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PubMed1994

Biological uniqueness and the definition of normality. Part 1--The concept of 'intrinsic' homeostasis.

The patterns of biochemical and physiological variables values are subject-specific and quite stable over time. Thus, within the limits imposed by physiological requirements, the composition of the 'milieu intérieur' varies between individuals. It follows that having all values of blood constituents within the norm (defined statistically from populations of healthy subjects) might not be sufficient to identify biological normality, and a revised definition of biological normality should take into account inter-individual differences. Our concept of 'intrinsic' homeostasis means that the differences between subjects' concentrations of blood constituents express subject-specific constraints in the organization of their physiology, and that these differences might play a greater role than usually recognized. We list the consequences for medical research of the existence of biological uniqueness and propose to give more importance to the study of biological 'fingerprints' and 'intrinsic' homeostasis in physiology and clinical medicine.

Homeostasis↗

PubMed1993

A model of human sleep homeostasis based on EEG slow-wave activity: quantitative comparison of data and simulations.

EEG slow-wave activity (SWA; spectral power in the 0.75-4.5 Hz band) is a function of the duration of prior waking and, thereby, an indicator of sleep homeostasis. We present a model that accounts for both the declining trend of SWA during sleep and for its variation within the successive nonrapid eye movement (non-REM) sleep episodes. The values of the model parameters were estimated by an optimization procedure in which empirical SWA of baseline nights (16 subjects, 26 nights) served as a reference. A sensitivity analysis revealed the model to be quite robust to small changes (+/- 5%) of the parameter values. The estimated parameter values were used to simulate data sets from three different experimental protocols (sleep in the evening or sleep in the morning after prolonged waking, or extended sleep initiated at the habitual bedtime; n = 8 or 9). The timing of the REM trigger parameter was derived from the empirical data. A close fit was obtained between the simulated and empirical SWA data, and even the occasional late SWA peaks during extended sleep could be reproduced. Minor discrepancies suggest indirect or direct circadian influences on SWA. The simulations demonstrate that the concept of sleep homeostasis as proposed in the two-process model of sleep regulation can be refined to account in quantitative terms for empirical data and to predict the changes induced by the prolongation of waking or sleep.

Adult↗

PubMedDate not supplied

Effect of atrial natriuretic factor (ANF) on water homeostasis of the neonate.

Atrial natriuretic factor (ANF) has been well known as a potent natriuretic peptide. The purpose of this study was to clarify the physiological role of ANF in neonates. We designed two types of study to investigate the role of ANF in neonates. (i) The role of ANF in neonatal fluid homeostasis; (ii) ANF and spontaneous diuresis. As a result, ANF may be released to control the extracellular volume and may have a role in the complex mechanisms that regulate the water homeostasis in neonates.

Atrial Natriuretic Factor↗

PubMed1985

Effects of high doses of manganese on carbohydrate homeostasis.

The effects of manganese (Mn) toxicity on carbohydrate homeostasis was examined in Sprague-Dawley and Osborne-Mendel rats. Mn injection was followed by increases in Mn concentration in both liver and pancreas. Concentrations of Mn in the pancreas increased more rapidly than in the liver. Plasma insulin levels decreased, plasma glucose levels increased, and a spike in glucagon concentration was observed following Mn injection. Increases in blood glucose in response to Mn injection were also observed in 24- and 48-h fasted rats, although the magnitude of the increase was less than that observed in fed rats. Both strains of rats appeared to respond similarly to Mn injection. The present studies demonstrate that acute Mn injection can affect glucose homeostasis. These effects may be mediated through altered endocrine pancreatic function.

Animals↗

PubMed1990

Cadmium-induced route-specific alterations in essential trace element homeostasis.

To determine if route-specific differences in essential trace element homeostasis occur after cadmium (Cd) exposure, selected metals (Zn, Fe, Ca, K, Cu, Mg, and Cd) were determined in testis, liver and lung after subcutaneous and intravenous Cd treatment. Cd by the subcutaneous route had the most pronounced effects on essential trace element homeostasis in the testes, increasing the concentration of Zn (51%), Fe (242%), Ca (95%), K (93%), and Cu (345%) in conjunction with a decrease of testicular Mg (46%), while few changes occurred with intravenous Cd. In the lung, modest changes of all elements except Ca and Cu were observed with Cd. However, alterations in Fe and Zn concentration were seen only in the liver. The present study suggests that levels of the essential metals in a particular tissue can be modified depending on the route of Cd administration.

Animals↗

PubMed1994

The effect of Rhazya stricta on glucose homeostasis in normal and streptozotocin diabetic rats.

The effect of R. stricta water extract on glucose homeostasis was studied in normal and streptozotocin diabetic rats. R. stricta had no effect on fasting glucose levels in normal and diabetic rats up to 7 h after its oral administration. In normal and diabetic rats R. stricta did not produce any significant effect on an oral glucose tolerance test (OGTT). Chronic administration of R. stricta in drinking water for 37 days did not produce any effect on the parameters of glucose homeostasis studied (plasma glucose, body weight, feed and fluid intake and plasma fructosamine) in the normal or diabetic phase of the experiment. The LD50 of R. stricta in mice was 2.36 g/kg body weight of the lyophilised extract and a daily administration of R. stricta to rats for 5 days did not produce any signs of organ damage.

Administration, Oral↗

PubMedDate not supplied

Arginine vasopressin and body fluid homeostasis in the fetal alcohol exposed rat.

Studies involving fluid homeostasis were carried out in adult Long-Evans rats born to mothers given liquid diets containing 35% of the calories derived from ethanol and compared to offspring of dams given isocaloric liquid diets containing no ethanol. Plasma levels of arginine vasopressin (AVP), plasma and urine osmolality, and urine production were determined in water-sated and water-deprived offspring. In the water-sated condition, the group exposed to alcohol prenatally had plasma levels of AVP seven-fold above control levels. This increase was associated with a large increase in within-group variability. Water consumption was also significantly elevated in the group of fetal alcohol exposed (FAE) rats. Plasma and urine osmolality and urine production were similar to control levels. In the control animals, 24-hr of water deprivation produced the expected increase in AVP, in plasma and urine osmolality, and decrease in urine production. The FAE animals, however, showed parallel changes in plasma and urine osmolality and urine production with no significant change in AVP. Examination of basal glucose metabolic rates in the cerebral structures involved in fluid homeostasis revealed that despite the large increase in AVP levels in the FAE rats, only the neurohypophysis and supraoptic nuclei showed significant increases in activity. These data suggest that fetal alcohol exposure causes a long-term disruption in the central mechanisms regulating vasopressin release and fluid homeostatic responses.

Animals↗

PubMed1995

Dysregulation of homeostasis of blood T-lymphocyte subpopulations persists in chronic multibacillary pulmonary tuberculosis patients refractory to treatment.

DESIGN: The dysregulation of homeostasis of blood-T lymphocyte subpopulations was studied in 21 cases of chronic, multibacillary pulmonary tuberculosis refractory to treatment. The clinico-bacteriological and immunological parameters studied in these cases (Gr A) were compared with those of a group of 10 newly-diagnosed drug sensitive cases of pulmonary tuberculosis (Gr B) at the beginning of the study and after 3 months of chemotherapy for tuberculosis. The chronic cases were treated with drugs selected from a reserve line. 10 normal healthy individuals were included in this study as a control group. RESULTS: At the beginning of the study the mean CD4/CD8 lymphocyte ratios in the refractory cases (0.69) and the newly diagnosed cases (0.81) were significantly lower than those of the normal control subjects (1.84). After 3 months of chemotherapy all but 3 of the newly-diagnosed cases showed clinical improvement, and all became sputum-negative. Their CD4/CD8 ratio recorded a rise to near normal (1.54). On the contrary, following 3 months of reserve-line regimen, only 7 of the 21 group A cases showed sputum conversion. In all of the refractory cases, irrespective of sputum conversion, the CD4/CD8 ratio remained low (1.05). CONCLUSION: This probably indicates that due to a long-standing bacillary load in drug resistant pulmonary tuberculosis patients the dysregulation of homeostasis of blood-T lymphocytes becomes persistent. This in turn delays their clinical and immunological recovery, even when therapy is adequate.

Adolescent↗

PubMed2006

Arabidopsis thaliana expresses two functional isoforms of Arvp, a protein involved in the regulation of cellular lipid homeostasis.

Arv1p is involved in the regulation of cellular lipid homeostasis in the yeast Saccharomyces cerevisiae. Here, we report the characterization of the two Arabidopsis thaliana ARV genes and the encoded proteins, AtArv1p and AtArv2p. The functional identity of AtArv1p and AtArv2p was demonstrated by complementation of the thermosensitive phenotype of the arv1Delta yeast mutant strain YJN1756. Both A. thaliana proteins contain the bipartite Arv1 homology domain (AHD), which consists of an NH(2)-terminal cysteine-rich subdomain with a putative zinc-binding motif followed by a C-terminal subdomain of 33 amino acids. Removal of the cysteine-rich subdomain has no effect on Arvp activity, whereas the presence of the C-terminal subdomain of the AHD is critical for Arvp function. Localization experiments of AtArv1p and AtArv2p tagged with green fluorescent protein (GFP) and expressed in onion epidermal cells demonstrated that both proteins are exclusively targeted to the endoplasmic reticulum. Analysis of beta-glucuronidase (GUS) activity in transgenic A. thaliana plants carrying chimeric ARV1::GUS and ARV2::GUS genes showed that ARV gene promoters direct largely overlapping patterns of expression that are restricted to tissues in which cells are actively dividing or expanding. The results of this study support the notion that plants, yeast and mammals share common molecular mechanisms regulating intracellular lipid homeostasis.

Amino Acid Sequence↗

PubMed2006

Molecular control of vertebrate iron homeostasis by iron regulatory proteins.

Both deficiencies and excesses of iron represent major public health problems throughout the world. Understanding the cellular and organismal processes controlling iron homeostasis is critical for identifying iron-related diseases and in advancing the clinical treatments for such disorders of iron metabolism. Iron regulatory proteins (IRPs) 1 and 2 are key regulators of vertebrate iron metabolism. These RNA binding proteins post-transcriptionally control the stability or translation of mRNAs encoding proteins involved in iron homeostasis thereby controlling the uptake, utilization, storage or export of iron. Recent evidence provides insight into how IRPs selectively control the translation or stability of target mRNAs, how IRP RNA binding activity is controlled by iron-dependent and iron-independent effectors, and the pathological consequences of dysregulation of the IRP system.

Animals↗

PubMed2005

Sleep homeostasis in rats assessed by a long-term intermittent paradoxical sleep deprivation protocol.

Numerous studies have evaluated the sleep homeostasis of rats after short- or long-periods of sleep deprivation, but none has assessed the effects of prolonged sleep restriction on the rat's sleep pattern. The purpose of the present study, therefore, was to evaluate the sleep homeostasis of rats under a protocol of chronic sleep restriction. Male Wistar rats were implanted with electrodes for EEG and EMG recordings. Using the single platform method, the animals were submitted to 18 h of sleep restriction, beginning at 16:00 h (lights on at 07:00 h), followed by a 6 h sleep window (from 10:00 h to 16:00 h) for 21 days. Immediately after this period, rats were allowed to sleep freely for 4 days (recovery period). The sleep-wake cycle was recorded throughout the entire experiment and the results showed that during the 6h sleep window there was an increase on the percentage of sleep time, reflected by augmented time in high amplitude slow wave sleep and in paradoxical sleep, when compared to baseline sleep, whereas bouts of awakening longer than 1.5 min were greatly reduced, with the animals exhibiting a monophasic-type sleep pattern. During the deprivation period, paradoxical sleep was abolished. High amplitude slow wave sleep was also greatly affected by the protocol. Nonetheless, one day of recovery was sufficient to restore the normal sleep pattern. These findings indicate that this protocol was capable to induce many changes in the rat's sleep patterns, suggesting that during the 6h sleep window there is a sleep adaptive homeostatic process.

Activity Cycles↗

PubMed2006

Sphingosine 1-phosphate receptors modulate intracellular Ca2+ homeostasis.

Ligation of sphingosine 1-phosphate (S1P) to a set of specific receptors named S1P receptors (S1PRs) regulates important biological processes. Although the ability of S1P to increase cytosolic Ca2+ in various cell types is well known, the role of the individual S1PRs has not been fully characterized. Here, we provide a complete analysis of S1P-dependent intracellular Ca2+ homeostasis in HeLa cells. Overexpression of S1P2, or S1P3, but not S1P1, leads to a significant increase in cytosolic and mitochondrial [Ca2+] in response to S1P challenge. Moreover, cells ectopically expressing S1P2, or S1P3 exhibited an appreciable decrease of the free Ca2+ concentration in the endoplasmic reticulum, dependent on stimulation of receptors by S1P endogenously present in the culture medium which was accompanied by a reduced susceptibility to C2-ceramide-induced cell death. These results demonstrate a differential contribution of individual S1PRs to Ca2+ homeostasis and its possible implication in the regulation of cell survival.

Calcium↗

PubMed2005

Protective effects of Ca2+ handling drugs against abnormal Ca2+ homeostasis and cell damage in myopathic skeletal muscle cells.

Deficiency of delta-sarcoglycan (delta-SG), a component of the dystrophin-glycoprotein complex (DGC), causes skeletal muscular dystrophy and cardiomyopathy in BIO14.6 hamsters. Here, we studied the involvement of abnormal Ca2+ homeostasis in muscle degeneration and the protective effect of drugs against Ca2+ handling proteins in vivo as well as in vitro. First, we characterized the properties of cultured myotubes from muscles of normal and BIO14.6 hamsters (30-60 days old). While there were no apparent differences in the levels of expression of various Ca2+ handling proteins (L-type Ca2+ channel, ryanodine receptor, SR-Ca2+ ATPase, and Na+/Ca2+ exchanger), muscle-specific proteins (contractile actin and acetylcholine receptor), or DGC member proteins except SGs, BIO14.6 myotubes showed a high degree of susceptibility to mechanical stressors, such as cyclic stretching and hypo-osmotic stress as compared to normal myotubes, as evidenced by marked increases in creatine phosphokinase (CK) release and bleb formation. BIO14.6 myotubes showed abnormal Ca2+ homeostasis characterized by elevated cytosolic Ca2+ concentration, frequent Ca2+ oscillation, and increased 45Ca2+ uptake. These abnormal Ca2+ events and CK release were significantly prevented by Ca2+ handling drugs, tranilast, diltiazem, and FK506. The calpain inhibitor E64 prevented CK release, but not 45Ca2+ uptake. Some of these drugs (tranilast, diltiazem, and FK506) also exerted a significant protective effect for muscle degeneration in BIO14.6 hamsters and mdx mice in vivo. These observations suggest that elevated Ca2+ entry through sarcolemmal Ca2+ channels predominantly contributes to muscle degeneration and that the drugs tested here may have novel therapeutic potential against muscular dystrophy.

Animals↗

PubMed2003

Disorders of calcium homeostasis.

To ensure a multitude of essential cellular functions, the extracellular concentration of calcium is maintained within a narrow physiological range. This depends on integrated regulation of calcium fluxes with respect to the intestine, kidneys and bone. The precise regulation of serum calcium is controlled by calcium itself, through a calcium receptor and several hormones, the most important of which are parathyroid hormone and 1,25(OH)(2) vitamin D. This balance can be disturbed by mutations in the calcium-sensing receptor, inappropriately high or low levels of parathyroid hormone, resistance to parathyroid hormone effects, insufficient intake or production of 1,25(OH)(2) vitamin D and inactivation of the vitamin D receptor. Mineral homeostasis is moreover influenced by many other systemic factors (e.g. sex steroid, thyroid and glucocorticoid hormones) or humoral factors (e.g. cytokines and growth factors). A specific example is the major abnormalities of mineral homeostasis in case of malignancy by excessive production of parathyroid hormone-related peptide resulting in hypercalcaemia. Several new drugs have been developed based on factors in this axis, including calcimimetics, calcilytics, vitamin D analogues and parathyroid hormone-related peptide inhibitors.

Animals↗

PubMed2005

Astrocytes: regulation of brain homeostasis via apolipoprotein E.

Astrocytes are derived from the ventricular and subventricular zones of the neural plate, though there is controversy over their derivation from astrocyte-specific precursor cells or radial glia intermediates. Astrocytes are the most abundant cell type in the brain and contribute to brain homeostasis in several ways, including buffering of extracellular K+, regulating neurotransmitter release, forming the blood-brain barrier (BBB), releasing growth factors, and regulating the brain immune response. In addition, astrocytes have been shown to release apolipoprotein E (ApoE), which has been shown to regulate neurotransmission, growth factor release, and immune responses. Due to the diverse functions of astrocytes, they may play a role in a variety of diseases such as hepatic encephalopathy, multiple sclerosis, epilepsy, and age-related diseases including Alzheimer's disease and Parkinson's disease. This review highlights many of the diverse roles played by astrocytes in regulating brain homeostasis and discusses their potential role in a variety of disorders.

Animals↗

PubMed2004

SREBP transcription factors: master regulators of lipid homeostasis.

Sterol regulatory element binding proteins (SREBPs) are a family of transcription factors that regulate lipid homeostasis by controlling the expression of a range of enzymes required for endogenous cholesterol, fatty acid (FA), triacylglycerol and phospholipid synthesis. The three SREBP isoforms, SREBP-1a, SREBP-1c and SREBP-2, have different roles in lipid synthesis. In vivo studies using transgenic and knockout mice suggest that SREBP-1c is involved in FA synthesis and insulin induced glucose metabolism (particularly in lipogenesis), whereas SREBP-2 is relatively specific to cholesterol synthesis. The SREBP-1a isoform seems to be implicated in both pathways. SREBP transcription factors are synthetized as inactive precursors bound to the endoplasmic reticulum (ER) membranes. Upon activation, the precursor undergoes a sequential two-step cleavage process to release the NH(2)-terminal active domain in the nucleus (designated nSREBPs). SREBP processing is mainly controlled by cellular sterol content. When sterol levels decrease, the precursor is cleaved to activate cholesterogenic genes and maintain cholesterol homeostasis. This sterol-sensitive process appears to be a major point of regulation for the SREBP-1a and SREBP-2 isoforms but not for SREBP-1c. Moreover, the SREBP-1c isoform seems to be mainly regulated at the transcriptional level by insulin. The unique regulation and activation properties of each SREBP isoform facilitate the co-ordinate regulation of lipid metabolism; however, further studies are needed to understand the detailed regulation pathways that specifically regulate each SREBP isoform.

Animals↗

PubMed2004

The relationship between vitamin D and parathyroid hormone: calcium homeostasis, bone turnover, and bone mineral density in postmenopausal women with established osteoporosis.

It is evident from several studies that not all patients with hypovitaminosis D develop secondary hyperparathyroidism. What this means for bone biochemistry and bone mineral density (BMD) remains unclear. The aim of this study was to investigate the effects of hypovitaminosis D (defined as a 25OHD < or = 30 nmol/l) and patients with a blunted PTH response (defined arbitrarily as a PTH within the standard laboratory reference range in the presence of a 25OHD < or = 30 nmol/l) in comparison to patients with hypovitaminosis D and secondary hyperparathyroidism (defined arbitrarily as a PTH above the standard laboratory reference range in the presence of a 25OHD < or = 30 nmol/l) and vitamin D-replete subjects (25OHD > 30 nmol/l). Four hundred twenty-one postmenopausal women (mean age: 71.2 years) with established vertebral osteoporosis were evaluated by assessing mean serum calcium, 25OHD, 1,25(OH)2D, bone turnover markers, and BMD. The prevalence of hypovitaminosis D was 39%. Secondary hyperparathyroidism was found in only one-third of these patients who maintained calcium homeostasis at the expense of increased bone turnover relative to the vitamin D-replete subjects (bone ALP mean difference: 43.9 IU/l [95% CI: 24.8, 59.1], osteocalcin: 1.3 ng/ml [95% CI: 1.1, 2.5], free deoxypyridinoline mean difference: 2.6 nmol/nmol creatinine [95% CI: 2.5, 4.8]) and bone loss (total hip BMD mean difference: 0.11 g/cm2 [95% CI: 0.09, 0.12]). Patients with hypovitaminosis D and a blunted PTH response were characterized by a lower serum calcium (mean difference: 0.07 mmol/l [95% CI: 0.08, 0.2]), a reduction in bone turnover (bone ALP mean difference: 42.4 IU/l [95% CI: 27.8, 61.9], osteocalcin: 1.6 ng/ml [95% CI: 0.3, 3.1], free-deoxypyridinoline mean difference: 3.0 nmol/nmol creatinine [95% CI: 1.9, 5.9]), but protection in bone density (total hip BMD mean difference: 0.10 g/cm2, [95% CI: 0.08, 0.11]) as compared to those with hypovitaminosis D and secondary hyperparathyroidism. This study identifies a distinct group of patients with hypovitaminosis D and a blunted PTH response who show a disruption in calcium homeostasis but protected against PTH-mediated bone loss. This has clinical implications with respect to disease definition and may be important in deciding the optimal replacement therapy in patients with hypovitaminosis D but a blunted PTH response.

Aged↗

PubMed2004

Modeling epithelial cell homeostasis: assessing recovery and control mechanisms.

Critical to epithelial cell viability is prompt and direct recovery, following a perturbation of cellular conditions. Although a number of transporters are known to be activated by changes in cell volume, cell pH, or cell membrane potential, their importance to cellular homeostasis has been difficult to establish. Moreover, the coordination among such regulated transporters to enhance recovery has received no attention in mathematical models of cellular function. In this paper, a previously developed model of proximal tubule (Weinstein, 1992, Am. J. Physiol. 263, F784-F798), has been approximated by its linearization about a reference condition. This yields a system of differential equations and auxiliary linear equations, which estimate cell volume and composition and transcellular fluxes in response to changes in bath conditions or membrane transport coefficients. Using the singular value decomposition, this system is reduced to a linear dynamical system, which is stable and reproduces the full model behavior in a useful neighborhood of the reference. Cost functions on trajectories formulated in the model variables (e.g., time for cell volume recovery) are translated into cost functions for the dynamical system. When the model is extended by the inclusion of linear dependence of membrane transport coefficients on model variables, the impact of each such controller on the recovery cost can be estimated with the solution of a Lyapunov matrix equation. Alternatively, solution of an algebraic Riccati equation provides the ensemble of controllers that constitute optimal state feedback for the dynamical system. When translated back into the physiological variables, the optimal controller contains some expected components, as well as unanticipated controllers of uncertain significance. This approach provides a means of relating cellular homeostasis to optimization of a dynamical system.

Biological Transport↗