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PubMed1975

Hepatic mitochondrial function in ketogenic states. Diabetes, starvation, and after growth hormone administration.

The study was designed to evaluate hepatic mitochondrial function during ketotic states. The ketogenic models studied were streptozotocin-induced diabetic ketoacidosis, 48 h of starvation, and after growth hormone administration. In the last-mentioned model we observed increased free fatty acids but not ketonemia. Oxidative phosphorylation was measured using the citric acid cycle substrates pyruvate and succinate, the amino acid glutamate, a ketone body beta-hydroxybutyrate, and a long-chain fatty acid palmitoyl-l-carnitine. State 3 (ADP stimulated) and state 4 (ADP limited) respiration, respiratory control ratio (state 3/state 4), and the ADP/O ratios were normal in the controls and the experimental groups. Uncoupled respiration produced by dinitrophenol with a variety of substrates was unchanged in the experimental groups compared to the controls. Fatty acid oxidation was studied in detail. The rate of utilization of palmitoyl-l-carnitine by controls or experimental groups did not depend on the product formed (citrate, acetoacetate). No significant changes were observed in the oxidation of palmitoyl-CoA (+ carnitine) or with an intermediate-chain fatty acid hexanoate. The specific activity of hepatic mitochondria carnitine palmitoyltransferase did not change in any of the three experimental groups. It is concluded that during diabetic ketoacidosis, starvation, and growth hormone administration, there is (a) no alteration in hepatic mitochondrial function; (b) no change in the intrinsic capacity of hepatic mitochondria to oxidize fatty acids; and (c) no change in the specific activity of mitochondrial carnitine palmitoyltransferase. The mechanism by which the body restrains flux through the mitochondrial oxidative machinery remains to be fully determined.

Acidosis↗
PubMed1984

Systemic response to thermal injury in rats. Accelerated protein degradation and altered glucose utilization in muscle.

Negative nitrogen balance and increased oxygen consumption after thermal injury in humans and experimental animals is related to the extent of the burn. To determine whether defective muscle metabolism is restricted to the region of injury, we studied protein and glucose metabolism in forelimb muscles of rats 48 h after a scalding injury of their hindquarters. This injury increased muscle protein degradation (PD) from 140 +/- 5 to 225 +/- 5 nmol tyrosine/g per h, but did not alter protein synthesis. Muscle lactate release was increased greater than 70%, even though plasma catecholamines and muscle cyclic AMP were not increased. Insulin dose-response studies revealed that the burn decreased the responsiveness of muscle glycogen synthesis to insulin but did not alter its sensitivity to insulin. Rates of net glycolysis and glucose oxidation were increased and substrate cycling of fructose-6-phosphate was decreased at all levels of insulin. The burn-induced increase in protein and glucose catabolism was not mediated by adrenal hormones, since they persisted despite adrenalectomy. Muscle PGE2 production was not increased by the burn and inhibition of prostaglandin synthesis by indomethacin did not inhibit proteolysis. The increase in PD required lysosomal proteolysis, since inhibition of cathepsin B with EP475 reduced PD. Insulin reduced PD 20% and the effects of EP475 and insulin were additive, reducing PD 41%. An inhibitor of muscle PD, alpha-ketoisocaproate, reduced burn-induced proteolysis 28% and lactate release 56%. The rate of PD in muscle of burned and unburned rats was correlated with the percentage of glucose uptake that was directed into lactate production (r = +0.82, P less than 0.01). Thus, a major thermal injury causes hypercatabolism of protein and glucose in muscle that is distant from the injury, and these responses may be linked to a single metabolic defect.

Adrenalectomy↗
PubMed1994

Effects of cigarette smoking and its cessation on lipid metabolism and energy expenditure in heavy smokers.

The relationship between thermogenic and potentially atherogenic effects of cigarette smoking (CS) and its cessation was investigated. Heavy smokers (n = 7, serum cotinine > 200 ng/ml, > 20 cigarettes/d) were maintained on isoenergetic, constant diets for 2 wk, 1 wk with and 1 wk without CS. Stable isotope infusions with indirect calorimetry were performed on day 7 of each phase, after an overnight fast. CS after overnight abstention increased resting energy expenditure by 5% (not significant vs. non-CS phase; P = 0.18). CS increased the flux of FFA by 77%, flux of glycerol by 82%, and serum FFA concentrations by 73% (P < 0.02 for each), but did not significantly affect fat oxidation. Hepatic reesterification of FFA increased more than threefold (P < 0.03) and adipocyte recycling increased nonsignificantly (P = 0.10). CS-induced lipid substrate cycles represented only 15% (estimated 11 kcal/d) of observed changes in energy expenditure. De novo hepatic lipogenesis was low (< 1-2 g/d) and unaffected by either acute CS or its chronic cessation. Hepatic glucose production was not affected by CS, despite increased serum glycerol and FFA fluxes. Cessation of CS caused no rebound effects on basal metabolic fluxes. In conclusion, a metabolic mechanism for the atherogenic effects of CS on serum lipids (increased hepatic reesterification of FFA) has been documented. Increased entry of FFA accounts for CS-induced increases in serum FFA concentrations. The thermogenic effect of CS is small or absent in heavy smokers while the potentially atherogenic effect is maintained, and cessation of CS does not induce a rebound lipogenic milieu that specifically favors accrual of body fat in the absence of increased food intake.

Adipocytes↗
PubMedDate not supplied

Factors contributing to increased energy expenditure in thermal injury: a review of studies employing indirect calorimetry.

In summary, a remarkably close agreement exists for the mean MEE measured in 28 studies of severe burn trauma. This is especially surprising given the variability in sample sizes, measurement techniques, study designs, and DPBs studied. The mean MEE calculated from the data published in these reports is listed in the final column of Table I. For more than 450 cases, an unweighted MEE is 2750 +/- 85 kcal/day. For those studies prior to 1980, the mean MEE exceeds 3000 kcal/day in eight of 14 reports vs only two of 14 published after 1980. Even so, the mean MEE for the pre-1980 reports differs by only 200 kcal/day (2960 +/- 120, n = 14). The accepted notion that the degree of elevation in MEE is in proportion to the % BSAB up to about 60% BSAB is useful in a general sense but must be applied with caution. The recent studies, which include proportionately more burns exceeding 80% BSAB, suggest an elevation in MEE in these cases. Nevertheless, a physiologic plateau apparently exists at or slightly below 2 x normal RMR at the peak of MEE. The magnitude of the MEE response results from an undefined interaction among several factors of which some have been examined while others such as inflammatory mediators are only beginning to receive study. The contributions to reduction in MEE from interventions to control cardiac output and peripheral cooling, core temperature, evaporative water (heat) loss, and substrate cycling have been reviewed. The importance of indirect calorimetry in patient care is highlighted by the large variability in similarly injured individuals and in the unexplained component of regression analyses.(ABSTRACT TRUNCATED AT 250 WORDS)

Burns↗
PubMedDate not supplied

The metabolic basis of the increase of the increase in energy expenditure in severely burned patients.

BACKGROUND: Severe burn trauma is characterized by an elevated rate of whole-body energy expenditure. APPROACH: In this short review, we have attempted to assess the metabolic characteristics of and basis for the persistent increase in energy expenditure during the flow phase of the injury. We consider some aspects of normal energy metabolism, including the contribution of the major adenosine triphosphate (ATP)-consuming reactions to the standard or basal metabolic rate. Rate estimates are compiled from the literature for a number of these reactions in healthy adults and burned patients, and the values are related to the increased rates of whole-body energy expenditure with burn injury. RESULTS: Whole-body protein synthesis, gluconeogenesis, urea production, and substrate cycles (total fatty acid and glycolytic-gluconeogenic) account for approximately 22%, 11%, 3%, 17%, and 4%, respectively, of the burn-induced increase in total energy expenditure. CONCLUSIONS: These ATP-consuming reactions, therefore, seem to explain approximately 57% of the increase in energy expenditure. The remainder of the increase may be due, in large part, to altered Na(+)-K(+)-ATPase activity and increased proton leakage across the mitochondrial membrane.

Adenosine Triphosphate↗
PubMed1997

Nutritional homeostasis in locusts: is there a mechanism for increased energy expenditure during carbohydrate overfeeding?

Maintenance of carbohydrate balance via changes in CO2 output volume was investigated in locusts using a flow-through respirometer. The effect of an imbalance in the dietary protein to digestible carbohydrate ratio on expired CO2 levels was measured in locusts fed one of two synthetic diets [7% protein, 21% digestible carbohydrate (7:21) and 21% protein, 7% digestible carbohydrate (21:7)]. Additionally, the effect of dietary dilution was investigated by feeding locusts one of two diets with a close-to-optimal ratio of protein to carbohydrate, one containing 7% protein and 7% digestible carbohydrate (7:7) and the other containing 21% protein and 21% digestible carbohydrate (21:21). For insects fed unbalanced diets, a higher CO2 output volume was measured during feeding on diet 7:21 when compared with insects fed on diet 21:7. Locusts also expired a greater volume of CO2 during the entire 2h observation period. This response is consistent with specific metabolic control of carbohydrate balance via enhanced respiration. For insects fed balanced diets, the total volume of CO2 expired over the duration of a meal was greater for insects fed diet 7:7 than for those fed diet 21:21, although this was due entirely to meals lasting longer on the more dilute diet. However, the basal level of respiration rate was greater for insects fed diet 21:21 and, as a result, over the entire 2h period, CO2 output volume did not differ between locusts fed diet 7:7 or 21:21. A possible mechanism for enhanced CO2 output volume on the nutritionally unbalanced diet was investigated, namely triglyceride/fatty-acid substrate cycling. There was no evidence for the presence of the thermogenic effect of this particular cycle on locusts as a means for dealing with excess ingested carbohydrate.

Journal Article↗
PubMedDate not supplied

Diphosphoinositol polyphosphates: the final frontier for inositide research?

The diphosphoinositol polyphosphates comprise a group of highly phosphorylated compounds which have a rapid rate of metabolic turnover through tightly-regulated kinase/phosphohydrolase substrate cycles. The phosphohydrolases occur as multiple isoforms, the expression of which is apparently carefully controlled. Cellular levels of the diphosphoinositol polyphosphates are regulated by cAMP and cGMP in a protein kinase-independent manner. These inositides can also sense a specific mode of intracellular Ca2+ pool depletion. In this review, we will argue that these are characteristics of highly significant cellular molecules.

Acid Anhydride Hydrolases↗
PubMed1985

The presence of glucose increases the lethal effect of alpha-chlorohydrin on ram and boar spermatozoa in vitro.

Ram cauda epididymal spermatozoa were incubated for 10 min at 34 degrees C with or without 1.0 mM-RS-alpha-chlorohydrin before (1) 5 mM-D-glucose or (2) 10 mM-L-lactate plus 1 mM pyruvate or (3) 5 mM-D-glucose plus 10 mM-L-lactate plus 1 mM-pyruvate or (4) no substrate was added. Without alpha-chlorohydrin, the motility, the ATP concentration and the energy charge of the spermatozoa were maintained for 240 min by substrate combinations 1-3 but with no added substrate (4) the motility declined after 60 min. All the values decreased dramatically after 10 min in spermatozoa exposed to alpha-chlorohydrin in substrate conditions 1 and 3 (glucose present) but alpha-chlorohydrin had no significant effect in conditions 2 and 4 (no glucose) except after prolonged incubation. In a dose-response experiment glucose-dependent ATP dissipation began to occur with 0.025 mM-RS-alpha-chlorohydrin. A similar effect was seen in boar spermatozoa exposed to 0.1-5.0 mM-alpha-chlorohydrin and 5 mM-D-glucose. With boar spermatozoa the presence of 10 mM-L-lactate and 1 mM-pyruvate as well as glucose prevented the loss of ATP. We conclude that this concerted action of alpha-chlorohydrin and glucose is probably responsible for the contraceptive action of alpha-chlorohydrin and propose that it may depend on 'futile substrate cycling' in the glycolytic pathway.

Adenosine Triphosphate↗
PubMed1988

Inhibitory effects of (S)-3-chlorolactaldehyde on the metabolic activity of boar spermatozoa in vitro.

(S)-alpha-Chlorohydrin and 3-chloro-1-hydroxyacetone inhibited the oxidative metabolism of fructose by boar spermatozoa only after a period of incubation in which they presumably underwent conversion to (S)-3-chlorolactaldehyde, an inhibitor of sperm glyceraldehyde 3-phosphate dehydrogenase. With glycerol as substrate, 3-chloro-1-hydroxyacetone had a similar effect, (S)-alpha-chlorohydrin was ineffective while (R,S)-3-chlorolactaldehyde was immediately effective with either substrate. All three compounds caused the accumulation of fructose 1,6-bisphosphate and dihydroxyacetone phosphate from fructose but not from glycerol which led to the conclusion that inhibition of triosephosphate isomerase was also associated with the anti-glycolytic action of (S)-3-chlorolactaldehyde. (S)-3-Chlorolactaldehyde caused the depletion of ATP in incubates of boar spermatozoa metabolizing fructose but not glycerol. This suggests that futile substrate cycling may play an important function in the anti-glycolytic action of (S)-3-chlorolactaldehyde and/or that boar spermatozoa can synthesize ATP from glycerol by a mechanism not involving the glycolytic pathway.

Acetone↗
PubMed2002

Unregulated elevation of glutamate dehydrogenase activity induces glutamine-stimulated insulin secretion: identification and characterization of a GLUD1 gene mutation and insulin secretion studies with MIN6 cells overexpressing the mutant glutamate dehydrogenase.

Glutamate dehydrogenase (GDH) is important in normal glucose homeostasis. Mutations of GDH result in hyperinsulinism/hyperammonemia syndrome. Using PCR/single-strand conformation polymorphism analysis of the gene encoding GDH in 12 Japanese patients with persistent hyperinsulinemic hypoglycemia of infancy (PHHI), we found a mutation (Y266C) in one PHHI patient. This mutation was not found in any of the control or type 2 diabetic subjects. The activity of the mutant GDH (GDH266C), expressed in COS-7 cells, was constitutively elevated, and allosteric regulations by ADP and GTP were severely impaired. The effect of the unregulated increase in GDH activity on insulin secretion was examined by overexpressing GDH266C in an insulinoma cell line, MIN6. Although glutamine alone did not stimulate insulin secretion from control MIN6-lacZ, it remarkably stimulated insulin secretion from MIN6-GDH266C. This finding suggests that constitutively activated GDH enhances oxidation of glutamate, which is intracellularly converted from glutamine to alpha-ketoglutarate, a tricarboxylic acid cycle substrate, which thereby stimulates insulin secretion. Interestingly, insulin secretion is also exaggerated significantly at low glucose concentrations (2 and 5 mmol/l) but not at higher glucose concentrations (8--25 mmol/l). Our results directly illustrate the importance of GDH in the regulation of insulin secretion from pancreatic beta-cells.

Adenosine Diphosphate↗
PubMed1990

Fructose-2,6-bisphosphate in control of hepatic gluconeogenesis. From metabolites to molecular genetics.

Hormonal regulation of hepatic gluconeogenic pathway flux is brought about by phosphorylation/dephosphorylation and control of gene expression of several key regulatory enzymes. Regulation by cAMP-dependent phosphorylation occurs at the level of pyruvate kinase and 6-phosphofructo-2-kinase (6PF-1-K)/fructose-2,6-bisphosphatase (Fru-2,6-P2ase). The latter is a unique bifunctional enzyme that catalyzes both the synthesis and degradation of fructose-2,6-bisphosphate (Fru-2,6-P2), which is an activator of 6PF-1-K and an inhibitor of Fru-1,6-P2ase. The bifunctional enzyme is a homodimer whose activities are regulated by cAMP-dependent protein kinase-catalyzed phosphorylation at a single NH2-terminal seryl residue/subunit, which results in activation of the Fru-2,6-P2ase and inhibition of the PF-1-K reactions. Hormone-mediated changes in the phosphorylation state of the bifunctional enzyme are responsible for acute regulation of Fru-2,6-P2 levels. 6PF-2-K/Fru-2,6-P2ase thus provides a switching mechanism between glycolysis and gluconeogenesis in mammalian liver. Pyruvate kinase is regulated by both phosphorylation and allosteric effectors. Fru-1,6-P2, an allosteric activator, also inhibits cAMP-dependent enzyme phosphorylation, and its steady-state concentration is indirectly determined by the level of Fru-2,6-P2. Therefore, acute regulation of both pyruvate kinase and the bifunctional enzyme provide coordinated control at both the pyruvate/phosphoenolpyruvate and Fru-6-P/Fru-1,6-P2 substrate cycles. The Fru-2,6-P2 system is also subject to complex multihormonal long-term control through regulation of 6 PF-2-K/Fru-2,6-P2ase gene expression. Glucocorticoids are the major factor in turning on this gene in liver, but insulin is also a positive effector. cAMP prevents the effects of glucocorticoids and insulin. Although Fru-2,6-P2 plays a key role in the regulation of carbon flux in the gluconeogenic pathway, the regulation of this flux depends on several factors and regulation of other key enzymes whose importance varies depending on the dietary and hormonal status of the animal. Molecular cloning of the cDNA encoding PF-2-K/Fru-2,6-P2ase has elucidated its structure and permitted analysis of its evolutionary origin as well as its tissue distribution and control of its gene expression. The rat liver and skeletal muscle isoforms arose by alternative splicing of a single gene. The muscle form differs from the liver form only at the NH2-terminal and does not have a cAMP-dependent protein kinase phosphorylation site. The hepatic enzyme subunit consists of 470 amino acids.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acid Sequence↗
PubMed1992

Recent developments in metabolism that impinge on research into the nature and treatment of diabetes mellitus.

It has been established that adenosine, its agonists, or antagonists can cause dramatic changes in insulin sensitivity in isolated soleus muscle and, moreover, can modify changes in sensitivity caused by pathophysiological conditions. Addition of adenosine deaminase to the incubation medium, which is known to lower the concentration of adenosine, increases the sensitivity of glycolysis to insulin. Addition of an adenosine-receptor agonist decreases sensitivity by about 10-fold, whereas addition of an adenosine-receptor antagonist increases sensitivity by about 10-fold. The latter totally removes the resistance of glucose utilization to insulin in the isolated soleus muscle obtained from either the genetically obese rat or from the rat fed a high sucrose diet. These findings strongly support the view that changes in insulin sensitivity in muscle can be brought about either by acute changes in the local concentration of adenosine or in the affinity or number of receptors for adenosine in muscle. However, in many of the conditions investigated, in which insulin sensitivity in muscle is changed, there was no correlation between the change in the adenosine content of the muscle and altered insulin sensitivity. It has also been shown that prostaglandin E1 can increase dramatically the sensitivity of glycolysis to insulin and that this is a specific effect of prostaglandins of the E series. It is not produced by prostacyclins, thromboxanes, or leukotrienes. It is unclear if there is a relationship between the effects of adenosine and prostaglandins. Chronic elevation of catecholamines may increase the sensitivity of glucose utilization to insulin and also increase the rate of thermogenesis by substrate cycling.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1992

A mathematical integration of energy and amino acid metabolism of lactating sows.

A dynamic mathematical model of energy and protein metabolism of lactating sows is described in this article. The model is designed to contribute to a systematic and quantitative understanding of the biological connection between diet and reproduction. It traces the flow of energy-containing nutrients from absorption through intermediary metabolism, into and out of body stores, and into milk. State variables (pools) include lysine, other amino acids, glucose, fatty acids, acetate, propionate, acetyl-coenzyme A, ATP, oxygen, carbon dioxide, urea, lean-body protein, visceral protein, storage triacylglycerol, milk protein, milk triacylglycerol, and milk lactose. The rate of each transaction is a function of substrate and inhibitor concentrations, assuming saturable kinetics. Protein and fat turnover, substrate cycles, and the energy cost of membrane transport are explicitly considered. Dynamic simulation of a complete lactation is accomplished by iterating the numerical integration of 16 first-order, nonlinear differential equations, each associated with a pool. Most kinetic parameters were estimated indirectly. Preliminary tests suggest the model is sound. It promises to be useful as a research tool and, with further development, as a guide to practical feeding strategies.

Absorption↗
PubMed1990

Some experiments on factors that can change insulin sensitivity.

Local hormones such as adenosine or prostaglandins can dramatically change the sensitivity of glucose transport in muscle to insulin. It is possible that these factors may play a role in changes in insulin sensitivity in vivo produced by such diverse conditions as treatment with furosemide, thyroid status or catecholamine status. In particular, there is evidence that chronic elevation of catecholamine or sympathetic stimulation improves insulin sensitivity. Evidence is also available to support the view that elevation of plasma catecholamine concentrations results in increased thermogenesis through activation of substrate cycling in a number of tissues. Consequently, insulin resistance and decreased thermogenesis may be explained by decreased levels of catecholamines and/or a decreased sensitivity of skeletal muscle and perhaps other tissues to catecholamines or a decreased activity of the sympathetic nervous system.

Adenosine↗
PubMed1998

Inhibitors of glutathione reductase as potential antimalarial drugs. Kinetic cooperativity and effect of dimethyl sulphoxide on inhibition kinetics.

We have developed inhibitors of glutathione reductase that improve on the inhibition of literature lead compounds by up to three orders of magnitude. Thus, analogues of Safranine O and menadione were found to be strong, reversible inhibitors of yeast glutathione reductase. Safranine O exhibited partial, uncompetitive inhibition with Ki and alpha values of 0.5 mM and 0.15, respectively. Thionine O was a partial (hyperbolic) uncompetitive inhibitor with Ki and alpha values of 0.4 microM and 0.15, respectively. LY83583 and 2-anilino-1,4-naphthoquinone also showed (hyperbolic) partial, uncompetitive inhibition with micromolar Ki values. For Nile Blue A a model for two-site binding with (parabolic) uncompetitive inhibition fitted the data with a Ki value of 11 microM and a kinetic cooperativity between the sites of 0.12, increased to 0.46 by preincubation of the enzyme and Nile Blue A in the presence of glutathione disulphide. Analysis of the effects of preincubation on the kinetics and cooperativity indicated the possibility of a slow conformational change in the homodimeric enzyme, the first such indication of kinetic cooperativity in the native enzyme to our knowledge. Further evidence of conformational changes for this enzyme came from studies of the effects of dimethyl sulphoxide which indicated that this co-solvent, which at low concentrations has no apparent effect on initial velocities under normal assay conditions, induced a slow conformational change in the enzyme. Thionine O, Nile Blue A and LY83583 were redox-cycling substrates producing superoxide ion, detectable by means of cytochrome c reduction, but leading to no loss of glutathione reductase activity, under aerobic or anaerobic conditions. The water-soluble Safranine analogues Methylene Blue, Methylene Green, Nile Blue A and Thionine O (5 mg/kg i.p. x 5) were effective antimalarial agents in vivo against P. berghei, but their effect was small and a higher dose (50 mg/kg i.p. x 1) was toxic in mice. Comparison was made with human glutathione reductase and its literature-reported interactions with several tricyclic inhibitors as studied by X-ray diffraction. It is possible that the conformational changes detected in the present study from alterations in detailed kinetic inhibition mechanisms may shed light on information transfer through the glutathione reductase molecule from the dimer interface ligand pocket to the active-site.

Animals↗
PubMed1991

Cellular energy metabolism and regulation.

Consistent with the increased demand for nutrients imposed by lactation and growth, those tissues directly involved in the digestion, absorption, and processing of the required additional nutrients show response to these states. During lactation, the rumen, upper intestine, and liver increase in size, and more energy is spent on Na+,K+ transport and on protein turnover. The massive endocrine influences during lactation suggest that the metabolism of other tissues besides these and mammary tissue would be influenced, but evidence is rather sparse. Ion transport and protein metabolism in some muscles may indeed be increased. Although substrate cycles characteristically account for a substantially smaller portion of the energy expenditure in the intact animal than do ion transport and protein turnover, stage of lactation influences some of these cycles, particularly the triacylglycerol fatty acid cycle. The needs for additional quantitative in vivo measurements of metabolic conversions and for mechanistic model description of metabolic events in nonmammary tissues are discussed.

Absorption↗
PubMed1998

[Energy expenditure at rest and obesity].

Adult human body has to have, because of every day fluctuating energy intake and energy needs, very precious adaptive mechanisms for maintenance of heat homeostasis in the body and nearly stable body weight and body composition, which are optimal for life and reproduction. These short term functioning adaptive mechanisms are called "empty biochemical mechanisms", where chemically bound energy is transformed to heat without work performance. These mechanisms are present on the cellular level (substrates cycles, uncoupling of respiration chain), on the interorgan metabolic level (glycolysis and gluconeogenesis between liver and adipose tissue-glucose-lactate cycle). Central nervous system controls them via many factors; the most important are catecholamines, leptin, insulin, thyroid hormones, cortisol, growth and sex hormones. Neurotransmitters and neuronal net influence energy intake and other behavior. Obesity seems to be associated with the amelioration or overcoming of possibilities of function short-term effective adaptive mechanisms.

Adaptation, Physiological↗
PubMed2001

Innovative low cost procedure for nutrient removal as an integrated element of a decentralised water management concept for rural areas.

The absence of large rivers with rather high niveau of self purifying effect in parts of east Germany leads to a discharging of the effluent of wastewater treatment plants into the groundwater in many cases. One useful consequence is the idea of realisation of decentralised measures and concepts in urban water resources management concerning municipal wastewater as well as rainfall, precipitation. At the same time, only the upper soil zone--a few decimetres--is water--saturated and thus discharge effective, even when extreme rainfall takes place. Underneath, however, there generally exists an unsaturated soil zone, which is up to now a rather unexplored retardation element of the hydrologic- and substrate-cycle. Nutrient removal in small wastewater treatment plants that are emptying into ground waters is often beneficial. The presented studies optimised an inexpensive method of subsequent enhanced wastewater treatment. The developed reactor is similar to a concentrated subsoil passage. The fixed bed reactor is divided in two sections to achieve aerobic and anoxic conditions for nitrification/denitrification processes. To enhance phosphorus removal, ferrous particles are put into the aerobic zone. Two series of column tests were carried out and a technical pilot plant was built to verify the efficiency of the process. The results show that this method can be implemented successfully.

Bioreactors↗