WASHINGTON UNIVERSITY IN ST. LOUIS SCHOOL OF MEDICINE PEDIATRICS FACULTY BESS A. MARSHALL, M.D.
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             Picture of Bess A. Marshall, M.D.
 
 
 
Bess A. Marshall, M.D.    contact information ]

Associate Professor of Pediatrics

Bess A. Marshall, M.D. joined the faculty of the Division of Pediatric Endocrinology and Diabetes in 1993. She is a native of Nashville, Tennessee and attended Vanderbilt University, where she received a B.S. in Mathematics from the College of Arts and Science in 1982 and an M.D. Degree from the School of Medicine in 1986. She served an internship and residency in Pediatrics at the University of Texas, Southwestern Health Sciences Center, Children's Medical Center of Dallas, and Parkland Memorial Hospital in Dallas from 1987-1990. From 1990-1993 she was a fellow in Pediatric Endocrinology and Metabolism at Washington University. She joined the faculty at Washington University in 1993.

Dr. Marshall's research interests include intermediary carbohydrate metabolism, glucose transporter structure and function mechanisms of insulin resistance, and metabolic control of insulin secretion. She has been funded by a National Institutes of Health Clinician- Investigator Development award, the Hardison Family Foundation and the National Institutes of Health NIDDK. She has been a scholar of the Child Health Research Center of Excellence in Developmental Biology at Washington University.

Dr. Marshall's clinical interests include diabetes and all aspects of endocrinology and metabolism. She is a fellow of the American Academy of Pediatrics and a member of the Lawson Wilkins pediatric Endocrine Society, the European Association for the Study of Diabetes, the International Diabetes Federation, the American Diabetes Association, the Endocrine Society, and is a charter member of the American Association of Clinical Endocrinologists. She is board certified in Pediatrics and Pediatric Endocrinology.

Selected Publications

  1. Cheverud JM, Pletscher LS, Vaughn TT, Marshall BA: Differential response to dietary fat in the Large (LG/J) and Small (SM/J) inbred mouse strains. Physiological Genomics 1999; 1: 33-39.

  2. Hsieh PS, Moore MC, Marshall BA, Pagliosotti MJ, Shay B, Szurkus D, Neal DW, Cherrington AD: The head arterial glucose level is not the reference for the generation of the portal signal in conscious dogs. American Journal of Physiology - Endocrinology & Metabolism 1999; 277(4):E678-E684.

  3. Ren J-M, Barucci N, Marshall BA, Hansen P, Mueckler MM, Shulman GI: Transgenic mice overexpressing Glut1 in muscle exhibit increased glycogenesis after exercise. American Journal of Physiology - Endocrinology & Metabolism 2000; 278(4):E588-E592.

  4. Koster JC, Marshall BA, Ensor NJ, Corbett JA, Nichols CG: Targeted overactivity of beta-cell KATP channels induces profound neonatal diabetes. Cell 2000; 100(6):645-654.

  5. Hansen PA, Marshall BA, Chen M, Holloszy JO, Mueckler MM: Transgenic overexpression of hexokinase II in skeletal muscle does not increase glucose disposal in wild-type or Glut1-overexpressing mice. Journal of Biological Chemistry 2000; 275(29):22381-22386.

  6. Davis A, Yarasheski K, White NH, Canter C, Marshall BA: Defective insulin receptors in Rabson-Mendenhall Syndrome cause complete peripheral insulin resistance but minimal glucocorticoid-suppressible hepatic insulin response remains. Pediatric Diabetes1 2000; 66-73.


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