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- NCIT_C39093 NCIT_NHC0 "C39093" @default.
- NCIT_C39093 NCIT_P106 "Functional Concept" @default.
- NCIT_C39093 NCIT_P108 "Food Intake and Energy Homeostasis Pathway" @default.
- NCIT_C39093 NCIT_P207 "C1517287" @default.
- NCIT_C39093 NCIT_P216 "h_ghrelinPathway" @default.
- NCIT_C39093 NCIT_P325 "The synthesis and release of growth hormone (GH) from the pituitary are controlled by the hypothalamic hormones GH-releasing hormone (GHRH) and somatostatin (SRIF), which in turn are regulated by feedback from blood GH and insulin-like growth factor-I (IGF-I) concentrations. The recently discovered endogenous GH-releasing peptide, called ghrelin, also stimulates GH release. Circulating GH acts directly on many organs to stimulate IGF-I production, with IGF-I production in the liver providing the main source of blood IGF-I. Most of the IGF-I in the circulation is bound to IGF-binding protein-3 (IGFBP-3) in a ternary complex with acid-labile subunit (ALS); a smaller fraction is bound to the five other IGFBP. A small fraction of the total IGF-I in blood is in a bioactive-free fraction. In the kidney, IGF-I increases renal plasma flow and GFR, whereas on bone it acts on the epiphysial plate, which leads to longitudinal bone growth. GH also has direct effects on many organs, including kidney and cartilage, which can be independent of IGF-I action. The GH/IGF-I axis in chronic renal failure (CRF) is changed markedly compared with the normal axis. In CRF, the total concentrations of the hormones in the GH/IGF-I axis are not reduced, but there is reduced effectiveness of endogenous GH and IGF-I, which probably plays a major role in reducing linear bone growth. The reduced effectiveness of endogenous IGF-I likely is due to decreased levels of free, bioactive IGF-I as levels of circulating inhibitory IGFBP are increased. In addition, less IGF-I is circulating in the complex with ALS and IGFBP-3 as a result of increased proteolysis of IGFBP-3. Together, these lead to decreased IGF-I receptor activation and a decreased feedback to the hypothalamus and pituitary. Low free IGF-I and high IGFBP-1 and -2 levels probably contribute to a reduced renal function and lead to a reduced stature. The direct effects of GH on bone, which are poorly understood, also are blunted. (This definition may be outdated - see the DesignNote.)" @default.
- NCIT_C39093 NCIT_P366 "Food_Intake_and_Energy_Homeostasis_Pathway" @default.
- NCIT_C39093 NCIT_P98 "The BIOCARTA Definition (ALT_DEFINITION) for this pathway concept was provided by BioCarta. This property was not created by, nor is it maintained by the NCI Thesaurus staff. Additionally, BioCarta is no longer updating its pathway data; thus, the BIOCARTA Definition might be outdated or inaccurate. Please see the Terms and Conditions for Use at http://www.biocarta.com/." @default.
- NCIT_C39093 normalizedInformationContent "79.853901415798049" @default.
- NCIT_C39093 referenceCount "21" @default.
- NCIT_C39093 hasExactSynonym "Food Intake and Energy Homeostasis Pathway" @default.
- NCIT_C39093 hasExactSynonym "Ghrelin: Regulation of Food Intake and Energy Homeostasis" @default.
- NCIT_C39093 type Class @default.
- NCIT_C39093 isDefinedBy ncit.owl @default.
- NCIT_C39093 label "Food Intake and Energy Homeostasis Pathway" @default.
- NCIT_C39093 subClassOf NCIT_C18611 @default.
- NCIT_C39093 subClassOf NCIT_C19779 @default.
- NCIT_C39093 subClassOf NCIT_C20633 @default.
- NCIT_C39093 subClassOf NCIT_C39093 @default.
- NCIT_C39093 subClassOf NCIT_C91822 @default.