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PubMed1988

A model for in vitro studies of epidermal homeostasis: proliferation and involucrin synthesis by cultured human keratinocytes during recovery after stripping off the suprabasal layers.

In normal epidermis there is a balance between the rate of cell division and the rate of terminal differentiation. This can be perturbed by injuries such as wounding or tape-stripping, but is reestablished during recovery. The aim of the studies described in this report was to assess whether cultures of human keratinocytes could be used as an experimental model for investigating the mechanism by which epidermal homeostasis is established and maintained. The suprabasal layers were stripped from confluent keratinocyte cultures by incubation in low-calcium medium (0.1 mM calcium ions). After return to normal medium (2 mM calcium ions), the basal layer regenerated a stratified culture of approximately the same thickness as controls. The kinetics of proliferation and terminal differentiation were monitored by measuring the total number of cells and proportion of involucrin-positive cells at intervals before, during, and after stripping. During recovery the proportion of cells expressing involucrin, assessed by immunofluorescence microscopy and polyacrylamide gel electrophoresis, rapidly returned to control levels, but the total number of cells per dish rose more slowly and often failed to reach control values. Thus, terminal differentiation was initially stimulated at the expense of proliferation. Our in vitro model of epidermal regeneration should provide a useful complement to intact skin and animal models for analyzing epidermal homeostasis.

Cell Differentiation↗
PubMed2001

Assessing homeostasis through circadian patterns.

An organism is thought to be in a dynamic state of homeostasis when each physiological and behavioral system reaches a delicate balance within the framework of other regulatory processes. Many biological systems target specific set-point variables and generate circadian patterns. In this article, we focus on specific measurements representative of two systems, namely deep-body temperature and activity counts. We examine data collected every 30 minutes in mice, assume there are underlying circadian patterns, and extend the approach presented in Brumback and Rice (1998, Journal of the American Statistical Association 93, 961-976) in order to obtain estimates in the presence of correlated data. We then assess homeostasis using these estimates and their statistical properties.

Animals↗
PubMed2004

The osmolyte strategy of normal human keratinocytes in maintaining cell homeostasis.

Compatible organic osmolytes, such as betaine, myoinositol, and taurine, are involved in cell volume homeostasis as well as in cell protection, for example, against oxidative stress. This so-called osmolyte strategy requires the expression of specific osmolyte transporting systems such as the betaine/gamma-amino-n-butyric acid (GABA) transporter, the sodium-dependent myoinositol transporter and the taurine transporter (TAUT). In contrast to liver, kidney, and neural cells, nothing is known about osmolytes in the skin. Here we report that primary normal human keratinocytes (NHK) express mRNA specific for the betaine/GABA transporter, for the sodium-dependent myoinositol transporter and for the TAUT. In comparison to normoosmotic (305 mosmol per L) controls, a 3-5-fold induction of mRNA expression for the betaine/GABA-, the sodium-dependent myoinositol- and the TAUT was observed within 6-24 h after hyperosmotic exposure (405 mosmol per L). Expression of osmolyte transporters was associated with an increased uptake of radiolabeled osmolytes. Conversely, hypoosmotic (205 mosmol per L) stimulation induced significant efflux of these osmolytes. Exposure to ultraviolet B (290-315 nm) or ultraviolet A (340-400 nm) radiation, which are major sources of oxidative stress in skin, significantly stimulated osmolyte uptake. Increased osmolyte uptake was associated with upregulation of mRNA steady-state levels for osmolyte transporters in irradiated cells. These studies demonstrate that NHK possess an osmolyte strategy, which is important for their capacity to maintain cell volume homeostasis and seems to be part of their response to UV radiation.

Betaine↗
PubMed2006

Longitudinal assessment of insulin sensitivity in pregnancy. Validation of the homeostasis model assessment.

OBJECTIVE: To validate the use of the homeostasis model assessment (HOMA) for measurement of insulin sensitivity in obese women during gestation and the postpartum period. DESIGN: Three consecutive measurements of insulin resistance (IR) were performed during and after pregnancy to compare the homeostasis model assessment insulin sensitivity index (HOMA-IR) to glucose utilization rates obtained during hyperinsulinaemic euglycaemic clamps (G(Rd)). PATIENTS: Six obese women (mean second trimester BMI = 30.4 kg/m(2)) with normal glucose tolerance were studied during the second and third trimesters of pregnancy and once in the postpartum period. Thus, there were a total of 18 measurements for analysis. RESULTS: Correlations between the rate of glucose disappearance (G(Rd)) (the gold standard) and the HOMA-derived metabolic parameters of insulin sensitivity were significant, with a multiple R(2) of 43.5% (P = 0.003). However, when controlling for variations between patients using dummy variables, we observed that one patient differed from the other five in the relationship between G(Rd) and HOMA-IR. Applying this regression we obtained a R(2) of 72.6% (P < 0.001). When the regression constant was omitted, we observed that the individual trends during pregnancy and postpartum in two patients differed statistically from the other patients between the two assessments, and we obtained a multiple R(2) of 97.3% (< 0.001). CONCLUSIONS: HOMA estimation of insulin resistance is appropriate for use during both the second and third trimesters of pregnancy and postpartum in obese women with normal glucose tolerance. It lacks sensitivity for the evaluation of individuals, where more precise measures of insulin sensitivity should be utilized.

Adult↗
PubMed2006

Functional characterization of calcium sensing receptor polymorphisms and absence of association with indices of calcium homeostasis and bone mineral density.

OBJECTIVES: Associations between calcium-sensing receptor (CaSR) polymorphisms and serum calcium, PTH and bone mineral density (BMD) have been reported by six studies. However, three other studies have failed to detect such associations. We therefore further investigated three CaSR coding region polymorphisms (Ala986Ser, Arg990Gly and Gln1011Glu) for associations with indices of calcium homeostasis and BMD and for alterations in receptor function. PATIENTS AND DESIGN: One hundred and ten adult, Caucasian, female, dizygotic twin pairs were investigated for associations between the three CaSR polymorphisms and serum calcium, albumin, PTH, 25-hydroxyvitamin D(3) (25OHD(3)), 1,25-dihydroxyvitamin D(3)[1,25(OH)(2)D(3)], urinary calcium excretion and BMD. Each polymorphic CaSR was also transfected into HEK293 cells and functionally evaluated. RESULTS: There was a lack of association between each of these three CaSR polymorphisms and serum calcium corrected for albumin, PTH, 25OHD(3), 1,25(OH)(2)D(3), urinary calcium excretion or BMD at the hip, forearm and lumbar spine. These findings were supported by a lack of functional differences in the dose-response curves of the CaSR variants, with the EC(50) values (mean +/- SEM) of the wild-type (Ala986/Arg990/Gln1011), Ser986, Gly990 and Glu1011 CaSR variants being 2.74 +/- 0.29 mm, 3.09 +/- 0.34 mm (P > 0.4), 2.99 +/- 0.23 mm (P > 0.4) and 2.96 +/- 0.30 mm (P > 0.5), respectively. CONCLUSIONS: Our study, which was sufficiently powered to detect effects that would explain up to 5%, but not less than 1%, of the variance has revealed that the three CaSR polymorphisms of the coding region have no major influence on indices of calcium homeostasis in this female population, and that they do not alter receptor function.

Adolescent↗
PubMed1992

Effects of the new somatostatin analogue (BIM 23014) on blood glucose homeostasis in normal men.

Changes in blood glucose homeostasis induced by the new somatostatin analogue BIM 23014 (BIM) were studied. Eight normal men (study 1) received either vehicle or 1000, 2000 and 3000 micrograms BIM as a 24 h s.c. infusion. Blood glucose, plasma insulin, C-peptide, glucagon and growth hormone (GH) were measured before treatment and then hourly for 24 h. In five normal men (study 2) an oral glucose tolerance test (OGTT) was performed during vehicle infusion and then on days 1 and 7 of a continuous s.c. infusion of 2000 micrograms BIM daily for 7 days. The same biological parameters as in study 1 were measured before OGTT and then twice-hourly for 5 h. Dose-dependent and transient glucose intolerance was observed in the first half of study 1. Except for glucagon, BIM significantly (P < 0.01) reduced plasma insulin, C-peptide and GH levels. In study 2 BIM infusion induced glucose intolerance and a drop in plasma insulin and C-peptide on day 1 which disappeared on day 7 of infusion. Higher on day 7 than on day 1, plasma GH secretion was significantly (P < 0.01) reduced throughout BIM infusion. In contrast plasma glucagon levels were not modified at any time. Side-effects were abdominal cramps and diarrhoea which were observed in most subjects when increasing BIM daily dose. In conclusion, BIM infusion induced transient changes in glucose homeostasis and insulin secretion in normal men. By contrast, plasma GH levels remained reduced throughout the treatment. BIM appears to be a useful tool to selectively inhibit GH secretion.

Adult↗
PubMed2005

T-cell homeostasis in mice exposed to airborne xenobiotics.

Many effects of environmental toxic agents contribute to the deregulation of immune system homeostasis. Here we demonstrate that the effect of airborne suspended matter (ASM) on the generation of mouse T cells is reversible. This reversal can be achieved by an active process that returns the T cells to homeostasis and does not result from the simple effect of ASM deprivation. An accelerated development of thymocytes and increased influx of T-cell progenitors to the thymus in mice exposed to environmental xenobiotics has been postulated. This hypothesis has been confirmed by parallel increases in the percentages of single-positive and triple-negative thymocytes. Enhanced expression of thymocyte surface markers related to positive selection has also been observed. The pathway of T-cell progenitor development is favoured in the bone marrow of mice exposed to ASM.

Air Pollutants↗
PubMed2006

Nickel homeostasis in Escherichia coli - the rcnR-rcnA efflux pathway and its linkage to NikR function.

The nickel physiology of Escherichia coli is dominated by its Ni-Fe hydrogenase isozymes, which are expressed under anaerobic growth conditions. Hydrogenase activity in E. coli requires the NikABCDE nickel transporter, which is transcriptionally repressed by NikR in the presence of excess nickel. Recently, a nickel and cobalt-efflux protein, RcnA, was identified in E. coli. This study examines the effect of RcnA on nickel homeostasis in E. coli. Under nickel-limiting conditions, deletion of rcnA increased NikR activity in vivo. Nickel and cobalt-dependent regulation of rcnA expression required the newly identified transcriptional repressor RcnR (formerly YohL). Deletion of rcnR results in constitutive rcnA expression and a corresponding decrease in NikR activity. Purified RcnR binds directly to the rcnA promoter DNA fragment and this interaction is inhibited by nickel and cobalt. Nickel accumulation is affected differently among deletion strains with impaired nickel homeostasis. Surprisingly, in low nickel growth conditions rcnA expression is required for nickel import via NikABCDE. The data support a model with two distinct pools of nickel ions in E. coli. NikR bridges these two pools by controlling the levels of the hydrogenase-associated pool based on the nickel levels in the second pool.

Amino Acid Sequence↗
PubMed2006

Use of the glucosyltransferase UGT71B6 to disturb abscisic acid homeostasis in Arabidopsis thaliana.

A glucosyltransferase (GT) of Arabidopsis, UGT71B6, recognizing the naturally occurring enantiomer of abscisic acid (ABA) in vitro, has been used to disturb ABA homeostasis in planta. Transgenic plants constitutively overexpressing UGT71B6 (71B6-OE) have been analysed for changes in ABA and the related ABA metabolites abscisic acid glucose ester (ABA-GE), phaseic acid (PA), dihydrophaseic acid (DPA), 7'-hydroxyABA and neo-phaseic acid. Overexpression of the GT led to massive accumulation of ABA-GE and reduced levels of the oxidative metabolites PA and DPA, but had marginal effect on levels of free ABA. The control of ABA homeostasis, as reflected in levels of the different metabolites, differed in the 71B6-OEs whether the plants were grown under standard conditions or subjected to wilt stress. The impact of increased glucosylation of ABA on ABA-related phenotypes has also been assessed. Increased glucosylation of ABA led to phenotypic changes in post-germinative growth. The use of two structural analogues of ABA, known to have biological activity but to differ in their capacity to act as substrates for 71B6 in vitro, confirmed that the phenotypic changes arose specifically from the increased glucosylation caused by overexpression of 71B6. The phenotype and profile of ABA and related metabolites in a knockout line of 71B6, relative to wild type, has been assessed during Arabidopsis development and following stress treatments. The lack of major changes in these parameters is discussed in the context of functional redundancy of the multigene family of GTs in Arabidopsis.

Abscisic Acid↗
PubMed2007

Single-stranded DNA binding factor AtWHY1 modulates telomere length homeostasis in Arabidopsis.

Telomere homeostasis, a process that is essential for the maintenance of chromosome integrity, is regulated by telomerase and a collection of associated proteins. By mass spectrometry we have identified a new telomeric protein encoded by the AtWHY1 (Arabidopsis thaliana Whirly 1) gene in Arabidopsis. AtWHY1 specifically binds the single-stranded plant telomeric DNA sequences, but not double-stranded telomeric DNA. To gain insights into the function of AtWHY1 in telomere biogenesis, we have identified two Arabidopsis lines harboring T-DNA insertions in AtWHY1. These lines exhibit neither growth nor developmental defects. However, AtWHY1-deficient plants show a steady increase in the length of telomere tracts over generations. This telomere elongation is correlated with a significant increase in telomerase activity. On the contrary, transgenic plants expressing AtWHY1 show a decreased telomerase activity and shortened telomeres. The evidence presented here indicates that AtWHY1 is a new family of telomere end-binding proteins that plays a role in regulating telomere-length homeostasis in Arabidopsis.

Amino Acid Sequence↗
PubMed1993

Effects of 2-, 4- and 12-hour fasting intervals on preoperative gastric fluid pH and volume, and plasma glucose and lipid homeostasis in children.

We evaluated 105 randomly-selected unpremedicated children aged 1-14 years to determine the effects of a 2-, 4- and 12-h preoperative fasting interval on the preoperative gastric fluid pH and volume, and plasma glucose and lipid homeostasis. Each child undergoing elective surgery ingested a large volume (approximately 10 ml/kg b.w.) of apple juice and then fasted for 2, 4 or 12 h before the estimated induction of anaesthesia. After induction of anaesthesia, gastric fluid was aspirated through a large-bore, multiorifice orogastric tube. Plasma concentrations of glucose, total ketone bodies, non-esterified fatty acid (NEFA), triglycerides, and cortisol were measured at the time of induction to evaluate the fasting interval effects on preoperative plasma glucose and lipid homeostasis. There were no significant differences between the three groups in either gastric fluid volume or pH. In addition, there were no significant differences between the groups with respect to the proportion with a pH < 2.5 and volume > 0.4 ml/kg b.w. Neither plasma concentrations of glucose, triglycerides, nor cortisol at the time of anaesthetic induction differed between the three groups. Both 4 and 12 h nil per os (NPO) caused an increase in lipolysis, which was presumably a compensatory mechanism to maintain normoglycaemia. The plasma NEFA and total ketone bodies concentrations were therefore significantly higher in these two fasting intervals than in 2 h NPO. These data suggest that a 2-h NPO, after a large volume of ingested apple juice, may offer additional benefits by preventing an increase in lipolysis during the fasting interval without either increasing the volume of gastric fluid or decreasing the gastric pH.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Homeostasis-securing therapy and statusmetria.

Statusmetria allows to define the effective levels of oxygen status. The conception of Syndrome Intensive Care (SIC) has exhausted itself and invariable outcomes of SIC of Multiorgan System Failure (MOSF) confirms that. Therefore, an alternative to SIC should be advanced. Efficiency of treatment has been assessed in 257 patients with MOSF using values of metabolic rate and ability of the organism to cover it by oxygen and substrate supply. Oxygen Pulse (OP) and Index of Efficacy of Oxygen Transport (IETO2) were monitored. Intensive care was considered to be Homeostasis-Securing Therapy (HST) if the energostructure deficit was eliminated and the necessary recovery of regeneration rate was restored. OP in patients with MOSF was 0.8 mL.m-2 or less and IETO2 was 2.4 units in SIC. We managed to maintain an OP of 1.0-1.7 mL.m-2 and an IETO2 of 1.9-2.4 units in HST. 41 patients out of 135 with MOSF survived in SIC and 96 patients out of 122 survived in HST. The efficiency of HST appeared to be twice as much as the efficiency of SIC. Conception of homeostasis-securing therapy is advancing. The conception provides restoration of regeneration rate due to the effective elimination of energostructure deficit compared to SIC. The concept may be a basis of a new technology for the treatment of MOSF.

Adult↗
PubMed1996

Abundant calcium homeostasis machinery in rat dental enamel cells. Up-regulation of calcium store proteins during enamel mineralization implicates the endoplasmic reticulum in calcium transcytosis.

UNLABELLED: Enamel cells handle large amounts of calcium, particularly during the developmental phase (termed maturation) when dental enamel is hypermineralized. The extent of intracellular calcium burden, and the nature of calcium homeostasis machinery used to accommodate it, are largely unknown. Here, the calcium-binding capacity of enamel cell cytosol was found to increase during development, in parallel with the putative transcellular flux of calcium. At maturation, the abundance of calcium-binding proteins in enamel cells exceeded that in brain and other established calcium-oriented tissues, which implies a large calcium burden. A search for likely cytosolic calcium transporters revealed only one high-affinity calcium-binding protein (12 kDa, distinguished from alpha-parvalbumin) that was up-regulated during maturation, but its low abundance (0.02% of soluble protein) precluded a major calcium transport or cytoprotective role. Two low-affinity calcium-binding proteins up-regulated during maturation (by 1.8-fold and 2.1-fold respectively) were identified as calreticulin and endoplasmin, both residents of the endoplasmic reticulum. Together, calreticulin and endoplasmin constituted an exceptionally high proportion (5%) of soluble protein during maturation, which gives an inferred calcium capacity 67-fold higher than that of the principal cytosolic calcium-binding protein. 28-kDa calbindin. Evidence that endoplasmin expression varied inversely with serum calcium concentration, and that the inositol trisphosphate receptor also was highly expressed during maturation, supported the novel hypothesis that non-mitochondrial calcium stores play a major role in transcellular calcium transport. IN CONCLUSION: (a) enamel cells contain a general high abundance of calcium homeostasis proteins, consistent with a heavy intracellular calcium burden; (b) the expression pattern (phenotype) of calcium-binding proteins varies with enamel cell function; (c) enamel cells appear to contain unusually large non-mitochondrial calcium stores; (d) contrary to the prevailing view that calcium passes mainly through the cytosol of calcium-transporting cells, the findings imply a route through the endoplasmic reticulum. This study gives novel information about how a highly calcium-oriented tissue avoids calcium toxicity, and provides a new focus for investigations into the mechanisms of transcellular calcium transport.

Animals↗
PubMedDate not supplied

Effects of draught load exercise and training on calcium homeostasis in horses.

This study was conducted to investigate the effects of draught load exercise on calcium (Ca) homeostasis in young horses. Five 2-year-old untrained Standardbred horses were studied in a 4-month training programme. All exercise workouts were performed on a treadmill at a 6% incline and with a constant draught load of 40 kg (0.44 kN). The training programme started with a standardized exercise test (SET 1; six incremental steps of 5 min duration each, first step 1.38 m/s, stepwise increase by 0.56 m/s). A training programme was then initiated which consisted of low-speed exercise sessions (LSE; constant velocity at 1.67 m/s for 60 min, 48 training sessions in total). After the 16th and 48th LSE sessions, SETs (SET 2: middle of training period, SET 3: finishing training period) were performed again under the identical test protocol of SET 1. Blood samples for blood lactate, plasma total Ca, blood ionized calcium (Ca(2+)), blood pH, plasma inorganic phosphorus (P(i)) and plasma intact parathyroid hormone (PTH) were collected before, during and after SETs, and before and after the first, 16th, 32nd and 48th LSE sessions. During SETs there was a decrease in ionized Ca(2+) and a rise in lactate, P(i) and intact PTH. The LSEs resulted in an increase in pH and P(i), whereas lactate, ionized Ca(2+), total Ca and intact PTH were not affected. No changes in Ca metabolism were detected in the course of training. Results of this study suggest that the type of exercise influences Ca homeostasis and intact PTH response, but that these effects are not influenced in the course of the training period.

Animals↗
PubMed1995

Role of atrial natriuretic peptide in long-term volume homeostasis.

1. Long-term volume homeostasis is linked very closely to long-term arterial pressure control through the renal-body fluid feedback mechanism. A key feature of this control system is the ability of the kidneys to respond to changes in arterial pressure by altering renal excretion of salt and water, often referred to as renal-pressure natriuresis. 2. Quantitative studies indicate that ANP secretion is relatively sensitive to changes in atrial pressure and that the rate of hormonal secretion does not adapt to continuous long-term stimulation. 3. Under normal conditions, the renal-body fluid feedback mechanism for arterial pressure control is very efficient in minimizing changes in body fluid volumes during alterations in sodium intake. Therefore, only small changes in atrial pressure and ANP secretion occur. Alterations in plasma ANP concentration within physiological levels have little effect on renal-pressure natriuresis and, therefore, have little impact on volume homeostasis. 4. When the renal-body fluid feedback mechanism for arterial pressure control is impaired and body fluid volumes are elevated, such as in heart failure, large increases in atrial pressure and ANP secretion occur. The resultant pathophysiological plasma levels of ANP exert sustained natriuretic effects and chronically shift renal-pressure natriuresis to lower arterial pressures. In the absence of this chronic effect of ANP on renal-pressure natriuresis, reduced arterial pressure in compensated heart failure would result in protracted retention of salt and water and additional increments in body fluid volumes.

Animals↗
PubMed1996

Integrative role of the lamina terminalis in the regulation of cardiovascular and body fluid homeostasis.

1. Cardiovascular and body fluid homeostasis depends upon the activation and co-ordination of reflexes and behavioural responses. In order to accomplish this, the brain receives and processes both neural and chemical input. Once in the brain, information from sources signalling the status of the cardiovascular system and body fluid balance travels, and is integrated, throughout a widely distributed neural network. Recent studies using neuroanatomical and functional techniques have identified several key areas within this neural network. One major processing node is comprised of structures located along the lamina terminalis. 2. Structures associated with the lamina terminalis include the median preoptic nucleus (MePO) and two sensory circumventricular organs (SCVO), the subfornical organ (SFO) and the organum vasculosum of the lamina terminalis (OVLT). Current evidence indicates that blood-borne signals, such as angiotensin II (AngII), reach SCVO (e.g. SFO) where they are transduced. This information is then carried via neural pathways to brain nuclei (e.g. MePO) where it is integrated with other inputs, such as those derived from systemic arterial blood pressure and volume receptors. 3. Because of their receptive and integrative functions, lamina terminalis structures are essential for the normal control of hormone release (e.g. vasopressin), sympathetic activation and behaviours (thirst and salt appetite), which collectively contribute to maintenance of cardiovascular and body fluid homeostasis.

Adrenergic Fibers↗
PubMed1998

Role of the mesolimbic dopamine system in cardiovascular homeostasis. Stimulation of the ventral tegmental area modulates the effect of vasopressin on blood pressure in conscious rats.

1. The possible role of the ventral tegmental area (VTA) and its dopaminergic projections in cardiovascular regulation is reviewed. 2. Our own work has shown that stimulation of the VTA by local microinjection of the substance P analogue DiMe-C7 caused an increase in blood pressure. The mechanism of the pressor response was an interaction of central dopaminergic activation, most likely at the level of the baroreflex, with the circulatory actions of vasopressin. 3. These findings are important for a possible role of the mesolimbic dopamine system in cardiovascular homeostasis. Several studies reviewed here show that neuronal activity of the VTA and its mesolimbic projections is altered by changes in blood pressure, salt and electrolyte balance, stress and food and water intake. 4. The VTA and mesolimbic dopamine system, while playing a widely accepted role in locomotor activity, cognition and reward mechanisms, may also be involved in the integration of sensory and behavioural information with cardiovascular homeostasis.

Animals↗
PubMed1977

Potassium homeostasis.

Potassium balance is regulated by appropriate changes in potassium excretion in the distal portion of the nephron. By contrast, potassium intake, absorption and proximal renal reabsorption do not show regulatory variation. Extracellular potassium concentration, which is a critical factor in membrane polarization, may at times vary in a direction opposite to total body content, because of altered distribution across cell membranes. Alterations in acid-base status frequently disturb homeostasis by altering potassium movement into cells, while insulin has an important regulatory effect on distribution. In general, the multiple renal and extra-renal mechanisms which prevent potassium overload are highly developed, while conservation is relatively ineffective. Consequently, depletion occurs more easily than spontaneous potassium overload. Homeostasis can be disturbed by renal impairment, excessive tissue breakdown, disturbances of acid-base balance, abnormal routes of loss, mineralocorticoid abnormalities and aberrations of sodium balance.

Acute Disease↗