Transgenic mice for the study of diabetes mellitus

Judith A. Shizuru, Nora Sarvetnick

Research output: Contribution to journalReview article

7 Citations (Scopus)

Abstract

Several recent studies have utilized transgenic technology to explore basic questions in the pathophysiology of diabetes mellitus. The ultimate expression of altered glucose homeostasis is a theme common to them. The experimental models have been diverse, however, and, in some instances, resulted in unexpected biologic effects. Many of the studies have examined the autoimmune etiology of insulin-dependent diabetes mellitus by expressing regulatory molecules of the immune system as transgenes in islet β cells. The molecules have included products of the major histocompatibility complex (MHC), cytokines, and other cell surface antigens. Ectopic expression of these transgenes resulted in altered immune responses directed against islets, and these transgenic mice now serve as important models to study mechanisms of immunologic tolerance. Transgenic technology is also being used to explore basic aspects of islet β-cell physiology and insulin metabolism. β-cell function is disrupted by transgenic β-cell expression of molecules such as calmodulin and H-ras. Hyperexpression of insulin as a transgene can result in a syndrome resembling features of non-insulin-dependent diabetes.

Original languageEnglish (US)
Pages (from-to)97-104
Number of pages8
JournalTrends in Endocrinology and Metabolism
Volume2
Issue number3
DOIs
StatePublished - Jan 1 1991

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Transgenes
Transgenic Mice
Diabetes Mellitus
Islets of Langerhans
Insulin
Technology
Cell Physiological Phenomena
Calmodulin
Surface Antigens
Major Histocompatibility Complex
Type 1 Diabetes Mellitus
Immune System
Homeostasis
Theoretical Models
Cytokines
Glucose

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

Transgenic mice for the study of diabetes mellitus. / Shizuru, Judith A.; Sarvetnick, Nora.

In: Trends in Endocrinology and Metabolism, Vol. 2, No. 3, 01.01.1991, p. 97-104.

Research output: Contribution to journalReview article

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