Search PubMed⌕ Search

Biomedical subjects

A Bruno

Publications and source records attributed to A Bruno.

At least 217 records · Page 12Linked to original sources
PubMed1984

Comparison of acute and subacute effects of deflazacort and prednisone on glucose metabolism in man.

Corticosteroid treatment produces glucose intolerance with insulin resistance. Recent reports have indicated that deflazacort (DF) is significantly less diabetogenic than prednisone (PN). A euglycaemic hyperinsulinaemic (100 microU/ml) glucose clamp ( EHGC ) and 3H-glucose infusion for 240 min were performed in 6 healthy volunteers (HV) after administration of 15 mg PN or 18 mg DF, 12 h and 2 h before test. The glucose metabolic clearance rate (MCR) was significantly (p = 0.02) higher after DF (4.75 +/- 0.58 ml/min X kg) than after PN (3.31 +/- 0.27 ml/min X kg). Basal hepatic glucose production (HGP) was significantly (p = 0.003) lower after DF (3.58 +/- 0.33 mg/kg X min) than after PN (4.44 +/- 0.23 mg/kg X min). A similar pattern was obtained for glucose volume (GV) and glucose pool (GP). The kinetic parameters of insulin were not significantly different after the two drugs. After 7 day of PN 30 mg/day or DF 36 mg/day, EHGC and 3H-glucose infusion for 240 min were performed in 10 HV. Glucose MCR values were significantly (p = 0.03) higher after DF (5.03 +/- 0.91 ml/min X kg) than after PN (2.80 +/- 0.26 ml/min X kg). HGP values did not different significantly after the two drugs. GV (p = 0.001) and GP (p = 0.002) were significantly lower after DF than after PN. Insulin kinetics were not significantly different after the two drugs. It is concluded that on acute and 7-day administration to healthy subjects DF, in an anti-inflammatory dose equivalent to PN, shows significantly less influence on glucose metabolism.

Adult↗
PubMed1984

Insulin resistance in the aged: a quantitative evaluation of in vivo insulin sensitivity and in vitro glucose transport.

It has recently been made clear that reduced sensitivity to exogenous insulin can be demonstrated in the course of aging. This phenomenon has been further investigated with the aid of sophisticated techniques, such as the euglycemic clamp, which, when coupled with the measurement of hepatic glucose production, showed that "impaired tissue sensitivity to insulin is the primary factor responsible for the decrease of glucose tolerance in advancing age." Nevertheless, this study did not establish whether such impairment reflects reduced sensitivity (receptor deficiency) or reduced response (postreceptor or receptor plus postreceptor defect), as shown in other diseases. Evidence in favor of the view that receptor deficiency is responsible can be seen in our observation of an approximately 50% reduction in receptors in a study of insulin binding on isolated human fat cells. Two aspects of this question appeared to require further investigation: tissue sensitivity to receptor-saturating insulin concentration (euglycemic clamp at about 1000 microU/mL plasma insulin), and the glucose transport system coupled to the receptor. A decrease in receptors alone should shift the insulin sensitivity curve to the right, both in vivo (euglycemic clamp) and in vitro (glucose transport), with no reduction of the maximum effect. A solution to this question is proposed in the light of a study conducted on young volunteers and subjects over 65 years old.

Adipose Tissue↗
PubMed1984

Hyperglycaemic clamp and insulin binding to isolated monocytes before and after glibenclamide treatment of mild type II diabetics.

The therapeutic action of 3.5 mg glibenclamide (HB 420) once a day for six weeks was evaluated in ten mild NID diabetics previously treated with diet only. Stable HbA1, insulin secretion during hyperglycaemic clamp (100 mg/dl over the baseline in the first study, and at the same level in the second one), peripheral sensitivity expressed as the amount of dextrose infused per Kg per min (M-coefficient), the glucose metabolic clearance rate (MCR) and the M/I ratio were measured. Circulating monocytes were separated to assess insulin binding before and after treatment. The results included a significant decrease in HbA1 (7.5 +/- 0.3 against 8.4 +/- 0.4%, P less than 0.005), increased steady-state (100-120 min.) plasma insulin (31 +/- 4.4 against 25.7 +/- 3.9 microU/ml), a significant increase in M-coefficient (4.02 +/- 0.62 against 2.49 +/- 0.31 mg/Kg/min, P less than 0.01), and MCR (1.90 +/- 0.34 against 1.18 +/- 0.18 ml/Kg/min, P less than 0.025) and an increase in the M/I ratio (14.6 +/- 1.9 against 11.2 +/- 1.7). All subjects displayed an increase in total insulin binding (4.03 +/- 0.31% against 2.79 +/- 0.34%, P less than 0.001) and affinity constants (Ke = 8.3 +/- 0.6 against 6.6 +/- 0.4 X 10(7) M-1, P less than 0.05). Since the M/I ratio increased in only 7/10 subjects and since there was no significant correlations between the percentage increase in M and MCR and the plasma insulin increase, whereas the increase in R0 was significant, it is felt that the euglycaemizing action of low doses of glibenclamide is primarily peripheral.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗
PubMed1984

Features of residual renal function in end-stage renal failure associated with spinal cord injury.

The characteristics of end-stage renal disease (ESRD) complicating spinal cord injury (SCI) were studied retrospectively in 43 male hemodialysis patients. A control group of male patients dialyzed in the same institution were studied for comparison. The SCI patients had significantly lower serum creatinine concentrations and daily urinary creatinine excretion than the control group, despite comparable creatinine clearances. Therefore, serum creatinine, when compared with the familiar values in non-SCI patients, may greatly underestimate the severity of the renal impairment. Urine output was higher, urine specific gravity lower, and renal glucosuria more common in the SCI patients. 24-hour urinary protein excretion was higher and serum albumin was lower in the SCI patients, with 48% of the patients exhibiting nephrotic range proteinuria. Urine pH was markedly elevated, and pyuria and bacteriuria were present in all SCI patients. Fractional excretion of potassium (159 +/- 16%) exceeded its filtered load in most SCI patients.

Adult↗
PubMed1983

An in vivo and in vitro study of the mechanism of prednisone-induced insulin resistance in healthy subjects.

Prednisone-induced insulin resistance may depend on either reduced sensitivity (receptor defect) or reduced response to insulin (postreceptor defect). To clarify the mechanism of prednisone-induced insulin resistance, a [3H]glucose infusion (1 microCi/min) was performed for 120 min before and during a euglycemic clamp repeated at approximately 100, approximately 1,000, and approximately 10,000 microU/ml steady state plasma insulin concentration in 10 healthy, normal weight subjects, aged 35 +/- 7 yr. Each test was repeated after 7-d administration of placebo or prednisone (15 plus 15 mg/d per subject), in a randomized sequence with an interval of 1 mo between the two tests. Mean fasting blood glucose (89.5 +/- 2.1 vs. 83.7 +/- 1.9 mg/dl) and mean fasting plasma insulin values (17.8 +/- 1.2 vs. 14.3 +/- 0.8 microU/ml) were significantly higher (P less than 0.01) after prednisone. The insulin sensitivity index (glucose metabolic clearance rate in ml/kg per min) was significantly lower (P less than 0.001) after prednisone at all three steady state plasma insulin levels: 2.8 +/- 0.3 vs. 7.4 +/- 1.1 at approximately 100 microU/ml; 6.0 +/- 0.5 vs. 12.2 +/- 1.1 at approximately 1,000 microU/ml; 7.4 +/- 0.6 vs. 14.4 +/- 0.5 at approximately 10,000 microU/ml. Fasting glucose production (in mg/kg per min) was significantly higher after prednisone: 3.7 +/- 0.2 vs. 2.9 +/- 0.2, P less than 0.001. Suppression of glucose production at steady state plasma insulin level of approximately 100 microU/ml was less after prednisone (1.01 +/- 0.35 vs. 0.14 +/- 0.13, NS), and total at approximately 1,000 and approximately 10,000 microU/ml after both prednisone and placebo. The metabolic kinetic parameters of insulin after prednisone were not significantly different from those after placebo. In addition, insulin binding and 3-ortho-methyl-glucose transport were studied in vitro on fat cells from 16 normal-weight surgical candidates aged 40 +/- 8 yr (10 treated with placebo and 6 with prednisone as above). No significant difference was observed with regard to specific insulin binding (tested with 1 ng/ml hormone only), whereas significant transport differences were noted at the basal level (0.40 +/- 0.10 vs. 0.54 +/- 0.12 pmol/10(5) cells, P less than 0.05), and at increasing concentrations up to the maximum stimulation values (5 ng/ml): 0.59 +/- 0.04 vs. 0.92 +/- 0.12 pmol/10(5) cells, P less than 0.005. These results suggest that (a) administration of an anti-inflammatory dose of prednisone for 7 d induces insulin resistance in man; (b) this is more dependent on depressed peripheral glucose utilization than on increased endogenous production; (c) total insulin binding on isolated adipocytes is not significantly affected; (d) insulin resistance is primarily the outcome of postreceptor defect (impaired glucose transport).

3-O-Methylglucose↗
PubMed1982

[Diagnostic value of echography in the study of thyroid nodules. Ultrasonographic and histological findings on 103 "cold" nodules].

This study examines the accuracy of ultrasonic scanning in the recognition of malignancy in 103 "cold" thyroid nodules. All nodules underwent to surgical ablation and to histopathological examination. 10 nodules were cistic, 72 solid and 21 mixed cistic-solid on echography. None of the cistic nodules showed malignant disease while six carcinomas were present in solid nodules and one (a papillary cancer) in a mixed cistic-solid lesion. However we were unable to find echographic abnormalities pathognomonic for malignancy. Only in one case (an undifferentiated carcinoma which involved adjacent blood vessels) the diagnosis of malignant tumour was made before operation; in the other cases the echo patterns of the carcinomatous nodules were similar to those observed in benign nodules. Similar ultrasonic findings were also seen in the various types of thyroid cancer (3 follicular, 2 papillary, 1 medullary, 1 undifferentiated) a part the papillary carcinoma which appeared as cistic-solid lesion. Our data seem to limit the diagnostic value of echography in the detection of malignant thyroid nodules, nevertheless they confirm the benignancy of echografically cistic nodules.

Adenoma↗
PubMed1977

Polymorphism of phenylbutazone: properties and compressional behavior of crystals.

Data from X-ray diffraction, thermal analysis, IR spectroscopy, and solubility studies were used for the identification and characterization of four crystalline modifications of phenylbutazone. The thermal behavior of the polymorphs under different treatment conditions also was investigated. Compression of the thermodynamically unstable forms, at a compression force of 1590--2040 kg, induced polymorphic changes in the crystals. Similar changes also were produced through grinding. The apparent equilibrium solubilties of polymorphs were determined, as was the dissolution of the polymorphs as compressed disks in an aqueous medium. The small effective surface area possessed by one polymorph resulted in slow dissolution.

Calorimetry, Differential Scanning↗
PubMedDate not supplied

Dietary guar gum supplementation does not modify insulin resistance in gross obesity.

Obesity is considered an insulin resistant state. Dietary guar gum supplementation is able to reduce blood glucose and plasma insulin response to a carbohydrate meal. In order to evaluate whether guar is able to reduce hyperinsulinemia and insulin resistance in gross obesity, we studied 9 obese patients, greater than 50% overweight with impaired glucose tolerance before and after 4 + 4 g/day guar for 6 weeks. Six patients repeated the treatment with 8 + 8 g/day guar after a 3-month interval. Guar was added to the usual diet in order to maintain the body weight constant. Pre-treatment and post treatment study included: total specific insulin binding on circulating monocytes; 3H-glucose infusion and euglycemic hyperinsulinemic clamp at approximately 100 microU/ml. The differences between post-treatment and pre-treatment values were not significant for any of the parameters studied. Fasting glucose production was: 2.17 +/- 0.33 SEM (pretreatment) vs 2.18 +/- 0.18 (4 + 4 g/day) vs 2.28 +/- 0.14 (8 + 8 g/day) mg/kg/min; glucose utilization was: 3.52 +/- 0.43 vs 3.22 +/- 0.44 vs 3.49 +/- 0.63 mg/kg/min; total specific insulin binding was: 2.80 +/- 0.20 vs 2.75 +/- 0.25 vs 2.78 +/- 0.31%; body weight was: 101.4 +/- 5.4 vs 100.2 +/- 6.2 vs 100.5 +/- 7.0 kg. These results indicate that dietary guar gum supplementation per se is unable to reduce insulin resistance in gross obesity if overweight is maintained constant.

Adult↗