Animal models provide insight into psychosomatic factors in diabetes.

Journal Article (Review)

OBJECTIVE: To review the literature regarding the use of animal models in research addressing psychosomatic aspects of diabetes. METHOD: We examine the key findings in animal model vs. human research in the area of stress and diabetes. Previous research has suggested that stress is a potential contributor to chronic hyperglycemia in diabetes. Stress affects metabolic activity via the stimulation of a variety of hormones that can result in elevated blood glucose levels. In patients with diabetes, due to a relative or absolute lack of insulin, stress-induced increases in glucose cannot be properly metabolized. Additionally, regulation of these stress hormones may be abnormal in diabetes. RESULTS: Human studies on the role of stress in the onset and course of type II diabetes are few and are limited by the constraints and logistics of examining life stress in humans. However, animal research allows for tight experimental control and the manipulation of factors that may contribute to the development and/or course of diabetes, such as stress, eating behavior, the nutrient content of food, and physical activity. Disease processes can be examined at a mechanistic level in animals which is typically limited in human research. CONCLUSIONS: There is a large body of animal work to support the notion that stress reliably produces hyperglycemia in type II diabetes. Furthermore, there is evidence that the autonomic nervous system plays a role in the pathophysiology of this condition in both animals and humans. Examination of eating behavior and nutrient content of food in animal models of diabetes has shed light on the role of these factors in the development of diabetes, as well as obesity. Finally, genetic research using animal models of diabetes will provide new directions for research in humans to delineate the genetic contribution to the development of diabetes.

Full Text

Duke Authors

Cited Authors

  • Surwit, RS; Williams, PG

Published Date

  • November 1996

Published In

Volume / Issue

  • 58 / 6

Start / End Page

  • 582 - 589

PubMed ID

  • 8948006

Pubmed Central ID

  • 8948006

International Standard Serial Number (ISSN)

  • 0033-3174

Digital Object Identifier (DOI)

  • 10.1097/00006842-199611000-00006


  • eng

Conference Location

  • United States