Growth Hormone Resistance-Special Focus on Inflammatory Bowel Disease.

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Term Occurence Count Dictionary
Insulin 3 endocrinologydiseasesdrugs
cortisol 1 endocrinologydiseasesdrugs
dexamethasone 2 endocrinologydiseasesdrugs
obesity 5 endocrinologydiseases
prednisone 1 endocrinologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
Insulin 1998 metabolic effects on the liver. Some, but not all, of these effects are brought about by the action of Insulin -like growth factor (IGF)-1 which is produced in response to GH in most tissues with the liver predominating.
Insulin 12906 apparently regulate GH response in order to control energy expenditure and maintain euglycemia [[51]]. Insulin has also been shown to directly impact both the expression and the protein level of GHR although the
Insulin 43146 process is key for effectively treating these patients.Figure 1Regulation of growth hormone (GH) and Insulin -like growth factor (IGF)-1 Secretion. GH secretion by the anterior pituitary into the circulation is
cortisol 19493 that high dose exogenous steroids may de-sensitize the positive effects of low levels of endogenous cortisol .3.2. Post-Transcriptional Regulation of GHR LevelsAlternative splicing of the GHR precursor mRNA can
dexamethasone 18967 secretion and GH responsiveness [[74]]. Erman A. et al. have shown that the synthetic glucocorticoid ( dexamethasone ) can lead to interaction between the glucocorticoid receptor and putative glucocorticoid response element
dexamethasone 19207 promoter/enhancer in HEK293 and SGBS cells [[68]]. This interaction induced a biphasic effect where low dose dexamethasone enhances the GHR expression, while high dose leads to alleviation of this effect with a return to normal
prednisone 39071 compared to placebo. Patients treated with GH also showed a decreased need for concomitant medication ( prednisone and immunosuppressants) relative to baseline compared to the placebo group. The positive results of
Select Disease Character Offset Disease Term Instance
obesity 10669 regulation of GHR expression is also controlled by factors including nutritional status, GH, insulin, and obesity /adiposity (Figure 3) [[34],[35],[36],[37]].The metabolic state and the availability of external nutrients
obesity 17137 reduced GHR expression in adipocytes from obese individuals, which possibly coincide with local low-grade obesity -related inflammation [[35]].The mechanisms by which IL-1β impacts GHR expression is less studied, and
obesity 21317 level of full length GHR and the 1–279 variant and found a positive correlation of the variant with obesity in subcutaneous fat. Due to the dominant negative effect of the GHR variant, a decreased responsiveness
obesity 21463 dominant negative effect of the GHR variant, a decreased responsiveness to GH is expected with increasing obesity [[35]]. Whether inflammatory mediators influence alternative splicing is still unclear, but regulation
obesity 45103 unknown mechanisms. Metabolic parameters including poor nutritional status, high insulin levels and obesity negatively impacts GHR expression. The effect of GH on GHR expression is imperfectly understood as applied

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