Joseph C. Dunbar Ph.D. (ad4730)

University Information

Title: Director, Academic
Unit: Physiology
Department: School of Medicine

Contact Information

313-577-5600
5057 Woodward
Office of the Vice President for Research
Suite 6409
Detroit, 48202

Physiology

Narrative Bio:

Our laboratory is interested in the endocrine mechanisms associated with diabetes mellitus and its complications. Diabetes or insulin insufficiency is characterized by changes in nutrient metabolism as well as chronic alterations in multiple physiological systems. Cardiovascular changes and hypertension are characteristic of diabetes and are the basis for the major complications of diabetes such as increased risk of heart attack, vascular dysfunction, and stroke. Since obesity is strongly associated with diabetes we are also investigating the role of insulin and adipose tissue hormones in the central nervous system (CNS)-mediated regulation of cardiovascular responses. We are investigating the hypothalamic factors mediating the leptin signaling cascade pathway. We have evaluated the interaction of the proopiomelanocortin system (POMC) and its major products aMSH and beta-endorphin and their receptors in this process. We are conducting studies on the mechanism of action of insulin and leptin in the regulation of blood flow dynamics. We are also conducting studies to evaluate the peripheral actions of these hormones contrasted to their actions mediated at the level of the central nervous system (CNS).
 

Office Address: 5057 Woodward, Suite 6049
Post Graduate Training:

1970-72 Post-Doctoral Diabetes Trainee, Sinai Hospital of Detroit
1972-81 Research Associate, Sinai Hospital of Detroit
 

Areas of Interest: Endocrinology; diabetes; metabolic and neural control of pancreatic secretion
Phone: (313) 577-5600
Publications:

A complete list of Dr. Dunbar's publications can be found at PubMed-Dunbar

Fax: (313) 577-5494
Laboratory Web Site: http://www.med.wayne.edu/physiology/facultyprofile/dunbar/dunbar.html
Email: jdunbar@med.wayne.edu
Categories: Cardiovascular Physiology,Endocrinology,Neurophysiology
Category Information:
  • Neural and cardiovascular changes induced by diabetes
Position Title: Professor and Associate Vice President for Research

Physiology - New

Narrative Bio:

When my lab was involved in research, we were interested in the endocrine mechanisms associated with diabetes mellitus and its complications. Diabetes or insulin insufficiency is characterized by changes in nutrient metabolism as well as chronic alterations in multiple physiological systems. Cardiovascular changes and hypertension are characteristic of diabetes and are the basis for the major complications of diabetes such as increased risk of heart attack, vascular dysfunction, and stroke. Since obesity is strongly associated with diabetes we also investigated the role of insulin and adipose tissue hormones in the central nervous system (CNS)-mediated regulation of cardiovascular responses. We investigated the hypothalamic factors mediating the leptin signaling cascade pathway. We have evaluated the interaction of the proopiomelanocortin system (POMC) and its major products aMSH and beta-endorphin and their receptors in this process. We conducted studies on the mechanism of action of insulin and leptin in the regulation of blood flow dynamics. We also conducted studies to evaluate the peripheral actions of these hormones contrasted to their actions mediated at the level of the central nervous system (CNS). It was our working hypothesis that many of the chronic pathologies associated with diabetes are mediated by alterations in the central nervous regulatory mechanisms that lead to the diabetic complications. We have demonstrated that insulin and leptin-mediated hormones can affect cardiovascular dynamics at the CNS level, and that these regulatory responses are altered in diabetes. We also had studies on the influence of diabetes on CNS neuronal apoptosis and the response to ischemia. We observed that diabetes is associated with a basal increase in apoptosis and this process is made worse by ischemia. We investigated the role of insulin and IGF-1 in this process and studied the mechanisms involved in this process.

Office Address: 5057 Woodward, Suit 6049
Post Graduate Training:
  • 1970-72 Post-Doctoral Diabetes Trainee, Sinai Hospital of Detroit
  • 1972-81 Research Associate, Sinai Hospital of Detroit
Areas of Interest: Endocrinology; diabetes; metabolic and neural control of pancreatic secretion
Phone: 313-577-5600
Publications:

 A complete list of Dr. Dunbar's publications can be found at PubMed-Dunbar

Fax: 313-577-5494
Laboratory Web Site: http://www.med.wayne.edu/physiology/facultyprofile/dunbar/dunbar.html
Categories: Cardiovascular Physiology,Endocrinology,Neurophysiology
Email: jdunbar@med.wayne.edu
Category Information:
  •  Neural and cardiovascular changes induced by diabetes
Position Title: Professor and Associate Vice President for Research

Division of Research

Email: joseph.dunbar@med.wayne.edu
Phone: 313-577-5600
Address: 5057 Woodward, Suite 6405.4
Title: Associate Vice President for Research and Assistant Dean of the Graduate School

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