Regulation of compensatory β-cell proliferation by inter-organ networks from the liver to pancreatic β-cells
Author:
Affiliation:
1. Department of Metabolism and Diabetes, Tohoku University Graduate School of Medicine
Publisher
Japan Endocrine Society
Subject
Endocrinology,Endocrinology, Diabetes and Metabolism
Link
https://www.jstage.jst.go.jp/article/endocrj/65/7/65_EJ18-0241/_pdf
Reference52 articles.
1. 1 Prentki M, Nolan CJ (2006) Islet beta cell failure in type 2 diabetes. J Clin Invest 116: 1802–1812.
2. 2 Terauchi Y, Takamoto I, Kubota N, Matsui J, Suzuki R, et al. (2007) Glucokinase and IRS-2 are required for compensatory beta cell hyperplasia in response to high-fat diet-induced insulin resistance. J Clin Invest 117: 246–257.
3. 3 Utzschneider KM, Prigeon RL, Carr DB, Hull RL, Tong J, et al. (2006) Impact of differences in fasting glucose and glucose tolerance on the hyperbolic relationship between insulin sensitivity and insulin responses. Diabetes Care 29: 356–362.
4. 4 Chick WL, Like AA (1970) Studies in the diabetic mutant mouse. 3. Physiological factors associated with alterations in beta cell proliferation. Diabetologia 6: 243–251.
5. 5 Edvell A, Lindstrom P (1999) Initiation of increased pancreatic islet growth in young normoglycemic mice (Umeå +/?). Endocrinology 140: 778–783.
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