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At least 937 records · Page 52Linked to original sources

PubMed2003

Creatine supplementation affects glucose homeostasis but not insulin secretion in humans.

AIMS: In this study, it was investigated whether the glucose homeostasis is affected by dietary creatine supplementation. For this purpose, the plasma glucose concentration and the plasma insulin response to an oral glucose load were measured in creatine-supplemented vegetarians. METHODS: The subjects were supplemented with either 5 g of creatine monohydrate (creatine-treated group, CREAT) or 5 g of maltodextrin (control group, CON) per day for 42 days. On days 0 and 43, blood samples were collected before as well as 10, 20, and 30 min following an oral glucose load and analyzed for plasma creatine, insulin, and glucose levels. RESULTS: Creatine supplementation resulted in an increase in plasma creatine (CREAT 92.7 +/- 14.6 micro M vs. CON 31.2 +/- 3.2 micro M; p = 0.001). There was a trend (p = 0.07) towards elevated fasting plasma glucose levels following creatine supplementation, while the plasma glucose response to the glucose load was enhanced (CREAT 168.2 +/- 5.3 mM. min vs. CON 129.6 +/- 14.7 mM.min; p = 0.05). There was no difference observed in the plasma insulin response to the glucose load between the groups. CONCLUSION: This study shows that creatine supplementation may result in abnormalities in glucose homeostasis in the absence of changes in insulin secretion.

Blood Glucose↗

PubMed2003

Effects of parathyroidectomy on iron homeostasis and erythropoiesis in hemodialysis patients with severe hyperparathyroidism.

AIMS: Secondary hyperparathyroidism (HPT) worsens anemia and may cause hyporesponsiveness to recombinant human erythropoietin therapy (r-HuEPO). To investigate the effect of parathyroidectomy (PTX) on iron homeostasis and erythropoiesis, we conducted a prospective study in chronic hemodialysis patients who underwent PTX. METHODS: Thirty-two patients were enrolled in this study. Based on the increases in hemoglobin level after PTX, patients were divided into responders and nonresponders. Iron homeostasis and erythropoiesis were assessed before and 1 and 3 months after PTX, hemoglobin and parathyroid hormone levels were monitored until 6 months after PTX. RESULTS: In the responders, increased hemoglobin levels were observed in 15 patients at 1 and 3 months after PTX (8.0 +/- 0.8 g/dl vs. 9.2 +/- 1.3 and 10.1 +/- 0.9 g/dl, p < 0.05). The nonresponders had higher pre-PTX hemoglobin levels than the responders (10.3 +/- 1.6 g/dl vs. 8.0 +/- 0.8 g/dl, p < 0.05). There was no further increase in hemoglobin at 6 months compared to 3 months after PTX in both groups. In neither group did PTX affect serum ferritin, transferrin saturation and serum erythropoietin level. Serum soluble transferrin receptor (sTfR) concentration was found to be higher in responders than in nonresponders (3.32 +/- 1.28 mg/l vs. 1.70 +/- 0.31 mg/l, p < 0.05). CONCLUSIONS: We conclude that PTX can improve anemia in hemodialysis patients with severe hyperparathyroidism and greater resistance to r-HuEPO therapy. The reversing of anemia does not involve altering iron mobilization. Pre-PTX hemoglobin and serum sTfR levels can predict the effect of PTX on correcting anemia.

Adult↗

PubMed2004

Role of insulin-like growth factor iin maintaining normal glucose homeostasis.

Insulin-like growth factor I (IGF-I) has significant structural homology with insulin. IGF-I has been shown to bind to insulin receptors to stimulate glucose transport in fat and muscle, to inhibit hepatic glucose output and to lower blood glucose while simultaneously suppressing insulin secretion. However, the precise role of IGF-I in maintaining normal glucose homeostasis and insulin sensitivity is not well defined. Studies in patients with diabetes have shown that in insulin-deficient states, serum IGF-I concentrations are low and increase with insulin therapy. Similarly, administration of insulin via the portal vein results in optimization of plasma IGF-I concentrations. A patient with an IGF1 gene deletion was shown to have severe insulin resistance that improved with IGF-I therapy. Studies conducted in experimental animals have shown that if IGF-I synthesis by the liver is deleted, the animals become insulin-resistant, and this is improved when IGF-I is administered. Likewise, deletion of the IGF-I receptor in muscle in mice induces severe insulin resistance. Administration of IGF-I to patients with type 2 diabetes mellitus has been shown to result in an improvement in insulin sensitivity and a reduction in the requirement for exogenously administered insulin to maintain glucose homeostasis. A polymorphism in the IGF1 gene that has been shown to reduce serum IGF-I results in an increased prevalence of type 2 diabetes. Taken together, these findings support the conclusion that IGF-I is necessary for normal insulin sensitivity, and impairment of IGF-I synthesis results in a worsening state of insulin resistance.

Adult↗

PubMedDate not supplied

Topical application of ionic polymers affects skin permeability barrier homeostasis.

We previously demonstrated that the external electric potential affected skin barrier homeostasis. On the other hand, topical application of an ionic polymer formed a diffusion electric double layer on the surface of the skin. Thus, we evaluated effects of topical application of ionic polymers on the damaged skin barrier. Application of a nonionic polymer did not affect barrier recovery. Application of sodium salts of anionic polymers accelerated barrier recovery, while that of cationic polymers delayed it. Topical application of a sodium-exchange resin accelerated barrier recovery, but application of a calcium-exchange resin had no effect even when the resins had the same structure. Application of a chloride-exchange resin delayed barrier recovery. Topical application of ionic polymers influenced skin barrier homeostasis.

Administration, Cutaneous↗

PubMed2005

Effects of lithium on endolymph homeostasis and experimentally induced endolymphatic hydrops.

There is evidence to suggest that water homeostasis in the inner ear is regulated via the vasopressin (VP)-aquaporin 2 (AQP2) system in the same fashion as in the kidney. The VP-AQP2 system in the kidney is well known to be inhibited by lithium, resulting in polyuria due to a decrease in reabsorption of water in the collecting duct of the kidney. Therefore, lithium is also likely to inhibit the VP-AQP2 system in the inner ear, and consequently exert some influence on inner ear fluid homeostasis. In this study, we investigated the effects of lithium on AQP2 expression in the rat inner ear, and on the cochlear fluid volume in hydropic ears of guinea pigs. A quantitative PCR study revealed that lithium reduced AQP2 mRNA expression in the cochlea and endolymphatic sac. Lithium application also decreased the immunoreactivity of AQP2 in the cochlea and endolymphatic sac. In a morphological study, lithium intake significantly reduced endolymphatic hydrops dose-dependently. These results indicate that lithium acts on the VP-AQP2 system in the inner ear, consequently producing a dehydratic effect on the endolymphatic compartment.

Animals↗

PubMedDate not supplied

Cytokine contribution to the repair processes and homeostasis recovery following anoxic insult: a possible IFN-gamma-regulating role in IL-1beta neurotoxic action in physiological or damaged CNS.

The cytokine contribution to the central nervous system (CNS) is currently being investigated, but conflicting results have frequently been found. Since, as stressed in the immune system, the cytokine action can be profoundly influenced by the synergistic and antagonistic interactions of the various cytokines present in the medium, a productive effect of the cytokine network in the repair processes and homeostasis recovery may also be dependent on their balanced response in the CNS. We, therefore, hypothesize that it is necessary to study the cytokine contribution to CNS events, evaluating cytokines both in their network and individually. Recent studies focus on interleukin 1 (IL-1) as a cytokine of primary importance for the outcome of diseases, and it seems to exert this role by regulating the synthesis of new proteins such as gamma interferon (IFN-gamma) cytokine which has been reported as having a very important early role in the balance of interactions in the cytokine network. On this basis, to verify the above hypothesis, we determined the release level of IL-1beta and IFN-gamma cytokines in media of cultured rat hippocampal neurons under physiological and anoxic conditions with and without 2-amino-5-phosphonopentanoate (AP5; an N-methyl-D-aspartate receptor antagonist). Our results show that these cytokines are released in these media, and the anoxic insult seems to determine an increase in IL-1beta and a decrease in IFN-gamma release levels as compared to those under the physiological condition. Moreover, while the IL-1beta and IFN-gamma releases covary positively in the physiological media (because an increase in the IL1-beta level is paralleled by an increase in IFN-gamma), the anoxic insult renders this interaction negative (as the IL-1beta level increase corresponds to a decrease in the IFN-gamma level). These data led us to suggest that IFN-gamma may have a physiological regulating role in the IL-1 neurotoxic action and homeostasis recovery following an insult. In fact, the addition of AP5 before anoxic exposure resulted in a significant increase of cellular survival, but also in a decrease of IL-1beta release and a re-establishment of IL-1beta and IFN-gamma release relations to the initial condition without stress. Our overall results, therefore, sustain our hypothesis on the importance of studying the role of cytokines both in their network and individually.

Animals↗

PubMed1994

Neurotrophin regulation of energy homeostasis in the central nervous system.

Our hypothesis is that one cause of neuronal cell death and shrinkage in the aged central nervous system is an inability of neurons to maintain oxidant homeostasis in the face of increased levels of reactive oxygen species, decreased endogenous antioxidants, and impaired energy metabolism associated with physiological senescence, Alzheimer's, and Parkinson's diseases. Since treatment with nerve growth factor (NGF) reverses behavioral impairments in aged rats and stimulates cholinergic activity in the basal forebrain, while brain-derived neurotrophic factor appears to play a similar role in the striatum, we propose that neurotrophin-mediated cell-sparing reflects effects on oxidant homeostasis. Neurotrophins may play a similar cell-sparing role in hypoxic/ischemic injury to the nervous system, which also is mediated in part by reactive oxygen species. The degradation of one such species, H2O2, is catalyzed by catalase and glutathione peroxidase (GSH Px). The activity of the latter enzyme is dependent on glutathione reductase and the availability of NADPH for regeneration of reduced GSH. The GSH redox cycle is also regulated by enzymes of the hexose monophosphate shunt. NGF protects PC12 cells from H2O2 injury by stimulating the synthesis of antioxidant enzymes including catalase, GSH Px, glucose-6-phosphate dehydrogenase, and gamma-glutamylcysteine synthetase, the rate-limiting enzyme for glutathione synthesis. NGF also enhances recovery from the NAD+ losses occurring as a consequence of H2O2 treatment.

Animals↗

PubMed1993

Involvement of the cervical sympathetic nervous system in the changes of calcium homeostasis during turpentine oil-induced stress in rats.

Hypocalcemia is a common finding during stress. The objective of this study was to examine: (a) the changes in circulating calcium, parathyroid hormone (PTH) and calcitonin (CT) concentration in rats stressed by being given a subcutaneous injection of turpentine oil, and (b) the involvement of the sympathetic cervical pathway in stress-induced changes of calcium homeostasis. Four hours after receiving turpentine oil or vehicle, rats were subjected either to hypocalcemia, by being given EDTA intraperitoneally, or to hypercalcemia, by being injected CaCl2 intraperitoneally. Significant changes in serum calcium (10% decrease), serum PTH (28% increase) and CT levels (40% decrease) were observed in stressed rats. EDTA administration brought about a significantly greater hypocalcemia, and a higher PTH secretory response in turpentine oil-stressed rats. During stress, the increase of serum calcium after CaCl2 was significantly smaller, and the rise of CT was greater than in controls. In the case of CT the changes were still observed in rats subjected to superior cervical ganglionectomy (SCGx) 14 days earlier. In the case of PTH, the increase found in stressed rats, but not the augmented response after EDTA, was blunted by SCGx. The potentiation of hypocalcemia brought about by turpentine oil was no longer observed in SCGx rats. In vehicle-treated controls, SCGx delayed PTH response to hypocalcemia, but did not affect the increased response of CT to CaCl2 challenge. The results indicate that a number of changes in calcium homeostasis arise during turpentine oil stress in rats. SCGx was effective to modify the set point for PTH release, but played a minor role in affecting the augmentation of CT release during stress.

Animals↗

PubMed1980

Influence of cholecalciferol on tissue zinc homeostasis in the rat.

A role for calciferol in zinc homeostasis was investigated by radioisotope uptake and compartmental analysis techniques. cholecalciferol was injected into rats 4-5 days prior to radioisotopic study of rapidly exchangeable pools (< 4 h). Kidney, liver, and duodenum had significant increases in zinc uptake rates. Bone and skeletal muscle had significant decreases. No other tissues had significant differences. Compartmental analysis models generated by the SAAM-25 digital computer program suggested a decrease in the fractional tissue to plasma coefficient to be the mechanism for the observed changes in the serum zinc concentration and tissue zinc accumulation rates. It is not clear whether this is a specific effect of calciferol on zinc homeostasis or is a nonspecific response which may reflect some role for zinc in calciferol metabolism.

Animals↗

PubMed1989

Interleukin-1 and glucose homeostasis: an example of the biological relevance of immune-neuroendocrine interactions.

Interleukin-1 (IL-1), a cytokine mainly produced by monocytes-macrophages, plays a crucial role in immunological and inflammatory processes. We have recently demonstrated that IL-1 can also affect neuroendocrine mechanisms. In this paper, we refer to the capacity of IL-1 to affect glucose homeostasis. In normal mice, low doses of IL-1 induce a long-lasting hypoglycemia which is not dependent on possible insulin-secretagogue actions of this cytokine. The hypoglycemic effect of IL-1 is also observed in insulin-resistant diabetic mice. Furthermore, IL-1 seems to adjust the 'set point' for glucose regulation to a lower level. The effects of IL-1 on glucose homeostasis constitute a clear example of the biological relevance of immune-neuroendocrine interactions.

Animals↗

PubMed1994

Effects of growth hormone treatment for short stature on calcium homeostasis, bone mineralisation, and body composition.

We investigated the effect of growth hormone (GH) treatment on mineral and vitamin D homeostasis, bone mineralisation, and body composition in short-statured children without GH deficiency (GHD). 11 children received GH (0.50 +/- 0.08 IU/kg/week) for 24 weeks. 1,25-Dihydroxyvitamin D3 levels (mean +/- SD in pmol/l) rose from a baseline of 73.7 +/- 39.2 to 114.0 +/- 32.7 at 8 weeks (p < 0.05) and 111.9 +/- 39.7 at 24 weeks (p < 0.01). Body composition evaluation using dual-energy X-ray absorptiometry revealed increased lean tissue mass and a reduction in fat tissue. As a percentage of total body mass, fat decreased from 19.0 +/- 11.8% at baseline to 17.3 +/- 11.5% at 8 weeks (p < 0.005) and 16.8 +/- 11.5% at 24 weeks (p < 0.05). L2-L4 bone mineral density was 0.637 +/- 0.155 g/cm2 at baseline and 0.666 +/- 0.160 g/cm2 at 24 weeks (NS). We conclude that recombinant human GH treatment of short children without GHD has significant effects on vitamin D homeostasis and body composition.

Body Composition↗

PubMed1996

Neuropeptide Y, the hypothalamus and the regulation of energy homeostasis.

Neuropeptide Y (NPY) neurones in the arcuate nucleus of the rodent hypothalamus may play a key role in responding to reductions in body energy stores with appropriate changes in energy homeostasis, namely an increase in food-seeking behaviour and hyperphagia, together with a reduction in heat production by brown adipose tissue. These adaptive responses are mimicked by the injection of NPY into the main sites of projection of the NPY neurones, and animals that are threatened by energy deficits (e.g. through starvation or insulin-deficient diabetes) show increased activity of these neurones. Genetically obese rodents also show hyperactivity of the NPY neurones, which is inappropriate to their energy needs and may contribute to their hyperphagia, reduced energy expenditure and excessive weight gain. The NPY neurones may be inhibited by insulin and leptin, which may both serve as signals of peripheral fat mass. Ultimately, characterization of the specific "feeding' receptors which mediate NPY's central effects on energy homeostasis may provide opportunities for designing drugs to manipulate and appetite and energy balance in man, notably obesity and the cachexia commonly associated with malignancy and chronic infection.

Animals↗

PubMed1990

Beneficial effects of angiotensin-converting enzyme inhibitor on renal function and glucose homeostasis in diabetics with hypertension.

The antihypertensive efficacy of enalapril and its effects on renal function and glucose homeostasis were investigated in 9 hypertensive patients with non-insulin-dependent diabetes mellitus. Enalapril therapy produced a significant fall in blood pressure (BP) (p less than 0.05) and a significant increase in renal blood flow (p less than 0.05) without a change in glomerular filtration rate. Furthermore, fasting plasma glucose was significantly reduced (p less than 0.01). Similarly, M value, as an index of plasma glucose control in diabetes, was significantly reduced from 19.6 to 10.1 (p less than 0.01). These findings suggested that the angiotensin-converting enzyme inhibitor enalapril was effective in reducing BP and improving renal function, and might improve glucose homeostasis in hypertensive diabetics.

Aged↗

PubMed1997

Derangement of pH homeostasis in the renal papilla: ochratoxin A increases pH in vasa recta blood.

It is reported that ochratoxin A (OTA) impairs urinary acidification by increasing the urinary pH and also increases the intracellular pH in Madin-Darby canine kidney cells. This study was designed to examine whether OTA deranges pH homeostasis in the interstitium (or vasa recta) of the renal papilla. Rats were injected once with OTA (3 micromol/kg body weight) intravenously (acute application) or with OTA (1.25 micromol/kg body weight/day) intraperitoneally for 6 days (subchronic application). We measured the pH values in both the descending and ascending vasa recta blood (VR) in the renal papilla. Both the acute and subchronic applications of OTA led to significant increases in pH values in both descending and ascending VR by 0.4-0.6 pH units. However, no significant increases in pH values in renal arterial and aortic blood in OTA-treated rats were observed. We also examined the pH changes in collecting-duct urine after OTA injection (3 micromol/kg body weight). We found a significant increase in pH values 30 min after OTA injection; this significant elevation of pH values was present during the whole experiment (120 min). The results of this study suggest that OTA deranges pH homeostasis in the interstitium of the renal papilla, in addition to the impairment of urinary acidification.

Animals↗

PubMed1987

Glucose homeostasis in the newborn: effects of an intravenous glucose infusion in normal and intra-uterine growth-retarded neonatal piglets.

Disturbances of glucose homeostasis are a common clinical problem in low birth weight human infants. Previous studies have demonstrated that the intra-uterine growth-retarded piglet is a suitable animal model for the study of such problems. The effects of an intravenous glucose infusion on glucose homeostasis have been studied in normal and intrauterine growth-retarded neonatal piglets using a non-steady state tracer technique. Despite suppression of hepatic glucose output, hyperglycaemia (plasma glucose greater than 10.0 mmol/l) developed in the majority of animals. The hyperglycaemia resulted from a failure to increase glucose utilisation adequately in response to the glucose infusion. Growth-retarded animals had an impaired ability to increase their rate of glucose utilisation, although, in common with the normally grown animals, they demonstrated a graded response to different infusion rates of glucose.

Animals↗

PubMed1994

Platelet calcium homeostasis is abnormal in patients with severe arteriosclerosis.

To evaluate platelet calcium homeostasis in a typical thrombosis-prone clinical condition, 14 patients with severe arteriosclerosis and 11 healthy control subjects were studied. Platelet intracellular free calcium concentration ([Ca2+]i) was evaluated by means of the fluorescent probe fura 2 under resting conditions and after challenge with 0.05, 0.1, and 0.5 U/mL thrombin (final concentrations). Three different concentrations of extracellular ionized calcium ([Ca2+]e) were used: 1 mmol/L, 1 mumol/L, and < 1 nmol/L. Resting platelet [Ca2+]i was significantly higher (P < .001) in patients than in control subjects. After addition of 0.05 U/mL thrombin, the relative increase of [Ca2+]i was lower in patients than in control subjects in each of the three [Ca2+]e conditions (P = .05 at 1 mmol/L, P = .02 at 1 mumol/L, and P = .04 at < 1 nmol/L). After addition of 0.1 U/mL thrombin, the relative increase of [Ca2+]i was lower in patients than in control subjects under two [Ca2+]e conditions, 1 mumol/L and < 1 nmol/L (P = .04 and P = .03 respectively). With 0.5 U/mL thrombin, a trend toward lower values in patients than in control subjects was observed, reaching statistical significance (P = .03) only at < 1 nmol/L [Ca2+]e. These results suggest that calcium homeostasis is abnormal in platelets from patients with severe arteriosclerosis and probably reflects a chronic activation.

Adult↗

PubMed1993

Intracellular calcium homeostasis in cardiac myocytes.

Calcium homeostasis in cardiac myocytes results from the integrated function of transsarcolemmal Ca2+ influx and efflux pathways modulated by membrane potential and from intracellular Ca2+ uptake and release caused predominantly by SR function. These processes can be importantly altered in different disease states as well as by pharmacological agents, and the resulting changes in systolic and diastolic [Ca2+]i can cause clinically significant alterations in contraction and relaxation of the heart. It may be anticipated that a rapid increase in our understanding of the pathophysiology of Ca2+ homeostasis in cardiac myocytes will be forthcoming as the powerful new tools of molecular and structural biology are used to investigate the regulation of Ca2+ transport systems.

Animals↗

PubMed2004

Transient receptor potential melastatin 7 ion channels regulate magnesium homeostasis in vascular smooth muscle cells: role of angiotensin II.

Magnesium modulates vascular smooth muscle cell (VSMC) function. However, molecular mechanisms regulating VSMC Mg2+ remain unknown. Using biochemical, pharmacological, and genetic tools, the role of transient receptor potential membrane melastatin 7 (TRPM7) cation channel in VSMC Mg2+ homeostasis was evaluated. Rat, mouse, and human VSMCs were studied. Reverse transcriptase polymerase chain reaction and immunoblotting demonstrated TRPM7 presence in VSMCs (membrane and cytosol). Angiotensin II (Ang II) and aldosterone increased TRPM7 expression. Gene silencing using small interfering RNA (siRNA) against TRPM7, downregulated TRPM7 (mRNA and protein). Basal [Mg2+]i, measured by mag fura-2AM, was reduced in siRNA-transfected cells (0.39+/-0.01 mmol/L) versus controls (0.54+/-0.01 mmol/L; P<0.01). Extracellular Mg2+ dose-dependently increased [Mg2+]i in control cells (Emax 0.70+/-0.02 mmol/L) and nonsilencing siRNA-transfected cells (Emax 0.71+/-0.04 mmol/L), but not in siRNA-transfected cells (Emax 0.5+/-0.01 mmol/L). The functional significance of TRPM7 was evaluated by assessing [Mg2+]i and growth responses to Ang II in TRPM7 knockdown cells. Acute Ang II stimulation decreased [Mg2+]i in control and TRPM7-deficient cells in a Na+-dependent manner. Chronic stimulation increased [Mg2+]i in control, but not in siRNA-transfected VSMCs. Ang II-induced DNA and protein synthesis, measured by 3[H]-thymidine and 3[H]-leucine incorporation, respectively, were increased in control and nonsilencing cells, but not in TRPM7 knockdown VSMCs. Our data indicate that VSMCs possess membrane-associated, Ang II-, and aldosterone-regulated TRPM7 channels, which play a role in regulating basal [Mg2+]i, transmembrane Mg2+ transport and DNA and protein synthesis. These novel findings identify TRPM7 as a functionally important regulator of Mg2+ homeostasis and growth in VSMCs.

Aldosterone↗