Literature DB >> 8968685

Insulin-like growth factor I (IGF-I) delays the onset of diabetes in non-obese diabetic (NOD) mice.

Y Kaino1, H Hirai, T Ito, K Kida.   

Abstract

It has been shown that prophylactic exogenous insulin treatment prevents the development of insulin-dependent diabetes mellitus (IDDM) in animal models and humans. In this study, we examined whether the development of diabetes and insulitis in female non-obese diabetic (NOD) mice could be affected by prophylactic administration of insulin-like growth factor I (IGF-I), which shares structural homology with insulin and has insulin-like metabolic effects. Two experiments which differed in duration and dosage of IGF-I treatment were carried out. In the first experiment, animals were treated from 4 to 9 weeks of age with IGF-I (17.9 nmol/day at 4-5 weeks of age and 35.9 nmol/day at 6-9 weeks of age) and observed up to 34 weeks of age. In the second experiment, the animals were treated from 4 to 34 weeks of age with IGF-I (1.79 nmol/day at 4-5 weeks of age, 3.59 nmol/day at 6-9 weeks of age, and 5.38 nmol/day at 10-34 weeks of age). The former treatment could significantly delay the onset of diabetes (P < 0.05) and decrease the insulitis score at 10 weeks of age (P < 0.01). On the other hand, the latter treatment did not affect the incidence of diabetes, the age at onset or the insulitis score. Our results suggest that the IGF-I treatment at the early age may provide protection against autoimmune beta-cell destruction in NOD mice.

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Year:  1996        PMID: 8968685     DOI: 10.1016/s0168-8227(96)01326-5

Source DB:  PubMed          Journal:  Diabetes Res Clin Pract        ISSN: 0168-8227            Impact factor:   5.602


  7 in total

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Authors:  J Størling; J Binzer; A K Andersson; R A Züllig; M Tonnesen; R Lehmann; G A Spinas; S Sandler; N Billestrup; T Mandrup-Poulsen
Journal:  Diabetologia       Date:  2005-08-25       Impact factor: 10.122

2.  Beta cell expression of IGF-I leads to recovery from type 1 diabetes.

Authors:  Mónica George; Eduard Ayuso; Alba Casellas; Cristina Costa; Jean Christophe Devedjian; Fatima Bosch
Journal:  J Clin Invest       Date:  2002-05       Impact factor: 14.808

3.  Insulin-like growth factor-1 stimulates regulatory T cells and suppresses autoimmune disease.

Authors:  Daniel Bilbao; Luisa Luciani; Bjarki Johannesson; Agnieszka Piszczek; Nadia Rosenthal
Journal:  EMBO Mol Med       Date:  2014-11       Impact factor: 12.137

4.  AAV-mediated pancreatic overexpression of Igf1 counteracts progression to autoimmune diabetes in mice.

Authors:  Cristina Mallol; Estefania Casana; Veronica Jimenez; Alba Casellas; Virginia Haurigot; Claudia Jambrina; Victor Sacristan; Meritxell Morró; Judith Agudo; Laia Vilà; Fatima Bosch
Journal:  Mol Metab       Date:  2017-05-17       Impact factor: 7.422

5.  Nonviral-mediated hepatic expression of IGF-I increases Treg levels and suppresses autoimmune diabetes in mice.

Authors:  Xavier M Anguela; Sabrina Tafuro; Carles Roca; David Callejas; Judith Agudo; Mercè Obach; Albert Ribera; Albert Ruzo; Christopher J Mann; Alba Casellas; Fatima Bosch
Journal:  Diabetes       Date:  2012-10-25       Impact factor: 9.461

Review 6.  Interactions Between the Neuroendocrine System and T Lymphocytes in Diabetes.

Authors:  Luz Andreone; María Laura Gimeno; Marcelo J Perone
Journal:  Front Endocrinol (Lausanne)       Date:  2018-05-17       Impact factor: 5.555

7.  Islet Macrophages Shift to a Reparative State following Pancreatic Beta-Cell Death and Are a Major Source of Islet Insulin-like Growth Factor-1.

Authors:  Dominika Nackiewicz; Meixia Dan; Madeleine Speck; Samuel Z Chow; Yi-Chun Chen; J Andrew Pospisilik; C Bruce Verchere; Jan A Ehses
Journal:  iScience       Date:  2019-12-14
  7 in total

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