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PubMed2003

Schematic illustration of some of the mechanisms for maintenance of homeostasis in organism.

The aim of the present paper is to illustrate schematically by a non-equal arm lever system the mechanisms that maintain the homeostasis of reactive oxygen species, glucose, mean arterial pressure and electrolytes. All regulating factors that increase the values of each physiological parameter are placed on the same arm of the lever system. The regulating factors that decrease this value are placed on the other arm of the lever. In this way the two types of factors interact with one another and maintain the lever system in a dynamic equilibrium, i.e., contribute to keeping the homeostasis. Illustrating the maintenance of homeostasis by a non-equal arm lever system gives the opportunity to express the quickness, flexibility, stability and effectiveness of physiological regulations.

Animals↗
PubMed1996

Disturbances of calcium homeostasis within the endoplasmic reticulum may contribute to the development of ischemic-cell damage.

It is widely accepted that disturbances of calcium homeostasis play a key role in the development of cell damage produced by transient cerebral ischemia. It is believed that the sharp increase in cytosolic calcium activity during ischemia activates a cascade of calcium-dependent metabolic processes which ultimately destroy the integrity of the cell. However, it has never been taken into account that ischemic cell damage may, at least in part, be caused by a disturbance of calcium homeostasis within the endoplasmic reticulum after transient cerebral ischemia. In fact, depletion of the endoplasmic reticulum from calcium induces metabolic changes resembling, in many respects, those produced by transient cerebral ischemia: it causes an inhibition of the activity of the eucaryotic initiation factor elF-2 alpha (by phosphorylation), a disaggregation of polyribosomes and thus an inhibition of global protein synthesis, and an increased expression of certain genes such as transcription factors (c-fos and c-jun) and the glucose-related protein grp78. Finally, a depletion of calcium in the endoplasmic reticulum induces tissue damage within the brain and triggers apoptosis in neuronal and non-neuronal cells. It is therefore concluded that cell damage induced by transient ischemia may, at least in part, be caused by a disturbance of calcium homeostasis within the endoplasmic reticulum.

Animals↗
PubMed1996

Dietary management of pancreatic beta-cell homeostasis and control of diabetes.

Undernutrition, overnutrition and malnutrition, in addition to several other environmental insults have been claimed to play roles in the etiopathogenesis of insulin-dependent and -independent diabetes. These factors are known to alter the beta-cell function and disturb its homeostasis, i.e. qualitative and quantitative changes in its activity. This can lead to disturbed glucose homeostasis and thereby diabetes. It is possible to stop this vicious cycle and reduce the incidence of diabetes by restoring the homeostasis of beta-cell function through proper diabetes management and maintainance of an appropriate dietary milieu. It has been suggested that beta-cell dysfunction or death occurs by oxyradical mediated processes. Adequate stimulation of beta cells through high carbohydrate and fibre intake, and reduced oxidative tone by caloric restriction (low protein and saturated fat), supplementation with antioxidants (vitamin E and D) and polyunsaturated essential fatty acids may prevent loss or even restore the beta-cell activity from environmental diabetogenic insults.

Animals↗
PubMed1988

Calcium, phosphorus, and magnesium homeostasis in ruminants.

Significant advances have been made in the last 30 years in the understanding of Ca, PO4, and Mg homeostasis in ruminants. Despite these advances, the primary cellular or molecular lesions responsible for failure of homeostasis have yet to be identified. Suggested causes, such as primary hormone deficiencies, have been eliminated, and we now believe that aging and nutrition can reduce the ability of intestine, bone, and kidney to respond rapidly to the hormone signals responsible for homeostasis during rapid increases in demand for these minerals. Further research is required before these lesions can be identified and new knowledge applied to the development of economical, effective programs that prevent milk fever and hypomagnesemic tetany. Until then, diseases such as milk fever will continue to affect 8 to 9 per cent of our dairy cows, and dairy farmers will continue to spend millions of dollars a year for treatment of the primary disease and the many secondary problems that result from these diseases.

Animals↗
PubMed1999

Serotonin neurons, neuroplasticity, and homeostasis of neural tissue.

Homeostasis is the process by which the internal milieu of the body is able to maintain equilibrium in the face of constant insults from the external world. Endocrine, immune, and vascular systems play pivotal roles in adjusting internal biochemical reactions to counteract assaults from the outside. Despite the vast accumulation of data over the last 50 years, a role for serotonin in brain homeostasis has not been proposed. In this chapter I will review the plasticity and anatomy of serotonergic neurons in integrating external sensory and motor systems as well as internal endocrine, glial and vascular signals with the various cellular elements comprising neural tissue. Steroids and neuropeptides have both been shown to alter the morphology of serotonergic neurons. In turn, alterations in serotonin levels in the adult brain can change the morphology of its target cells. A pivotal role for serotonin in the homeostasis of neural tissue is consistent with the function of serotonin throughout evolution and explains the large number of biological systems, behavioral activities, and clinical diseases associated with serotonergic neurons.

Adult↗
PubMed2002

Genomic scale mutant hunt identifies cell size homeostasis genes in S. cerevisiae.

BACKGROUND: In most eukaryotic cells, there is a relationship between cell size and proliferative capacity. For example, in order to commit to cell division, the yeast Saccharomyces cerevisiae must attain a "critical cell size." This mechanism coordinates growth with cell division to maintain cell size homeostasis. Because very few cell size control genes are known, the genetic pathways responsible for cell size homeostasis remain obscure. Furthermore, elucidation of the mechanism of cell size homeostasis has been recalcitrant to genetic analysis primarily due to the difficulty in cloning cell size control genes. RESULTS: To identify new size control genes, the effect of 5958 single gene deletions (4792 homozygous and 1166 heterozygous gene deletions) on cell size in yeast grown to saturation was systematically determined. From these data, 49 genes were identified that dramatically altered cell size. Of these, 34 are involved in transcription, signal transduction, or cell cycle control; 88% of these genes have putative human homologs. Sixteen genes regulate cell size in a dosage-dependent manner, and the majority of mutants identified fail to correctly exit the cell cycle. Many of these genes are components of Ccr4-Not transcriptional complexes or function in the PKC-MAP kinase pathway. These genes may modulate cell size by altering the expression or activity of G1-phase cyclins. CONCLUSIONS: These results illustrate how systematic genetic screens can be used to dissect intricate biological processes that are refractory to classic genetic approaches. This genomic-wide genetic screen yielded 46 new cell size mutants and systematically assessed the effect of 5958 single gene deletions on cell size as cells exited the cell cycle.

Cell Cycle↗
PubMed2003

Local regulation of homeostasis favors chromosomal instability.

Tissues of long-lived multicellular organisms have to maintain a constant number of functioning cells for many years. This process is called homeostasis. Homeostasis breaks down when cells emerge with mutations in tumor suppressor genes or oncogenes. Such mutated cells can have increased net rates of proliferation, which is increased somatic fitness. We show that the best protection against such mutations is achieved when homeostasis is regulated locally via small compartments. Small compartments, on the other hand, allow the accumulation of cells with reduced somatic fitness. Cells with mutations conferring genetic instability normally have a reduced somatic fitness because they have an increased probability of producing deleterious mutations or triggering apoptosis. Thus, small compartments protect against mutations in tumor suppressor genes or oncogenes but promote the emergence of genetic instability.

Cell Transformation, Neoplastic↗
PubMed2003

Fas (CD95/Apo-1) ligand regulation in T cell homeostasis, cell-mediated cytotoxicity and immune pathology.

Members of the tumor necrosis factor (TNF) superfamily are crucially involved in the regulation of T cell activation, homeostasis and cytotoxicity. In particular, Fas ligand (FasL), expressed by activated T lymphocytes, induces cell-mediated cytotoxicity and may also be responsible for apoptotic suicide. Tight regulation of this death-inducing ligand is a prerequisite for proper immune defense and homeostasis. In this review, we will discuss various aspects of FasL regulation in cell-mediated cytotoxicity, immune homeostasis and the immunopathology of diseases.

Animals↗
PubMed1999

Regulation of phosphatidylcholine homeostasis by calcium-independent phospholipase A2.

Phosphatidylcholine (PtdCho) is the most abundant phospholipid in mammalian cell membranes and is essential for cell viability. The levels of this lipid must be tightly controlled to maintain homeostasis. Therefore, changes in the rate of PtdCho synthesis are generally balanced by changes in PtdCho catabolism and vice versa. It is commonly accepted that the rate of PtdCho synthesis is regulated by CTP:phosphocholine cytidylyltransferase (CT). However, it is not certain if PtdCho mass is regulated by specific catabolic enzyme(s). Our goal is to determine if PtdCho homeostasis is regulated by a phospholipase A2 (PLA2). To this end, we have prepared Chinese hamster ovary (CHO) cell lines that overexpress CT. CT activity is 7-10-fold higher in the transfected cells than in parental CHO cells. This increase in CT activity is associated with increases in both PtdCho synthesis and PtdCho catabolism. Glycerophosphocholine is the PtdCho catabolite that accumulates in the transfected cells, which suggests that PtdCho turnover is mediated by a phospholipase A2 (PLA2). Indeed, higher levels of calcium-independent PLA2 activity are measured in the cytosols of the CHO cells that overexpress CT, compared to parental CHO cells. The elevated calcium-independent PLA2 activity is associated with increases in the expression of the 80-kDa calcium-independent PLA2 (iPLA2). Together, these data suggest that the 80-kDa iPLA2 may be modulated in response to changes in PtdCho levels and therefore is involved in the regulation of PtdCho homeostasis in CHO cells.

Animals↗
PubMed2004

Renin cells are precursors for multiple cell types that switch to the renin phenotype when homeostasis is threatened.

Renin-synthesizing cells are crucial in the regulation of blood pressure and fluid-electrolyte homeostasis. Adult mammals subjected to manipulations that threaten homeostasis increase circulating renin by increasing the number of renin-expressing/-releasing cells. We hypothesize that the ability of adult cells to synthesize renin does not occur randomly in any cell type, depending instead on the cell's lineage. To determine the fate of renin-expressing cells, we generated knockin mice expressing cre recombinase in renin-expressing cells and crossed them with reporter mice. Results show that renin-expressing cells are precursors for a variety of cells that differentiate into non-renin-expressing cells such as smooth-muscle, epithelial, mesangial, and extrarenal cells. In the kidney, these cells retain the capability to synthesize renin when additional hormone is required to reestablish homeostasis: specific subpopulations of apparently differentiated cells are "held in reserve" to respond (repeatedly) by de-differentiating and expressing renin in response to stress, and re-differentiating when the crisis passes.

Animals↗
PubMedDate not supplied

Zinc metabolism and homeostasis: the application of tracer techniques to human zinc physiology.

Tracer kinetic techniques based on zinc stable isotopes have a vital role in advancing knowledge of human zinc physiology and homeostasis. These techniques have demonstrated the complexity of zinc metabolism, and have been critical to estimating the size and interrelationships of those pools of zinc that exchange rapidly with zinc in plasma and which are likely to be especially important for zinc dependent biology. This paper presents findings from recent research linking a steady state compartmental model with non-steady state post-prandial sampling from the intestine, utilizing a combination of intestinal intubation/perfusion and stable isotope tracer kinetic techniques. The gastrointestinal tract has a central role in maintaining whole body zinc homeostasis. While the fractional absorption of zinc from a meal depends on the quantity of exogenous zinc and on such dietary factors as phytic acid, the fractional absorption does not appear to be dependent on the size of the rapidly exchanging pool of the host. In contrast, the quantity of endogenous zinc excreted via the intestine is positively correlated with both the amount of absorbed zinc and the zinc 'status' of the host, and thus this process has an equally critical role in maintaining zinc homeostasis. The observed alterations in zinc metabolism in some disease states can be understood in the context of known homeostatic processes. In other conditions, however, such alterations as inflammation-associated hyperzincuria and zinc redistribution, the links between homeostatic perturbation and cellular biology are yet to be explained. Thus the challenge remains for research at the whole body level to carefully characterize zinc distribution and exchange under diverse circumstances, while research at the cellular level must elucidate the regulatory processes and the factors to which they respond.

Digestive System↗
PubMedDate not supplied

Zinc homeostasis and functions of zinc in the brain.

The brain barrier system, i.e., the blood-brain and blood-cerebrospinal fluid barriers, is important for zinc homeostasis in the brain. Zinc is supplied to the brain via both barriers. A large portion of zinc serves as zinc metalloproteins in neurons and glial cells. Approximately 10% of the total zinc in the brain, probably ionic zinc, exists in the synaptic vesicles, and may serve as an endogenous neuromodulator in synaptic neurotransmission. The turnover of zinc in the brain is much slower than in peripheral tissues such as the liver. However, dietary zinc deprivation affects zinc homeostasis in the brain. Vesicular zinc-enriched regions, e.g., the hippocampus, are responsive to dietary zinc deprivation, which causes brain dysfunctions such as learning impairment and olfactory dysfunction. Olfactory recognition is reversibly disturbed by the chelation of zinc released from amygdalar neuron terminals. On the other hand, the susceptibility to epileptic seizures, which may decrease vesicular zinc, is also enhanced by zinc deficiency. Therefore, zinc homeostasis in the brain is closely related to neuronal activity. Even in adult animals and probably adult humans, adequate zinc supply is important for brain functions and prevention of neurological diseases.

Amygdala↗
PubMed2006

Soma-germline interactions coordinate homeostasis and growth in the Drosophila gonad.

The ability of organs such as the liver or the lymphoid system to maintain their original size or regain it after injury is well documented. However, little is known about how these organs sense that equilibrium is breached, and how they cease changing when homeostasis is reached. Similarly, it remains unclear how, during normal development, different cell types within an organ coordinate their growth. Here we show that during gonad development in the fruitfly Drosophila melanogaster the proliferation of primordial germ cells (PGCs) and survival of the somatic intermingled cells (ICs) that contact them are coordinated by means of a feedback mechanism composed of a positive signal and a negative signal. PGCs express the EGF receptor (EGFR) ligand Spitz, which is required for IC survival. In turn, ICs inhibit PGC proliferation. Thus, homeostasis and coordination of growth between soma and germ line in the larval ovary is achieved by using a sensor of PGC numbers (EGFR-mediated survival of ICs) coupled to a correction mechanism inhibiting PGC proliferation. This feedback loop ensures that sufficient numbers of PGCs exist to fill all the stem-cell niches that form at the end of larval development. We propose that similar feedback mechanisms might be generally used for coordinated growth, regeneration and homeostasis.

Animals↗
PubMed1995

Failure of T-cell homeostasis preceding AIDS in HIV-1 infection. The Multicenter AIDS Cohort Study.

We and others have postulated that a constant number of T lymphocytes is normally maintained without regard to CD4+ or CD8+ phenotype ('blind' T-cell homeostasis). Here we confirm essentially constant T-cell levels (despite marked decline in CD4+ T cells and increase in CD8+ T cells) in homosexual men with incident human immunodeficiency virus, type 1 (HIV-1), infection who remained free of acquired immunodeficiency syndrome (AIDS) for up to eight years after seroconversion. In contrast, seroconverters who developed AIDS exhibited rapidly declining T cells (both CD4+ and CD8+) for approximately two years before AIDS, independent of the time between seroconversion and AIDS, suggesting that homeostasis failure is an important landmark in HIV disease progression. Given the high rate of T-cell turnover in HIV-1 infection, blind T-cell homeostasis may contribute to HIV pathogenesis through a CD8+ T lymphocytosis that interferes with regeneration of lost CD4+ T cells.

Acquired Immunodeficiency Syndrome↗
PubMed2024

Osteocalcin of maternal and embryonic origins synergize to establish homeostasis in offspring.

Many physiological osteocalcin-regulated functions are affected in adult offspring of mothers experiencing unhealthy pregnancy. Furthermore, osteocalcin signaling during gestation influences cognition and adrenal steroidogenesis in adult mice. Together these observations suggest that osteocalcin may broadly function during pregnancy to determine organismal homeostasis in adult mammals. To test this hypothesis, we analyzed in unchallenged wildtype and Osteocalcin-deficient, newborn and adult mice of various genotypes and origin maintained on different genetic backgrounds, the functions of osteocalcin in the pancreas, liver and testes and their molecular underpinnings. This analysis revealed that providing mothers are Osteocalcin-deficient, Osteocalcin haploinsufficiency in embryos hampers insulin secretion, liver gluconeogenesis, glucose homeostasis, testes steroidogenesis in adult offspring; inhibits cell proliferation in developing pancreatic islets and testes; and disrupts distinct programs of gene expression in these organs and in the brain. This study indicates that osteocalcin exerts dominant functions in most organs it influences. Furthermore, through their synergistic regulation of multiple physiological functions, osteocalcin of maternal and embryonic origins contributes to the establishment and maintenance of organismal homeostasis in newborn and adult offspring.

Animals↗
PubMed2006

Basis for improved permeability barrier homeostasis induced by PPAR and LXR activators: liposensors stimulate lipid synthesis, lamellar body secretion, and post-secretory lipid processing.

Previously, we demonstrated that topical applications of peroxisome proliferator-activated receptors (PPARs) and liver X receptor (LXR) activators improve permeability barrier homeostasis. We showed further that stimulation of epidermal differentiation provides one mechanism that could account for such improvement. Here, we studied the effects of these agents on the lipid matrix of the stratum corneum. Hairless mice were treated topically with activators of PPARalpha (WY14643), PPARdelta (GW1514), PPARgamma (ciglitazone), and LXR (22(R)-cholesterol or TO901317) or vehicle twice daily for 3 days. All activators significantly increased epidermal cholesterol, fatty acid, and sphingolipid synthesis, including the production of barrier-specific ceramide species. In addition, lamellar body (LB) formation, secretion, and post-secretory processing accelerated significantly following acute barrier disruption in PPAR/LXR-activator-treated animals. Finally, the activity of epidermal beta-glucocerebrosidase, a key lipid-processing enzyme, increased in PPAR/LXR-activator-treated animals. Thus, topical PPAR and LXR activators stimulate epidermal lipid synthesis, increase LB secretion, and accelerate extracellular lipid processing, providing additional mechanisms that further account for their ability to improve epidermal permeability barrier homeostasis. Since the liposensors are activated by endogenous lipid metabolites, they may serve as unique regulators of barrier homeostasis.

Animals↗
PubMed2006

Novel roles of NM23 proteins in skin homeostasis, repair and disease.

Keratinocyte growth factor (KGF) is an important regulator of epidermal homeostasis and repair. Therefore, the identification of KGF target genes in keratinocytes should contribute to our understanding of the molecular mechanisms underlying these processes. In a search for KGF-regulated genes, we identified the gene encoding the nucleoside diphosphate kinase NM23-H1. Apart from a housekeeping function, NM23 proteins are involved in the regulation of many cellular processes as well as in tumor metastasis, but their functions in epidermal homeostasis and repair are largely unknown. Here, we show a high expression of NM23-H1 and NM23-H2 in the KGF-responsive keratinocytes of the hyperproliferative epidermis of mouse skin wounds and of patients suffering from the skin disease psoriasis. To determine if this overexpression is functionally important, we generated HaCaT keratinocyte cell lines overexpressing NM23-H1 and/or -H2. Whereas the enhanced levels of NM23 did not affect cell proliferation in monoculture, NM23-H2 and double transfectants but not NM23-H1 transfectants formed a strongly hyperthickened epithelium in three-dimensional organotypic cultures. The abnormal epithelial morphology resulted from enhanced proliferation, reduced apoptosis and alterations in the differentiation pattern. These findings suggest that epidermal homeostasis depends on a tight regulation of the levels of NM23 isoforms.

Adult↗
PubMed2000

Disordered calcium homeostasis of sepsis: association with calcitonin precursors.

BACKGROUND: Hypocalcemia and increased serum levels of calcitonin precursors are common in critically ill patients, especially in those with sepsis. We investigated calcium homeostasis in such patients. PATIENTS AND METHODS: Serum concentrations of total and ionized calcium and known factors influencing or reflecting calcium homeostasis were measured in 101 consecutive patients of a medical intensive care unit. Calcitonin precursor levels were determined using a highly sensitive radioimmunoassay. RESULTS: Critical illness per se was associated with decreased serum total and ionized calcium levels, which correlated with the severity of the underlying disease as measured by the APACHE II score. In addition, total and ionized hypocalcemia was more pronounced with increasing severity of infection (P < 0.02), and occurred in parallel with a marked increase of calcitonin precursors (P < 0.001). Mature calcitonin levels, however, remained normal. Changes of serum ionized calcium concentrations from admission to discharge correlated significantly with changes in the serum calcitonin precursor concentration (r2 = - 0.14, P < 0.001). Circulating vitamin D levels, parathyroid hormone levels and other markers reflecting calcium homeostasis did not correlate with the severity of infection. CONCLUSIONS: In critically ill patients with sepsis, markedly elevated circulating calcitonin precursors might play a role in the development of the pronounced hypocalcemia. The specific calcitonin precursor(s) responsible for this effect and the pathophysiological mechanism remain to be elucidated.

Adult↗