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Biomedical subjects

F Corica

Publications and source records attributed to F Corica.

At least 55 records · Page 3Linked to original sources
PubMed1999

Platelet magnesium depletion in normotensive and hypertensive obese subjects: the role of salt-regulating hormones and catecholamines.

We measured plasma and platelet magnesium concentrations, plasma epinephrine and norepinephrine, and plasma aldosterone and renin concentrations in normotensive (NT-Ob, n = 19, BMI 35.7 +/- 7.4 kg/m2, WHR 0.92 +/- 0.05) and hypertensive (HT-Ob, n = 11, BMI 35.2 +/- 3.6 kg/m2, WHR 0.93 +/- 0.07) obese subjects, and in a group of age- and sex-matched lean controls (n = 14, BMI 23.1 +/- 1.8 kg/m2, WHR 0.79 +/- 0.05). Plasma aldosterone and renin concentrations were significantly higher in obese subjects with respect to controls. Moreover, plasma norepinephrine and epinephrine levels were significantly increased in obese subjects, and plasma norepinephrine was higher in HT-Ob when compared to NT-Ob group. Platelet magnesium concentrations were significantly reduced in both normotensive and hypertensive obese subjects with respect to controls (controls 2.65 +/- 0.35 mumol/10(8) cells, NT-Ob 2.02 +/- 0.19 mumol/10(8) cells--p < 0.001, HT-Ob 1.98 +/- 0.18 mumol/10(8) cells--p < 0.001), while a slightly significant decrease in plasma magnesium levels was only detectable in HT-Ob group. Urinary magnesium and magnesium fractional excretion were significantly increased in hypertensive obeses. Pearson's correlation analysis, separately performed in each group of subjects, showed that plasma aldosterone, renin, epinephrine, norepinephrine and magnesium fractional excretion were negatively correlated to platelet magnesium levels in NT-Ob and HT-Ob groups, but not in lean controls. The multiple linear regression analysis performed in the whole group of obese subjects considering platelet magnesium as a dependent variable showed that platelet magnesium decrease together with the increase in plasma epinephrine (p = 0.046) and norepinephrine (p = 0.020), also after adjusting for age, sex, BMI, WHR, HOMA IR and diagnosis of hypertension. Furthermore, platelet magnesium showed a trend for negative association (p < 0.1) to plasma aldosterone and magnesium fractional excretion in multivariate analysis. The impairment in platelet magnesium handling observed in normotensive and hypertensive obese patients seems to be associated to a rise in renin-angiotensin-aldosterone and sympathetic systems activity. Our results suggest that platelet magnesium depletion, together with disturbances of salt-regulating hormones and catecholamines, may be involved in the pathophysiology of cardiovascular complications from obesity.

Adult↗
PubMed1998

Effects of water deprivation and angiotensin II intracerebroventricular administration on brain nitric oxide synthase activity.

Intracranial administration of L-arginine causes a reduction of the water intake induced by water deprivation or by intracerebroventricular (i.c.v.) injection of angiotensin II (angiotensin II), through the release of nitric oxide (NO) in the central nervous system. We studied the effects of i.c.v. angiotensin II (120 ng/rat) in association with i.c.v. L-arginine (2.5-10 microg/rat) on blood pressure. We also studied the effects of both peripheral and central angiotensin II injection (1.5-6 mg kg(-1) i.p. and 30-120 ng rat(-1) i.c.v., respectively) on NO synthase activity in the cortex, diencephalon and brainstem, after water deprivation (24 h), conditions producing activation of the renin-angiotensin system. L-arginine dose dependently antagonized the increase in blood pressure induced by i.c.v. angiotensin II (P < 0.001). Peripheral administration of angiotensin II produced a dose-dependent reduction of NO synthase activity in the brainstem and cortex (P < 0.001), but not in the diencephalon. Water deprivation produced similar effects on brain NO synthase activity. Angiotensin II i.c.v. injection caused NO synthase activity reduction in all brain regions studied (P < 0.001). Our findings suggest that NO and angiotensin II could play opposite roles in brain regulation of blood pressure and drinking behaviour.

Angiotensin II↗
PubMed1998

Effects of intracerebroventricular leptin administration on food intake, body weight gain and diencephalic nitric oxide synthase activity in the mouse.

1. Intracranial administration of leptin reduces both food intake and body weight gain in the mouse. Inhibitors of nitric oxide (NO) synthase produce similar effects. 2. To investigate the role of the brain L-arginine/NO pathway in mediating this effect of leptin, we have evaluated food intake and body weight gain after daily (5 days) intracerebroventricular (i.c.v.) administration of leptin (0.5-2 microg) alone or in association with L-arginine (10 microg). Moreover, we measured diencephalic nitric oxide synthase (NOS) activity after a single i.c.v. leptin (0.25-2 microg) injection and after consecutive doses of leptin (0.25-2 microg) over 5 days. The time course of the effect of leptin on NOS activity was also evaluated. 3. I.c.v. injected leptin (1 and 2 microg) significantly and dose-dependently reduced food intake and body weight gain with respect to vehicle (food intake: 5.97+/-0.16 g 24 h(-1) and 4.27+/-0.18 g 24 h(-1), respectively, vs 8.05+/-0.34 g 24 h(-1), P<0.001, n=6 for each group; body weight gain: -10.7+/-0.46% and -15.7+/-0.65%, respectively, vs 5.14+/-0.38%, P<0.001, n=6 for each group). This effect was antagonized by L-arginine (food intake: 7.90+/-0.37 g 24 h; body weight gain: 5.11+/-0.31%, n=6). Diencephalic NOS activity was significantly reduced by the highest doses of leptin with respect to vehicle (vehicle: 0.90+/-0.04 nmol citrulline min(-1) g(-1) tissue; leptin 1 microg: 0.62+/-0.03 nmol citrulline min(-1) g(-1) tissue, P<0.001; leptin 2 microg: 0.44+/-0.03 nmol citrulline min(-1) g(-1) tissue, P<0.001, n=6 for each group). Similar results were obtained in animals treated with daily consecutive doses of leptin. The inhibitory effect appeared rapidly (within 30 min) and was long lasting (up to 12 h). 4. Our results suggest that the brain L-arginine/NO pathway may be involved in the central effect of leptin on feeding behaviour and body weight gain in mice.

Animals↗
PubMed1998

Reduced blood bcl-2 protein concentration in patients on hemodialysis.

The concentrations of bcl-2 protein that can block programmed cellular death in various cell lines were evaluated in blood samples from 10 uremic patients on hemodialysis, 10 uremics not yet on hemodialysis, and in 10 healthy controls. The bcl-2 protein variations (in uremics on dialysis) were ascertained in patients during the dialysis session. Oxidative stress was evaluated in all groups by assaying the products of intraerythrocytic lipoperoxidation. Dialyzed and nondialyzed uremic patients had higher bcl-2 protein concentrations than healthy subjects. Dialysis causes a significant reduction in the concentrations of bcl-2 protein which becomes statistically significant during the 3rd hour. In both groups of uremic patients a positive correlation was found between bcl-2 protein and products of lipoperoxidation.

Aged↗
PubMed1998

Increased transforming growth factor-beta1 plasma concentration is associated with high plasma 3,3',5'-tri-iodothyronine in elderly patients with nonthyroidal illnesses.

OBJECTIVE: To study transforming growth factor-beta1 (TGF-beta1) plasma concentrations in elderly patients with nonthyroidal illnesses (NTI). DESIGN: Case-control study. METHODS: We measured plasma concentrations of tri-iodothyronine (T3), reverse T3 (rT3), thyroxine (T4), free T3 (fT3) and free T4 (fT4) estimates, TSH, and TGF-beta1 in 48 elderly NTI patients consecutively admitted in our Division of Internal Medicine and Metabolic Diseases, and in 11 healthy age- and sex-matched controls. RESULTS: The data on thyroid hormones enabled us to identify three groups: Group A, subjects (8 patients) with T3 and fT3 levels comparable to those in controls: Group B, subjects (30 patients) with T3 and fT3 levels lower than controls but rT3 levels comparable to those of controls; Group C, subjects (10 patients) with T3 and fT3 levels lower than those of controls and higher rT3 levels. The patients of Group C showed higher plasma levels of TGF-beta1 compared with controls. Moreover, we found a positive correlation between TGF-beta1 and rT3 (rs = 0.38, P < 0.01) in the whole group of NTI patients. CONCLUSIONS: Our data seem to confirm the hypothesis that TGF-beta1 could play a role in the pathogenesis of some modifications of thyroid function observed in patients with nonthyroidal illnesses.

Aged↗
PubMed1998

Plasma (total and ionized), erythrocyte and platelet magnesium levels in renal transplant recipients during cyclosporine and/or azathioprine treatment.

We evaluated total and ionized plasma magnesium levels, and erythrocyte and platelet magnesium concentrations from two groups of renal transplant recipients treated either with cyclosporine, azathioprine and prednisolone (group CAP, n = 8) or with azathioprine and prednisolone (group AP, n = 13), and in a group of age- and sex-matched healthy subjects (n = 10). Reduced plasma (total and ionized), erythrocyte and platelet magnesium concentrations were found in both CAP and AP groups with respect to controls (CAP: total plasma Mg median 0.61 vs 0.86 mmol/L, p < 0.01, ionized plasma Mg median 0.43 vs 0.58 mmol/L, p < 0.001, erythrocyte Mg median 2.18 vs 2.56 mmol/L, p < 0.05, platelet Mg median 1.75 vs 2.84 mmol/10(8) cells, p < 0.001; AP: total plasma Mg median 0.62 vs 0.86 mmol/L, p < 0.01, ionized plasma Mg median 0.48 vs 0.58 mmol/L, p < 0.001, erythrocyte Mg median 2.30 vs 2.56 mmol/L, p < 0.05, platelet Mg median 1.75 vs 2.84 mumol/10(8) cells, p < 0.001), while no difference was found between the two groups of transplant recipients as regards plasma and intracellular magnesium levels. Magnesium fractional excretion was higher in transplant recipients than in the control group (Mg fractional excretion median AP 18.6 per cent and CAP 12.8 per cent vs controls 3.5 per cent), whereas no difference was found between patients and control subjects for urinary magnesium 24h excretion. Moreover, in the whole group of transplant recipients (n = 21), urinary magnesium showed an inverse correlation with platelet (rs = -0.54, p < 0.05) and ionized plasma magnesium (rs = -0.48, p < 0.05), and time after transplantation showed a negative correlation with platelet magnesium concentrations (rs = -0.73, p < 0.001), and a direct correlation with fractional magnesium excretion (rs = 0.53, p < 0.05). Finally, a direct relationship between platelet magnesium and ionized plasma magnesium was also detected in the whole group of transplant recipients (rs = 0.47, p < 0.05). Both intraplatelet magnesium depletion and ionized plasma magnesium reduction induced by immunosuppressive therapy could be involved in the increased risk from atherosclerotic disease in renal transplant recipients.

Arteriosclerosis↗
PubMed1998

[Obesity and hypertension: the role of magnesium].

We focus on the recent "ionic hypothesis", in which an alteration of ionic metabolism represents a peculiar event in the pathogenesis of obesity and hypertension. We report the results from our original studies in which we evaluated intraplatelet magnesium levels. In a study on normotensive and hypertensive patients with non insulin-dependent diabetes mellitus and healthy control subjects, we showed a common reduction of plasma, erythrocyte and platelet magnesium levels in both normotensive and hypertensive diabetics with respect to control. Anyway, hypertensive diabetics showed a greater reduction of intraplatelet magnesium concentrations when compared to normotensive diabetics. Using the same technique, we found reduced erythrocyte and platelet magnesium concentrations in patients with essential hypertension with respect to the control group. In a successive study, we found, in the group of normotensive obese, that erythrocyte and platelet magnesium levels were significantly lower than those of the control group, while in hypertensive obese patients a reduction of plasma magnesium levels has been also detected. In conclusion, in these studies has been confirmed the existence of a reduction of the intracellular magnesium concentrations, which is common in hypertensive and obese patients.

Blood Platelets↗
PubMed1998

[Leptin: adipocyte hormone].

The authors reviewed the most recent literature on leptin, a protein produced by adipocytes which exerts its action on hypothalamus, modifying eating behavior and inhibiting the lust for food consumption. This one appeared to be the main, if not the only, physiologic action of leptin. Later leptin has been acknowledged a major role in the homeostasis. The regulation of the synthesis, and the mechanisms by which the protein modulates both food intake and energetic balance have been evaluated, and the hypotheses on the regulatory function exerted by leptin on the homeostasis, by acting on neuroendocrine system, on sexual maturity and fertility, on the sympathetic nervous system, on hemopoiesis and hydroelectrolytic balance have been discussed, some of which being already supported by experimental evidences.

Adipose Tissue↗
PubMed1997

Plasma, erythrocyte and platelet magnesium levels in type 1 diabetic patients with microalbuminuria and clinical proteinuria.

We evaluated plasma, erythrocyte and platelet magnesium levels in patients with insulin-dependent diabetes mellitus (IDDM) with normoalbuminuria (N = 10), microalbuminuria (N = 10), and clinical proteinuria (N = 7), and in a group of healthy subjects (N = 10). We found that IDDM patients had lower platelet magnesium levels when compared to controls. Lower platelet magnesium concentrations were found in patients with microalbuminuria (1.859 +/- 0.47 vs 2.340 +/- 0.46 mumol/10(8) cells, p < 0.05) and in those with clinical proteinuria (1.522 +/- 0.19 vs 2.340 +/- 0.46 mumol/10(8) cells, p < 0.01) with respect to the group with normoalbuminuria. In the groups with microalbuminuria and clinical proteinuria we detected a negative correlation between HbA1c and both plasma and platelet magnesium. Our findings indicate that microalbuminuria and clinical proteinuria are associated with an altered magnesium homeostasis. In particular, decreased platelet magnesium concentrations could represent an additional risk factor in the pathogenesis of microvascular complications of diabetes.

Adult↗
PubMed1997

Reduced plasma concentrations of transforming growth factor beta1 (TGF-beta1) in obese women.

OBJECTIVE: To evaluate Transforming Growth Factor beta1, (TGF-beta1) plasma concentrations and the possible relationship between this growth factor and various hormones in obese women. DESIGN: Case-control study. SETTING: Outpatient's Service for the Prevention and Treatment of Obesity at the University Hospital. SUBJECTS: Twenty-five women with mild to moderate obesity, and 15 non-obese healthy women were used as controls. MEASUREMENTS: Evaluation of TGF-beta1, insulin, prolactin, sex-hormone binding globulin, androstenedione, free triiodothyronine, free tetraiodothyronine, thyroid-stimulating hormone, dehydroepiandrosterone-sulfate, testosterone, insulin-like growth factor 1, cortisol and adrenocorticotropic hormone plasma concentrations in obese women. Blood samples were taken from fasting subjects for the determination of the above parameters. RESULTS: In obese women plasma TGF-beta1 concentrations were lower than in controls. The obese subjects also had lower GH, IGF-1 and SHBG plasma concentrations and increased insulinaemia. A positive correlation was found between TGF-beta1 and both IGF-1 (r = 0.52; P < 0.01) and DHEA-S (r = 0.43; P < 0.05), while a negative correlation was found between TGF-beta1 and SHBG (r = -0.49; P < 0.05). CONCLUSIONS: The reduction in TGF-beta1, an antilipogenic factor, may play a role in the pathogenesis of obesity and could be involved in the development of some obesity-related endocrine alterations.

Adult↗
PubMed1997

Renal failure from mitochondrial cytopathies.

Mitochondrial cytopathies are metabolic diseases, expressing mutations in nuclear DNA, punctiform mutations or depletions in mitochondrial DNA. These genetic lesions alter mitochondrial oxidative phosphorylation, with a reduction in energy produced for cell activity. Renal disease may be the first sign of mitochondrial cytopathy, or it may appear together with neurological and neuromuscular signs. Fanconi's syndrome, a benign sign of renal tubulopathy, is particularly frequent in newborns with mitochondrial cytopathy, whereas tubulointerstitial nephropathy, which affects infants and adults, is more serious because it develops into terminal uremia. Findings of hyperlactatemia and reduced enzymatic activity on the respiratory chain in tissue biopsies are of diagnostic significance in mitochondrial cytopathy. A breakthrough is being made in our understanding of genetic alterations in mitochondrial DNA, and with future therapy, the kidney, a target organ, may be safeguarded.

Adult↗
PubMed1997

Cold pressor test raises serum concentrations of ICAM-1, VCAM-1, and E-selectin in normotensive and hypertensive patients.

In patients with essential hypertension, elevated soluble E-selectin (sE-selectin) levels may indicate endothelial cell injury or activation. We therefore sought to ascertain whether arterial blood pressure increased by the cold pressor test can modify serum concentrations of sE-selectin and other soluble forms of adhesion molecules, such as soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1), or the expression of any adhesion molecules in circulating monocytes and lymphocytes. Our findings show that levels of sE-selectin, sVCAM-1, and sICAM-1 are higher in patients with essential hypertension than in normotensive subjects (sICAM-1, 380 +/- 52 versus 262 +/- 96 ng/mL, P<.05; sVCAM-1, 720 +/- 52 versus 625 +/- 38 ng/mL, P<.05; and sE-selectin, 75 +/- 21 versus 61 +/- 22 ng/mL, P<.05). Furthermore, in normotensive and hypertensive patients, the cold pressor test caused an increase in serum concentrations of sICAM-1, sVCAM-1, and sE-selectin, but it did not cause changes in the expression of adhesion molecules in circulating monocytes and lymphocytes. High arterial blood pressure may therefore increase the production of serum adhesion molecules, probably through endothelial activation.

Blood Pressure↗
PubMed1996

Magnesium levels in plasma, erythrocyte, and platelet in hypertensive and normotensive patients with type II diabetes mellitus.

The authors, by means of a recently introduced method, evaluated the intraplatelet concentrations of magnesium in 45 normotensive patients with type II diabetes mellitus, in 45 hypertensive diabetics and in 15 healthy controls. They also evaluated plasma and erythrocyte concentrations of the cation through direct current plasma spectrometer. Both normotensive and hypertensive diabetics showed a reduction in plasma, erythrocyte, and platelet concentrations of magnesium compared to controls. On the contrary, no significant difference was found between hypertensive and normotensive diabetics with regard to plasma and erythrocyte magnesium, whereas intraplatelet assay of the ion pointed out significantly lower concentrations of magnesium in hypertensive compared to normotensive patients (56.4 +/- 9.0 vs 60.7 +/- 10.2 micrograms/10(8) cells--p < 0.05). The authors believe that intraplatelet assay of magnesium may be the most reliable method for the evaluation of the cation in hypertensive diabetics, probably because platelets share common features with smooth muscle cells, including the alpha-2-adrenoceptor cyclase system and a coupling mechanism concerning the calcium-dependent contraction.

Aged↗