Dataset Information

Kraan199_Kinetics of Cortisol Metabolism and Excretion.

ABSTRACT: A new model is proposed to study the kinetics of [3H]cortisol metabolism by using urinary data only. The model consists of 5 pools, in which changes of the fractions of dose are given by a system of 5 ordinary differential equations. After i.v. administration of [3H]cortisol to 8 multiple pituitary deficient (MPD) patients (group I) the urines from each patient were collected in 9-15 portions during the following 3 days. From the urinary data the rate constants of cortisol metabolism were calculated. A published set of urinary data from patients with a normal cortisol metabolism (group II) was used for comparison. The overall half-life of the label in the circulation was 30 min for both groups; the half-life of the label excretion by both groups was 6 h and the time of maximal activity in the main metabolizing pool was 1.8 h in group I and 1.5 h in group II. The 20% of normal cortisol production rate (CPR) in the 8 MPD patients amounted to 7.2 + 1.9/zmol/(m2*d). Therefore, the low CPR but normal rate constants, i.e. a normal metabolic clearance rate of cortisol, in the MPD patients suggest a sensitive adjustment of the cortisol response in the target organs.

SUBMITTER: Ahmad Zyoud

PROVIDER: BIOMD0000000916 | BioModels | 2024-09-02

REPOSITORIES: BioModels

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	BIOMD0000000916?filename=Kraan1992-biopax2.owl	Owl
	BIOMD0000000916?filename=Kraan1992-biopax3.owl	Owl
	BIOMD0000000916?filename=Kraan1992-matlab.m	Other
	BIOMD0000000916?filename=Kraan1992-octave.m	Other
	BIOMD0000000916?filename=Kraan1992.cps	Other

Items per page:

1 - 5 of 12

Publications

Kinetics of cortisol metabolism and excretion. A hypothetic model based on the cumulative urinary radioactivity in eight multiple pituitary deficient patients.

Kraan G P GP Drayer N M NM de Bruin R R

The Journal of steroid biochemistry and molecular biology 19920401 2

A new model is proposed to study the kinetics of [3H]cortisol metabolism by using urinary data only. The model consists of 5 pools, in which changes of the fractions of dose are given by a system of 5 ordinary differential equations. After i.v. administration of [3H]cortisol to 8 multiple pituitary deficient (MPD) patients (group I) the urines from each patient were collected in 9-15 portions during the following 3 days. From the urinary data the rate constants of cortisol metabolism were calcul ...[more]

PMID: 1567783

Similar Datasets

Project description:This a model from the article: A computer simulation of the hypothalamic-pituitary-adrenal axis. Gonzalez-Heydrich J, Steingard RJ, Kohane I. Proc Annu Symp Comput Appl Med Care 1994;:1010 7949852 , Abstract: This paper describes the construction of a computer model that simulates the hypothalamic-pituitary-adrenal axis (HPA axis) regulation of cortisol production. It is presented to illustrate the process of physiological modeling using standard "off the shelf" technologies. The model simulates components of the HPA axis involved in the continuous secretion and elimination of cortisol, adrenocorticotropin (ACTH), and corticotropin releasing hormone (CRH). The physiological relations of these component pieces were modeled based on the current knowledge of their functioning. Rate constants, half lives, and receptor affinities were assigned values derived from the experimental literature. At its current level of development the model is able to accurately simulate the timing, magnitude and decay of the ACTH and cortisol concentration peaks resulting from the ovine-CRH stimulation test in normal and hypercortisolemic patients. The model will be used to predict the effects of lesions in different components of the HPA axis on the time course of cortisol and ACTH levels. We plan to use the model to explore the experimental conditions required to distinguish mechanisms underlying various disorders of the HPA axis, particularly depression. Efforts are currently underway to validate the model for a large variety of normal and pathological perturbations of the HPA axis. This model was taken from the CellML repository and automatically converted to SBML. The original model was: Gonzalez-Heydrich J, Steingard RJ, Kohane I. (1994) - version02 This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information. In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not.. To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.