Διαταραχές στον άξονα της αυξητικής ορμόνης σε ασθενείς της μονάδας εντατικής θεραπείας με σήψη

2013 ◽  
Author(s):  
Χρυσούλα Παπαστάθη
Keyword(s):  
Septic Shock ◽  
Severe Sepsis ◽  
Growth Factor ◽  
Interleukin 6 ◽  
Insulin Like Growth Factor ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Septic Episode ◽  
Igf I ◽  
Igfbp 3

Objective: To investigate the Growth Hormone (GH)/Insulin-like Growth Factor-I (IGF-I)axis and identify the factors that determine IGF-I levels in adult septic patients of variable severity,i.e., with sepsis, severe sepsis or septic shock, in the acute phase of disease.Design: Prospective study comparing septic patients treated in a general intensive care unitand healthy volunteers.Methods: In 107 consecutive septic patients (44 with sepsis, 13 with severe sepsis, and 50with septic shock), GH, IGF-I, Insulin-like Growth Factor Binding Protein-3 (IGFBP-3), insulin,cortisol, albumin, thyroid hormones, C-reactive protein and interleukin-6 serum levels weremeasured once within 48 hrs after onset of a septic episode. Twenty-nine healthy volunteers servedas controls.Results: IGF-I and IGFBP-3 levels were decreased in patients with sepsis and severe sepsis(versus controls), decreasing further in patients with septic shock (versus sepsis). IGF-I levels were positively related to IGFBP-3, albumin, triiodothyronine and thyroxine, and inversely related to cortisol, sepsis severity, C-reactive protein, interleukin-6 and age. In multiple regression analysis, IGF-I levels were independently related to IGFBP-3 and albumin (lower in patients with decreasedIGFBP-3 and albumin levels) (p<0.001 and p=0.01, respectively), and cortisol (lower in patientswith increased cortisol levels) (p=0.04). IGFBP-3 accounted for most of the variance explained bythe model (R2=0.519). GH levels were not related to IGF-I levels or mortality. IGF-I and IGFBP-3levels were associated with mortality.Conclusions: The GH/IGF-I axis is severely disrupted in septic patients. IGFBP-3 is themajor determinant of IGF-I levels, whereas albumin and cortisol are secondary determinants.

scholarly journals Soluble membrane receptors, interleukin 6, procalcitonin and C reactive protein as prognostic markers in patients with severe sepsis and septic shock

PLoS ONE ◽  
2017 ◽  
Vol 12 (4) ◽  
pp. e0175254 ◽  
Author(s):  
Juan-Jesús Ríos-Toro ◽  
Mercedes Márquez-Coello ◽  
José-María García-Álvarez ◽  
Andrés Martín-Aspas ◽  
Ricardo Rivera-Fernández ◽  
...  
Keyword(s):  
Septic Shock ◽  
Severe Sepsis ◽  
Interleukin 6 ◽  
Prognostic Markers ◽  
Membrane Receptors ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Sepsis And Septic Shock

Specimen processing time and measurement of total insulin-like growth factor-I (IGF-I), free IGF-I, and IGF binding protein-3 (IGFBP-3)

2006 ◽  
Vol 16 (2) ◽  
pp. 86-92 ◽  
Author(s):  
Tiffany G. Harris ◽  
Howard D. Strickler ◽  
Herbert Yu ◽  
Michael N. Pollak ◽  
E. Scott Monrad ◽  
...  
Keyword(s):  
Growth Factor ◽  
Processing Time ◽  
Binding Protein ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Igf I ◽  
Specimen Processing ◽  
Igf Binding ◽  
Igf Binding Protein ◽  
Igfbp 3

Growth hormone deficiency in 'little' mice results in aberrant body composition, reduced insulin-like growth factor-I and insulin-like growth factor-binding protein-3 (IGFBP-3), but does not affect IGFBP-2, -1 or -4

1993 ◽  
Vol 136 (1) ◽  
pp. 91-104 ◽  
Author(s):  
L. R. Donahue ◽  
W. G. Beamer
Keyword(s):  
Body Composition ◽  
Growth Factor ◽  
Gh Deficiency ◽  
Body Water ◽  
Insulin Like Growth Factor ◽  
Gh Therapy ◽  
Factor I ◽  
Igf I ◽  
Body Compartments ◽  
Igfbp 3

ABSTRACT Although GH is known to regulate somatic growth during development, its role in regulating adult body composition is less well defined. The effects of GH on individual body compartments – water, fat, protein and mineral – are achieved both by the action of GH and by a GH-induced hormone, insulin-like growth factor-I (IGF-I). We used a genetic model of GH deficiency, the 'little' (gene symbol lit) mouse, to determine the GH regulation of IGF-I and its insulin-like growth factor-binding proteins (IGFBPs) and to define the interaction between these hormones and each body compartment in adults. Our results showed that GH-deficient lit/lit mice had reduced levels of serum IGF-I (range 38–130 μg/l) compared with normal lit/+ littermates (range 432–567 μg/l) between 2 and 52 weeks of age. The lit/lit mice did not experience the fivefold increase in IGF-I between 2 and 4 weeks of age that was seen in lit/+ mice. In lit/lit serum, overall binding of 125I-labelled IGF-I to the four IGFBPs was reduced, solely in response to a reduced amount of IGFBP-3. No overall differences were found between lit/lit and lit/+ mice in the binding of 125I-labelled IGF-I to IGFBP-2, -1 or -4. Age-related declines in IGF-I and IGFBPs were seen in lit/lit mice. However, adult levels of IGF-I were maintained in lit/+ mice to at least 52 weeks of age, as were levels of IGFBP-1 and -4, while IGFBP-3 and -2 declined with age. With respect to body composition, comparison of lit/lit with lit/+ mice showed that the lit/lit mice were characterized by abnormally large adipose tissue stores and reduced body water, protein and mineral from 2 weeks onward. These changes occurred despite normal energy intake in lit/lit mice up to 52 weeks of age, indicating that neither undernutrition nor hyperphagia is characteristic of this GH-induced model of obesity. Furthermore, lit/lit males accrued more body fat beginning at an earlier age than lit/lit females. With advancing age, the per cent body fat increased in both lit/lit and lit/+ mice, while the per cent body water and mineral declined. In lit/lit but not lit/+ mice, per cent protein also declined with age. The changes in body water and fat are attributable to lack of adequate GH in the genetically GH-deficient lit/lit mouse. On the other hand, the changes in body protein are more likely to be effects of IGF-I. Changes in mineral observed in lit/lit mice could be the result of action by GH, IGF-I or both hormones. Therefore, when GH is chronically manipulated by GH deficiency as in lit/lit mice, by GH excess as in acromegaly, or by GH therapy, all four body compartments are affected, suggesting that GH therapy is most valuable when the treatment goal is to alter overall body composition. Journal of Endocrinology (1993) 136, 91–104

scholarly journals A substitution model of dietary manipulation is an effective means of optimising lipid profile, reducing C-reactive protein and increasing insulin-like growth factor-1

2004 ◽  
Vol 92 (5) ◽  
pp. 809-818 ◽  
Author(s):  
Adrian H. Heald ◽  
Cheryl Golding ◽  
Reena Sharma ◽  
Kirk Siddals ◽  
Sara Kirk ◽  
...  
Keyword(s):  
Growth Factor ◽  
Dietary Intervention ◽  
Short Interval ◽  
The Other ◽  
Fat Intake ◽  
Insulin Like Growth Factor ◽  
C Reactive Protein ◽  
High Fat ◽  
Substitution Model ◽  
Reactive Protein

There are two key methods in which fat intake may be manipulated; the ‘substitution model’ and the ‘reduction model’. However insufficient information is known about the mechanisms of dietary fat reduction in individuals who have successfully reduced their fat intake, to be clear as to which strategy offers the greatest chance of success. Our objective was to ascertain the most effective dietary intervention for improving cardiovascular risk profile. Eighty female volunteers (high fat consumers) were recruited. Each subject was randomly allocated into one of the following groups. Substitution of high-fat foods was made with reduced-fat products, by the reduction of high-fat foods, by a combination of substitution and reduction strategies, or no advice was given. Each intervention lasted 3 months. Anthropometric measures and fasting blood samples were taken at baseline and follow-up. The substitution intervention resulted in weight loss (mean −1.4 (95% CI −2.4, −0.2) kg) and reduced percentage body fat (mean −1.3 (95% CI −2.0, −0.5)%). There was no significant weight change with the other interventions. Fasting triacylglycerols (−0.2 (SEM 0.07) mM; P=0.04), cholesterol and C-reactive protein (CRP) levels (0.8 (SEM 0.2) mg/l; P=0.04) fell with the substitution intervention, but not with the other interventions. Insulin-like growth factor-1 increased with both substitution and reduction (P=0.02). There was no significant change in fasting insulin or glucose with any intervention. The substitution model of dietary intervention is effective even over a relatively short interval of time in reducing fasting total cholesterol, triacylglycerols and CRP. Although the group size for the present study was small and involved females only, it has significant implications for population intervention strategies.

scholarly journals Genetic Determinants of Circulating Insulin-Like Growth Factor (IGF)-I, IGF Binding Protein (BP)-1, and IGFBP-3 Levels in a Multiethnic Population

2007 ◽  
Vol 92 (9) ◽  
pp. 3660-3666 ◽  
Author(s):  
Iona Cheng ◽  
Katherine DeLellis Henderson ◽  
Christopher A. Haiman ◽  
Laurence N. Kolonel ◽  
Brian E. Henderson ◽  
...  
Keyword(s):  
Growth Factor ◽  
Binding Protein ◽  
Insulin Like Growth Factor ◽  
Genetic Determinants ◽  
Igf I ◽  
Igf Binding ◽  
Multiethnic Population ◽  
Igf Binding Protein ◽  
Igfbp 3

Regulation and localization of the insulin-like growth factor system in small bowel during altered nutrient status

1995 ◽  
Vol 268 (4) ◽  
pp. G631-G640 ◽  
Author(s):  
D. E. Winesett ◽  
M. H. Ulshen ◽  
E. C. Hoyt ◽  
N. K. Mohapatra ◽  
C. R. Fuller ◽  
...  
Keyword(s):  
Growth Factor ◽  
Small Bowel ◽  
Lamina Propria ◽  
Elemental Diet ◽  
Nutrient Status ◽  
Insulin Like Growth Factor ◽  
Nutrient Regulation ◽  
Igf I ◽  
Ad Libitum ◽  
Igfbp 3

Insulin-like growth factor-I (IGF-I) may regulate small bowel growth. Analyses here in ad libitum-fed, fasted, and refed rats demonstrate that during fasting and refeeding changes in jejunal mass correlate with changes in serum IGF-I and jejunal IGF-I mRNAs. These data indicate that circulating and locally expressed IGF-I contribute to nutrient regulation of jejunal mass. During refeeding, jejunal IGF binding protein 3 (IGFBP-3) mRNA abundance was reduced relative to that of IGF-I, possibly amplifying enterotrophic actions of IGF-I. Localization of IGFBP-3 to subepithelial cells in lamina propria of jejunum indicates that IGFBP-3 derived from lamina propria may modulate IGF-I action on adjacent epithelium. Ileum differed from jejunum in that refeeding did not increase bowel mass or IGF-I mRNA to ad libitum values. Differences in exposure to luminal nutrient may underlie distinct responses of the two segments. Rats fed elemental diet intravenously showed reduced jejunal mass but not reduced jejunal IGF-I mRNA compared with rats fed oral elemental diet. Elemental nutrient given intravenously or orally therefore does not differ in effects on jejunal IGF-I expression. Complex luminal nutrient may, however, regulate jejunal IGF-I expression.

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