1999
DOI: 10.1155/edr.2000.9
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Changes in the Growth Hormone‐IGF‐I Axis in Non‐obese Diabetic Mice

Abstract: We investigated the changes in GH-IGF-I axis in non-obese diabetic

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Cited by 21 publications
(13 citation statements)
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“…In contrast, human diabetes is characterised by GH hypersecretion positively correlated to the diabetic aberration (Yde 1969, Hansen & Johansen 1970, Hansen 1972. In concert with this we observed elevated barbital-stimulated GH levels in the present study, which have been demonstrated previously in the same model (Flyvbjerg et al 1999) and also in NOD mice (Landau et al 2000). It is therefore suggested that the diabetic mouse models, with respect to changes in GH, mimic human type 1 diabetes better than diabetic rats.…”
Section: Discussionsupporting
confidence: 89%
“…In contrast, human diabetes is characterised by GH hypersecretion positively correlated to the diabetic aberration (Yde 1969, Hansen & Johansen 1970, Hansen 1972. In concert with this we observed elevated barbital-stimulated GH levels in the present study, which have been demonstrated previously in the same model (Flyvbjerg et al 1999) and also in NOD mice (Landau et al 2000). It is therefore suggested that the diabetic mouse models, with respect to changes in GH, mimic human type 1 diabetes better than diabetic rats.…”
Section: Discussionsupporting
confidence: 89%
“…Although evidence of apoptosis has been described in cancer cachexia, 18,19,52 it has not been reported in chemically-induced diabetic rats. 53 Insulin-like growth factor-1 (IGF-1), a protein that is significantly reduced both in human TID 54 and in the diabetic NOD mouse, 55 inhibits caspase 3-mediated apoptosis. 56 Therefore, it is tempting to speculate that the mechanism for TID-induced cachexia involves apoptosis by a mechanism that involves a deficiency in IGF-1, and that the NOD model of cachexia provides a model to study mechanisms of apoptosis that are specific to TID cachexia.…”
Section: Discussionmentioning
confidence: 99%
“…Some studies showed that tissue IGF-1 gene expression might be affected by systemic or local factors or both in diabetes, i.e. decrease of GH receptors in target cells and its binding affinity [13] , and by reduced or absent pulsatile pattern secretion of GH, metabolic abnormality of insulin like growth factor binding proteins (IGFBPs) [6,14] , negative nitrogen balance [15,16] etc. All these may probably lead to a decline of IGF-1.…”
Section: Discussionmentioning
confidence: 99%