic effects of estrogen and progesterone. The goal of this research is to understand why both menopause and use of certain types of postmenopausal estrogen replacement therapy promote body fat gain in women. The specific hypothesis tested is that, whereas physiological estrogen increases energy expenditure and thereby decreases adipose tissue deposition, pharmacological estrogen treatment limits hepatic lipid oxidation and thereby promotes adipose tissue deposition. Her work has shown that high-dose estrogen treatment may limit lipid oxidation by lowering hepatic expression of the enzyme CPT-1 and elevating portal insulin concentrations. Current research involves both basic and clinical studies. The ovariectomized rat model is used to examine how physiological vs pharmacological estrogen affect substrate partitioning, as assessed with indirect calorimetry and with Northern analysis of mRNA for enzymes affecting lipid oxidation. The parallel clinical arm is an intervention study in which energy expenditure, substrate metabolism, and body composition are assessed in postmenopausal women both before and after treatment with estrogen.

Selected Publications 
Publication PUBMEDID
Herd, SL. Gower, BA, Dashti, N, Goran MI. Body fat, fat distribution and serum lipid, lipoprotein and apolipoprotein concentrations in African American and Caucasian American prepubertal children Int J Obesity, in press.   
Gower, BA, L Nyman. 2000. Associations between oral estrogen use, free testosterone concentration, and lean body mass among postmenopausal women J. Clin. Endo. Metab. 85:4476-4480.    
Kurtz, DM, L Tian, BA Gower, TR Nagy, CA Pinkart, and PA Wood. 2000. Transgenic studies of fatty acid oxidation gene expression in nonobese diabetic mice. J. Lipid Res. 41:2063 2070.   
Sun, M, BA Gower, AA Bartolucci, GR Hunter, R Figueroa-Colon, MI Goran. 2001. A longitudinal study of body composition and resting energy expenditure during puberty in African-American and White children and adolescents. Am. J. Clin. Nutr. 73:308-315.   
Gower, BA, SL Herd, MI Goran. 2001. Antilipolytic effects of insulin in African-American and Caucasian prepubertal boys Obesity Res. 9:224-228.   
Bamman MM, JR Shipp, J Jiang, BA Gower, GR Hunter, A Goodman, CL McLafferty, RJ Urban. 2001. Mechanical load increases muscle IGF I and androgen receptor mRNA concentrations in humans. Am J Physiol. 280:E383-E390..   
Hunter GR, RL Weinsier, BA Gower, C Wetzstein. 2001. Age-related decrease in resting energy expenditure in sedentary white women: effects of regional differences in lean and fat mass. Am. J. Clin. Nutr. 73:333-337.   
Weinsier RL, Hunter GR, Gower BA, Schutz Y, Darnell BE, Zuckerman PA. 2001. Body fat distribution in white and black women: different patterns of intra-abdominal and subcutaneous abdominal adipose tissue utilization with weight loss. Amer. J. Clin. Nutr. 74: 631-636.   
Higgins PB, Gower BA, Hunter GR, Goran MI. 2001. Defining health-related obesity in prepubertal children. Obesity Res. 9: 233-240.   
Higgins PB, Fields D, Hunter GR, Gower BA. 2001. Effect of scalp and facial hair on air displacement plethysmography estimates of percentage body fat. Obesity Res. 9: 326-330.