Stanley Andrisse

Stanley Andrisse, Ph.D, MBA

Assistant Professor

Contact Information: 
E-mail: stanley.andrisse@howard.edu
Office: Numa P. G. Adams Bldg, Suite: 2420, Room 2414-A
Office Telephone: 202-806-4928
Laboratory: Numa P. G. Adams Bldg, Suite: 2508D

 
 
Education & Experience
B.S., Lindenwood University (2006)
M.B.A., Lindenwood University (2008)
Ph.D., Saint Louis University (2014)
Postdoctoral Fellow, Johns Hopkins Medicine (2014-2017)
Adjunct Assistant Professor, Johns Hopkins Medicine (2017-present)
 
Teaching:
Reproductive Endocrinology
Metabolism
 
Research:
Insulin signaling
Energy metabolism
Mechanisms of insulin resistance and diabetes
 
Grants and Funding:
American Physiological Society, Predoctoral Fellowship (2012-2014)
NIH, NIDDK, T32 Postdoctoral Fellowship (2014-2016)
Johns Hopkins University, Provost Fellowship (2016-2017)
 

Research Interests: My research investigates the intersecting pathways of different insulin resistant states. I am actively recruiting trainees and technicians (contact me). Dysregulated hepatic glucose metabolism plays a pivotal role in the pathophysiology of metabolic syndrome, type 2 diabetes and insulin resistance. The pathways that regulate hepatic gluconeogenesis, glycogen synthesis, and glycogenolysis are complex. Increasing evidence from my work and others has revealed many intersecting pathways that influence the traditional PI3K/AKT insulin action pathway. Discovering these mechanistic interactions, using cutting-edge molecular technologies is the focus of my work. I will employ the use of animal models, cell culture models and clinical collaborations.

Research Significance: The current pandemic of obesity and comorbid conditions of fatty liver disease and T2D is highly associated with insulin resistance. Much work has been devoted to delineating the pathogenesis of insulin resistance. The insulin regulated shift of hepatic glucose metabolism to-and-from glucose production and storage is a crucial process in physiology and pathophysiology. Insulin resistance prohibits hepatic glucose storage and increases hepatic glucose production (HGP) facilitating disease. However, the differing comorbidities associated with insulin resistance display different mechanisms. Thus, uncovering the intersecting pathways modulating insulin action will lead to more specific and targeted therapies.

Androgen-induced Insulin Resistance

Publications:

  1. Andrisse S, Fisher JS. AMP-activated protein kinase. Encyclopedia of Exercise Medicine in Health and Disease. Publisher: Springer Verlag GmbH, Heidelberg, DE. (2011) [review]
  2. Andrisse S, Patel GD, Chen JE, Webber AM, Spears LD, Koehler RM, Robinson-Hill RM, Ching JK, Jeong I, Fisher JS. ATM and GLUT1-S490 phosphorylation regulate GLUT1 mediated transport in skeletal muscle. PLOS One, 2013 Jun 11;8(6): e66027.
  3. Ching JK, Spears LD, Armon JL, Renth AL, Andrisse S, Collins IV RL, and Fisher JS. Impaired insulin-stimulated glucose transport in ATM-deficient skeletal muscle. Applied Physiology, Nutrition, and Metabolism, 2013 Jun;38(6):589-96.
  4. Andrisse S, Koehler RM, Chen JE, Patel GD, Vallurupalli VR, Ratliff BA, Warren DE, Fisher JS. Role of GLUT1 in regulation of reactive oxygen species. Redox Biology, 2014 Mar 25;2:764-71.
  5. Ma. Y, Andrisse S, Chen Y, Childress S. Ping X, Wang Z, Jones D, Ko C, Divall S, Wu S. Androgen receptor in the ovary theca cells plays a critical role in androgen-induced reproductive dysfunction. Endocrinology, 2017 Jan 1;158(1):98-108.
  6. Andrisse S, Childress S, Ma Y, Billings K, Chen Y, Xue P, Wolfe A, Wu S. Low dose dihydrotestosterone drives metabolic Dysfunction via cytosolic and nuclear hepatic androgen receptor mechanisms in female mice. Endocrinology, 2017 Mar 1;158(3):531-544.