PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 6806187

[What is catabolism?].

K Schultis
View original source ↗Export metadata ↓

Abstract

Disease can be differentiated from health by some stereotype phenomena of which catabolism is one of the most fundamental. It is not only a feature of the postaggression syndrome but also of the pathophysiological activity observed with chronically consuming diseases, including starvation. Any catabolic state ultimately leads to a malnutrition syndrome. Without catabolism the total vegetative switch-over to development of ergotropy as described by Hoff, is inconceivable. Ergotropy fundamentally ensures that emergency situations can be overcome, in other words, ensures survival in spite of risk to vital systems. Due to disturbed regulations, for example risk to vital systems. Due to disturbed regulations, for example induced by secondary diseases, malnutrition syndromes occurring as a result of catabolism will themselves ultimately jeopardize vital systems. Thus, they may become factors determining prognosis. The art of managing such situations is part of the progress currently available to modern-day medicine through the therapeutic device of requirement-adapted nutrition.

Explore related subjects

Energy MetabolismHumansNitrogenNutrition DisordersNutritional RequirementsParenteral NutritionPostoperative PeriodStress, PhysiologicalEnglish AbstractJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

K Schultis. 1982. [What is catabolism?].. https://pubmed.ncbi.nlm.nih.gov/6806187/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Impact of maternal nutrition and metabolism on health of the offspring.

Since the original publication of the theory of the fetal origins of adult diseases more than 15 years ago, extensive epidemiological studies have linked the environment in utero to adult health. Maternal nutrition and metabolism are major mechanisms by which the intrauterine environment programs the health of the offspring. Both growth-restricted and overgrown fetuses are at risk for postnatal disease. This paper summarizes the nutritional and metabolic causes of both these conditions and also reviews the interventions that have been tested to mitigate these effects.

Energy Metabolism↗
PubMed2006

The regulation of energy generating metabolic pathways by p53.

The function of p53 as a tumor suppressor remains undisputed. p53 has a central role in cellular stress responses as well as affecting cancer development and progression. The word "central", however, is becoming increasingly more of an understatement as the list of p53-regulated pathways and processes is ever expanding. Although much focus continues to center on p53-mediated signaling cascades that control cell growth arrest and/or apoptosis, recent work has begun to define a role for p53 in the regulation of metabolic pathways typically thought of as essential for maintaining life. With the first potential link between p53 and glycolysis reported nearly ten years ago, the topic has gained a renewed interest. Recent studies now demonstrate the ability of p53 to regulate the expression of several novel genes including PGM (phosphoglycerate mutase), TIGAR (TP53-induced glycolysis and apoptosis regulator) and, SCO2 (synthesis of cytochrome c oxidase 2), each intimately linked to the processes of glycolysis and oxidative phosphorylation. With this discovery, yet another novel means by which p53 carries out its tumor suppressor function is brought into light.

Energy Metabolism↗
PubMed2006

Bringing metabolic networks to life: convenience rate law and thermodynamic constraints.

BACKGROUND: Translating a known metabolic network into a dynamic model requires rate laws for all chemical reactions. The mathematical expressions depend on the underlying enzymatic mechanism; they can become quite involved and may contain a large number of parameters. Rate laws and enzyme parameters are still unknown for most enzymes. RESULTS: We introduce a simple and general rate law called "convenience kinetics". It can be derived from a simple random-order enzyme mechanism. Thermodynamic laws can impose dependencies on the kinetic parameters. Hence, to facilitate model fitting and parameter optimisation for large networks, we introduce thermodynamically independent system parameters: their values can be varied independently, without violating thermodynamical constraints. We achieve this by expressing the equilibrium constants either by Gibbs free energies of formation or by a set of independent equilibrium constants. The remaining system parameters are mean turnover rates, generalised Michaelis-Menten constants, and constants for inhibition and activation. All parameters correspond to molecular energies, for instance, binding energies between reactants and enzyme. CONCLUSION: Convenience kinetics can be used to translate a biochemical network--manually or automatically--into a dynamical model with plausible biological properties. It implements enzyme saturation and regulation by activators and inhibitors, covers all possible reaction stoichiometries, and can be specified by a small number of parameters. Its mathematical form makes it especially suitable for parameter estimation and optimisation. Parameter estimates can be easily computed from a least-squares fit to Michaelis-Menten values, turnover rates, equilibrium constants, and other quantities that are routinely measured in enzyme assays and stored in kinetic databases.

Energy Metabolism↗