GK

Inbr. F40 (Galli et al, 1996).

Colour: Albino.

Genet. c.

Origin: Developed from outbred Wistar rats with selection for high glucose levels in and oral glucose tolerance test (Goto et al 1975).

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Characteristics

Shows several non-insulin dependent diabetes mellitus (NIDDM)-related phenotypes including fasting hyperglycemia, impared secretion of insulin in response to glucose both in vivo and in isolated pancreata, hepatic and peripheral insulin resistance, with late complications which include nephropathy and neuropathy (Suzuki et al, 1992, Hughes et al, 1994, Villar-Palasi and Farese, 1994). Three independent loci affecting NIDDM, and a major locus affecting body weight but not glucose tolerance have been identified in a cross with non-diabetic F344 rats (Galli et al, 1996).

HCS

Origin: Harvard to Liverpool, UK in 1960.

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Goto Y., Kakizaki M., and Masaki N. (1975) Spontaneous diabetes produced by selective breeding of normal Wistar rats. Proc. Japan. Acad. Sci. 51, 80-85. \par

Hughes sj, Suzuki K., and Goto Y. (1994) The role of islet secretory function in the development of diabetes in the GK Wistar rat. Diabetologia 37, 863-870. \par

Suzuki K.-I., Goto Y., and Toyota T. (1992) Spontaneously diabetic GK (Goto-Kakizaki) rats, in Lessons from Animal Diabetes (Shafrir E., ed), pp. 107-116. Smith-Gordon, London. \par

Villar-Palasi C. and Farese R. V. (1994) Impaired skeletal muscle glycogen synthase activation by insulin in the Goto-Kakizaki (GK) rat. Diabetologia 37, 885-888. \par

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INBRED STRAINS OF RATS
Updated 9 Apr. 1998
Michael FW Festing
MRC Toxicology Unit, Hodgkin Building,
University of Leicester, UK