Tsuura, Y., Ishida, H., Okamoto, Y., Kato, S., Sakamoto, K., Horie, M., Ikeda, H., Okada, Y. and Seino, Y. (1993) Glucose Sensitivity of ATP-Sensitive K+ Channels Is Impaired in Beta-Cells of the GK Rat. A New Genetic Model of NIDDM. Diabetes, 42, 1446-1453.
https://doi.org/10.2337/diab.42.10.1446

has been cited by the following article:

• TITLE: Non-Obese Type 2 Diabetic Rat Models-GK Rat and SDT Rat

  AUTHORS: Takeshi Ohta, Tomohiko Sasase, Takayuki Gotoh, Masami Shinohara, Phanthila Sirichaiyakul, Suhattaya Furuta, Rumpar Techasakulsin, Taiichiro Kamiya, Chikako Yoshida, Takahisa Yamada

  KEYWORDS: Diabetic Model, GK Rat, SDT Rat, Type 2 Diabetes

  JOURNAL NAME: Open Journal of Animal Sciences, Vol.8 No.4, September 13, 2018

  ABSTRACT: The number of diabetic patients has recently been increasing all over the world together with lifestyle changes including sedentary life and high-calorie diet intake, and as a result the increase in these suffering from diabetes mellitus has become a global issue. Diabetic animal models play a key role in bettering our understanding of the pathophysiology of diabetes and in developing new therapies for the disease. Diabetes is classified into two types, type 1 and type 2, and type 2 diabetes is chiefly caused by a depletion of insulin secretion in the pancreas and insulin resistance in peripheral tissues. The Goto-Kakizaki (GK) rat and the Spontaneously Diabetic Torii (SDT) rat are genetic non-obese type 2 diabetic models, and the both rats are considered to be suitable models for investigating the etiology of the depletion of insulin secretion and impaired glucose tolerance. In this review, we overviewed the outline of pathophysiological features in GK rats and SDT rats, including biological parameters and pharmacological responses.