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At least 361 records · Page 20Linked to original sources

PubMed1977

Potassium homeostasis in chronic diabetes mellitus.

Potassium homeostasis was evaluated in 13 patients with diabetes mellitus. In eight, plasma renin activity was low; plasma aldosterone concentration was decreased in all; seven had a history of spontaneous hyperkalemia. After administration of glucose orally, there were paradoxical increases in serum potassium levels in seven patients. After potassium loading, maximal values and increments of serum potassium were higher and fractional potassium excretion was lower in the diabetic than in the control subjects, although the differences were not statistically significant. Abnormalities of potassium homeostasis in diabetes are probably related to insulin and mineralocorticoid deficiency. Diabetic patients with hypoaldosteronism have the potential for severe hyperkalemia should renal or extrarenal mechanisms for potassium homeostasis be challenged by severe acidosis be challenged by severe acidosis, diminished renal function, marked hyperglycemia, or administration of potassium salts or potassium-sparing diuretics.

Adult↗

PubMed1985

Abnormalities in blood pressure homeostasis that contribute to falls in the elderly.

Aging is associated with abnormalities in blood pressure homeostasis and may precipitate falls through transient underperfusion of the brain. Age-related declines in baro-reflex sensitivity, cerebral blood flow, and renal sodium conservation threaten normal blood pressure regulation and cerebral perfusion. Common clinical conditions associated with abnormal blood pressure homeostasis and falls in the elderly include postural hypotension, postprandial hypotension, carotid sinus hypersensitivity, and cardiac arrhythmias, all of which are exacerbated by hypertension. Further research is needed to understand the physiologic basis of abnormal blood pressure homeostasis, to explore the potential relationship between hypertension and falling, and to design new therapeutic approaches to this important cause of falls in the elderly.

Accidents↗

PubMed1979

The role of hepatic control of glucose homeostasis in the etiology of neonatal hypo- and hyperglycemia.

Precise control of glucose homeostasis is well recognized in the adult. Going from a period of complete dependence on the maternal organism for delivery of substrate, the fetus is born not only with a need to furnish himself with glucose for energy and rapid growth but also with the need to maintain a balance between glucose deficiency and excess. This is especially difficult because of the intermittent nature of exogenous oral intake in the neonatal period. Development of glucose homeostasis requires a balance between substrate availability (both absolute and relative) and coordination of hormonal, neural and enzymatic systems. The large number of conditions producing or associated with both hypo- and hyperglycemia in the newborn, especially the low birth weight or sick neonate, emphasizes this vulnerability. Newer techniques including stable isotope methodology, now being employed with increasing frequency, will help define maturation of neonatal carbohydrate homeostasis and further clarify nutritional requirements in this transitional period.

Adult↗

PubMed1985

Presence of a nonmetabolizable solute that is translocated with Na+ enhances Na+-dependent pH homeostasis in an alkalophilic Bacillus.

The presence of a nonmetabolizable solute whose uptake is coupled to the inward translocation of Na+ has been found to enhance Na+-dependent pH homeostasis and survival of an obligately alkalophilic bacterium. Upon shift of cells of Bacillus firmus RAB from growth medium to buffers at pH 10.5, viability and maintenance of a relatively acidified cytoplasm depended upon the presence of Na+ and was augmented by the inclusion of alpha-aminoisobutyric acid in the buffer. Similarly, when cells were first equilibrated at pH 8.5 and then shifted to buffer at pH 10.5, an extraordinary capacity to maintain a relatively low pHin was exhibited, but only in the presence of Na+. In this protocol, the inclusion of alpha-aminoisobutyric acid actually resulted in an early overshoot of proton influx and also rendered a suboptimal concentration of Na+ efficacious in pH homeostasis. When a protonophoric uncoupler was added to the equilibration and shift buffers, Na+-dependent acidification of the interior was inhibited at early time points. The results support the conclusion drawn from earlier work that a Na+/H+ antiporter plays a critical role in pH homeostasis in the obligately alkalophilic bacilli. Moreover, the current findings indicate that the Na+/solute symporters are a physiologically functional pathway for completing the sodium cycle that controls pHin.

Aminoisobutyric Acids↗

PubMed1983

Endocrine regulation of calcium homeostasis during pregnancy.

The principal maternal physiologic adjustment with respect to calcium metabolism is increasing PTH secretion, which maintains the serum ionic calcium level within its characteristically narrow physiologic limits in the face of an expanding extracellular fluid volume, increased urinary excretion, and calcium transfer to the fetus. Additionally, PTH promotes increased renal synthesis of 1,25-(OH)2D3, which acts in concert with PTH to meet the calcium demands of gestation. Whether or not calcitonin secretion increases as well is not clear; if so, this effect may be important in protecting the maternal skeleton. The primary characteristic of perinatal calcium metabolism is the active placental transport of calcium ions from mother to fetus, making the fetus relatively hypercalcemic. Since none of the calcitropic hormones cross the placenta, hypercalcemia apparently suppresses either secretion or activity of PTH by the fetus and stimulates fetal calcitonin release, creating an environment (high calcium, low PTH, high calcitonin) favorable to skeletal growth. With birth, the transplacental calcium source terminates abruptly and the serum calcium level declines for 24 to 48 hours, after which it stabilizes and then rises slightly. Neonatal calcium homeostasis probably reflects multiple influences, including the respective calcitropic hormones and other involved ions such as magnesium and phosphate. The physiologic mechanisms regulating calcium homeostasis during pregnancy and the perinatal period generally operate very effectively. Thus, aberrations leading to clinically evident disease states are relatively infrequent. Maternal hyperparathyroidism causes several complications, notably hypocalcemic tetany in the newborn, and maternal hypoparathyroidism may be associated with perinatal hyperparathyroidism. Diabetic pregnancy leads to altered calcium metabolism in mother, fetus, and newborn; the primary feature may be chronic hypomagnesemia, which leads to hypoparathyroidism to mother and fetus. There is some suggestion of an etiologic role for calcium in hypertensive disorders, and, in any event, magnesium sulfate therapy influences calcium homeostasis. Finally, leg cramps in the pregnant woman may reflect alterations in calcium metabolism.

Animals↗

PubMed1984

Calcium homeostasis in morbid obesity.

Calcium homeostasis in morbidly obese subjects has attracted little attention. Prompted by reports of elevated serum levels of parathyroid hormone in such patients, calcium homeostasis was investigated in 36 patients with morbid obesity and in 44 normal weight controls. Concerning serum immunoreactive parathyroid hormone (C-terminal), serum ionized calcium (Ca++) and serum albumin corrected magnesium no significant differences between the groups were detected. When albumin corrected, serum total calcium turned out to be significantly elevated (p less than 0.0001) in the obese subjects. Also, serum alkaline phosphatase activity was significantly raised in the obese state. The results demonstrate that calcium homeostasis, as expressed by the metabolically active serum Ca++, is normal in morbid obesity. But the results also point towards an abnormal calcium binding due to either an increased calcium binding to albumin or to calcium complexing small anions.

Adult↗

PubMed1983

Parenteral level of glucose intake on glucose homeostasis, tumor growth, gluconeogenesis, and body composition in normal and tumor-bearing rats.

To determine the effects of different levels of glucose intake on glucose homeostasis, gluconeogenesis, body composition, and tumor growth, we gave 8 days of total parenteral feeding of a defined liquid formula diet to groups of Buffalo rats, with and without a transplantable Morris 7777 hepatoma. The level of glucose intake was held at levels which ranged from 0 to 9.5 g/100 body weight per day while the levels of all other nutrients were held constant. Measurements were made on tumor growth rate, terminal blood plasma glucose and whole blood lactate levels, gluconeogenesis, body and organ weight, muscle nitrogen content, liver glycogen, and urine analysis. Tumor-bearing rats (TB) at low glucose intake but not non-tumor-bearing rats (NTB) were found to be dependent on gluconeogenesis for maintenance of blood glucose homeostasis (normoglycemia). Body weight was dependent on glucose intake level in both TB and NTB rats with glucose intake rates of 5.7 g/100 g/day being the point between weight loss or gain. However, under these feeding conditions, tumor growth rate was not dependent on the glucose intake rate. The weight of epididymal fat pad and the size of fat cells were positively correlated with glucose intake rate in both TB and NTB rats, but the fat pad weight in TB rats showed a greater dependence on the rate of glucose intake than it did in the NTB rats. Glucose intake of 3.8 g/100 g/day or less leads to significant loss of muscle mass and loss of muscle nitrogen (protein) in TB but not in NTB rats. Some liver glycogen was detected in all groups of rats except those TB rats with zero glucose intake. TB rats with high glucose intake (5.7 to 9.5 g/100 g/day) had higher blood lactate and lower urine pH than did NTB rats. Thus, TB rats at low glucose intake (3.8 g/100 g/day or less), as opposed to NTB rats, demonstrated a significant dependence on gluconeogenesis for glucose homeostasis, mobilized more of their liver glycogen, and catabolized more of their muscle proteins to supply the increased energy needs of the growing tumor and to maintain normoglycemia.

Animals↗

PubMed1995

Glutathione and protein thiol homeostasis in brain during reperfusion after cerebral ischemia.

The status of glutathione (GSH) and protein thiol homeostasis was examined in rat brain regions during reperfusion after moderate and severe cerebral ischemia. GSH levels were decreased in brain regions during reperfusion for 1 hr after moderate or severe ischemia for 0.5 hr. Maximal loss of GSH (50-66%) was observed in the striatum and hippocampus. The GSH lost from the brain regions was essentially recovered as protein-glutathione mixed disulfide (PrSSG) with concomitant loss of protein thiols (PrSH). The activities of enzymes such as Na+K+ ATPase, NADH dehydrogenase and glutathione reductase were also inhibited but were restored after incubation of the brain homogenate with dithiothreitol. The depletion of GSH was also accompanied by an increase in the levels of malondialdehyde and reactive oxygen species. The total GSH recovered as sum of GSH and PrSSG was significantly higher than the sham-operated controls in the hippocampus and striatum after 1 hr of reperfusion, after moderate ischemia for 0.5 hr, and at the end of 24 hr of reperfusion the GSH-protein thiol homeostasis was restored. In contrast after 1 hr of reperfusion after severe ischemia, the GSH recovered as sum of GSH and PrSSG was not significantly different from sham-operated controls and at the end of 24 hr, 7 of 9 animals died. The recuperation of the brain from oxidative stress during reperfusion after moderate ischemia was thus preceded by increased recovery of total GSH essentially in the form of PrSSG. Thus, rapid restoration of thiol homeostasis in the brain during reperfusion may help the brain recover from reperfusion injury.

Animals↗

PubMed1995

Comparative study of the effect of sodium fluoride and sodium monofluorophosphate on glucose homeostasis in the rat.

The effect of acute and chronic administration of sodium fluoride (NaF) or sodium monofluorophosphate (MFP) on the glucose homeostasis of the rat are compared. The oral administration of a single dose of 40 mumol/100 g b.w. of either compound produced similar increases in plasma glucose (up to 1.8 g/l) and diffusible fluoride (up to 130 mumol/l). In long-term experiments (three months of duration), treatment with NaF (a 5 mmol/l solution as the water supply) produced, in the first month of experiment, abnormal glucose tolerance tests and increased plasma diffusible fluoride levels (range: 2-12 mumol/l). Treatment with MFP, on the other hand, did not affect glucose homeostasis; plasma diffusible fluoride was always below 2 mumol/l. The results of these experiments indicate that glucose homeostasis is affected when plasma diffusible fluoride exceeds 5 mumol/l. The basal and glucose-stimulated insulin secretion of isolated Langerhans rat islets (incubated with solutions containing 2, 5, 10 and 20 mumol/l NaF) was significantly inhibited by 5 to 20 mumol/l fluoride. No effect was observed under similar conditions with MFP at concentrations of 2, 5, 10, 20 and 50 mumol/l.

Animals↗

PubMed1993

Divergent neuroprotective effects of nimodipine in PDD and MID provide indirect evidence of disturbances in Ca2+ homeostasis in dementia.

Evidence suggesting that increased cytotoxic Ca2+ concentrations due to disturbances of Ca2+ homeostasis are involved in neuronal deterioration in dementia has accumulated but has not yet been explicitly confirmed. Here we report of divergent neuroprotective effects of nimodipine, a Ca2+ channel blocker with high lipophilic properties, in primary degenerative dementia (PDD) and multiinfarct dementia (MID). Our clinical data show that nimodipine improves clinical symptomatology and cognitive functions in dementia significantly better than placebo but is more effective in PDD than in MID. This fact becomes explicitly apparent by comparison of the mean value differences of each of the 18 SCAG items between onset and termination of treatment in the two diagnostic groups. The divergent therapeutic response in PDD and MID suggests that the neuroprotective effects of nimodipine can not be due mainly to unspecific cognition enhancing mechanisms or vasodilatation of cerebral blood vessels but must primarily be the consequence of a direct activity in depolarized neuronal cells and of its ability to protect neuronal tissue from Ca2+ overload. Hence, we conclude that disturbances in Ca2+ homeostasis play an important role in the process of neuronal deterioration in dementia. Although we can not entirely rule out the possibility that pharmacological activities besides the modulation of neuronal Ca2+ influx contribute to the effects of nimodipine, from a clinical view our results provide indirect evidence of disturbances in Ca2+ homeostasis as one of the primary factors in the demential process. Our results further support the usefulness of nimodipine in the pharmacotherapy of age-related mental deficits.

Aged↗

PubMedDate not supplied

Iron chelation and tumor cell calcium homeostasis.

The effects of iron chelation on calcium homeostasis of Ehrlich carcinoma cells were studied using 59Fe-ferric lactate and 45CaCl2. Desferrioxamine action on bound iron is characterized by the presence of an insoluble fraction located deep in the cell membrane and another soluble fraction on the cell surface. The competitive binding by albumin suggests that the iron is bound by protein containing molecular structures of the cell. The modification of cellular calcium homeostasis induced by ferric lactate, which is a phenomenon inherent in cell injury, is not caused by lipid peroxidation. The role of iron-induced cellular calcium homeostasis in carcinogenesis is discussed.

Animals↗

PubMedDate not supplied

[Characteristics of several indicators of colloid-osmotic homeostasis in middle-aged and aged persons].

Basic indexes of colloid-osmotic homeostasis have been studied in 50 patients. 25 elderly and old patients without surgical pathology have been examined, 25 young healthy persons were controls. It has been found that in elderly patients blood plasma COP tends to decrease, while blood plasma osmolality increases. The nature of changes gives evidence of lower reliability of colloid-osmotic homeostasis in geriatric patients. The results show that it is unjustified to use standard values of colloid-osmotic homeostasis characteristic of young and middle-aged patients during infusion therapy in geriatric patients.

Adolescent↗

PubMed1996

Calcium homeostasis in pregnancy.

The demands of fetal growth lead to an adaptation of maternal homeostasis in order to provide the required calcium from enhanced intestinal absorption rather than from mobilization of maternal skeletal reserves. In large part this adaptive process depends on the interrelationship between PTH and 1,25(OH)2D which shows quantitative rather than qualitative changes from the non-pregnant state. In contrast the maintenance of fetal mineral homeostasis largely depends on PTHrP which regulates active placental calcium transfer and the calcium fluxes across the kidney and bone. The major source of PTHrP is the fetal parathyroid gland although some is provided by the placenta. It may be this latter component which passes into the maternal circulation where it may play a role in calcium homeostasis by acting through the PTH receptor.

Biological Transport↗

PubMed1996

Calcium homeostasis in cultured embryonic rat septohippocampal neurons is altered by ethanol and nerve growth factor before and during depolarization.

Ethanol and nerve growth factor (NGF) affect the survival of septohippocampal (SH) neurons. The effect of ethanol and NGF on calcium (Ca2+) homeostasis in these neurons was investigated in this study. Changes in intracellular-free Ca2+ concentration ([Ca2+]i) were measured using indo-1 in cultured embryonic (E21) SH neurons before stimulation (basal) and during stimulation with 30 mM potassium cloride (KCl+). SH neurons were treated with 0, 100, 200, 400, or 800 mg% ethanol with NGF (+NGF) or without NGF (-NGF). NGF treatment decreased, while ethanol did not affect basal [Ca2+]i. The combination of ethanol and NGF treatment led to increases in basal [Ca2+]i. While [Ca2+]i was lower during stimulation with KCl+ following ethanol or NGF treatment, ethanol and NGF treatment together led to significantly greater increases or decreases in [Ca2+]i compared to similarly treated NGF neurons. Responses of SH neurons were compared to those of medial septal (MS) neurons. Changes in [Ca2+]i during treatment with ethanol and/or NGF were reduced in SH neurons compared with MS neurons. We conclude that changes in Ca2+ homeostasis can occur in SH neurons in the presence of ethanol and/or NGF. The changes following ethanol treatment are enhanced by NGF. By altering Ca2+ homeostasis, NGF may enhance the survival of SH neurons during ethanol-induced neurotoxicity.

Animals↗

PubMed1996

Hormonal regulation of calcium homeostasis.

Several hormones play a role in calcium homeostasis. PTH and 1,25(OH)2D exert their effects on the skeleton, kidney, and gastrointestinal tract, maintaining normal levels of calcium and phosphate in both blood and extracellular fluid. Regulation of bone turnover, reabsorption of calcium and phosphate from the glomerular filtrate, and absorption of calcium and phosphate from the diet are mechanisms by which homeostasis is preserved. Calcitonin may be involved in calcium homeostasis, but its role is less well defined.

Calcitonin↗

PubMedDate not supplied

Effects of iron complexes on brain calcium homeostasis.

The effects of two physiological low molecular weight iron complexes, ferric lactate and ferric adenosine triphosphate (ATP) on brain Ca2+ homeostasis modification, have been studied in vitro and in vivo. In vitro ferric ATP complex shows a higher efficiency as modifier of Ca2+ homeostasis. This higher reactivity and the in vivo observed effect of increased brain uptake of iron from ferric lactate provoked by the presence of ATP, corroborate in vitro results showing an iron transfer from ferric lactate to ATP, as well as the mediator role of ATP in the iron-induced cellular Ca2+ homeostasis modification process. The possible role of this process in Parkinson's disease is discussed.

Adenosine Triphosphate↗

PubMed1997

Regulation of Ca2+ homeostasis by glucose metabolism in rat brain.

In a previous communication we reported that glucose deprivation from KHRB medium resulted in a marked stimulation of Ca2+ uptake by brain tissue, suggesting a relationship between glucose and Ca2+ homeostasis in brain tissue. Experiments were carried out to investigate the significance of glucose in Ca2+ transport in brain cells. The replacement of glucose with either D-methylglucoside or 2-deoxyglucose, non-metabolizable analogues of glucose, resulted in stimulation of Ca2+ uptake just as by glucose deprivation. These data show that glucose metabolism rather than glucose transfer was necessary to stimulate Ca2+ uptake in brain tissue. Inhibition of glucose metabolism with either NaF, NaCN, or iodoacetate resulted in stimulation of Ca2+ uptake similar to that produced by glucose deprivation. These results lend further support for the concept that glucose metabolism is essential for Ca2+ homeostasis in brain. Anoxia promotes glucose metabolism through glycolytic pathway to keep up with the demand for ATP by cellular processes (the Pasteur effect). Incubation of brain slices under nitrogen gas did not alter Ca2+ uptake by brain tissue, as did glucose deprivation and the inhibitors of glucose metabolism. We conclude that glucose metabolism resulting in the synthesis of ATP is essential for Ca2+ homeostasis in brain. Verapamil and nifedipine which block voltage-gated Ca2+ channels, did not alter Ca2+ uptake stimulated by glucose deprivation, indicating that glucose deprivation-enhanced Ca2+ uptake was not mediated by Ca2+ channels. Tetrodotoxin which specifically blocks Na2+ channels, abolished Ca2+ uptake enhanced by glucose deprivation, but had no effect on Ca2+ uptake in presence of glucose (controls). These results suggest that stimulation of Ca2+ uptake by glucose deprivation may be related to Na2+ transfer via NaCa exchange in brain.

Animals↗

PubMedDate not supplied

Granulocyte-macrophage colony-stimulating factor and pulmonary surfactant homeostasis.

Pulmonary surfactant lining the alveolus of the lung is critical to postnatal adaptation to air breathing. Precise concentrations of surfactant proteins and lipids are maintained in the alveolar space by a careful balance among synthesis, recycling, and catabolism. Pulmonary alveolar proteinosis is a rare pulmonary disease associated with accumulation of surfactant lipids and proteins in the alveolar spaces. Recent work with transgenic mice demonstrated that disruption of the production of granulocyte-macrophage colony-stimulating factor (GM-CSF) or the common beta-subunit of the GM-CSF receptor caused alveolar proteinosis that was histologically similar to that seen in human patients. The defect in surfactant homeostasis is caused by decreased surfactant clearance, mediated (at least in part) by dysfunction of the alveolar macrophage. Local production of GM-CSF corrects the alveolar proteinosis in the GM-CSF knockout mouse. Likewise, transplantation of wild-type bone marrow cells expressing the common beta-chain of the GM-CSF receptor restores surfactant homeostasis in the GM-CSF receptor knockout mouse. These studies demonstrate the previously unanticipated role of GM-CSF signaling in surfactant homeostasis, mediated (at least in part) by its actions on the clearance of surfactant lipids and proteins by the alveolar macrophage. These findings may have important implications for the diagnosis and treatment of pulmonary alveolar proteinosis syndromes in humans.

Animals↗