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Biomedical subjects

P Pavan

Publications and source records attributed to P Pavan.

At least 37 records · Page 2Linked to original sources
PubMed1997

Forearm nitric oxide balance, vascular relaxation, and glucose metabolism in NIDDM patients.

Endothelium-dependent and -independent vascular responses were assessed in 10 NIDDM patients and 6 normal subjects with no evidence of atherosclerotic disease. Changes in forearm blood flow and arteriovenous (AV) serum nitrite/nitrate (NO2-/NO3-) concentrations were measured in response to intra-arterial infusion of acetylcholine (ACh) (7.5, 15, 30 microg/min, endothelium-dependent response) and sodium nitroprusside (SNP) (0.3, 3, 10 microg/min, endothelium-independent response). Insulin sensitivity (determined by minimal model intravenous glucose tolerance test) was lower in NIDDM patients (0.82 +/- 0.20 vs. 2.97 +/- 0.29 10(4) min x microU(-1) x ml(-1); P < 0.01). Baseline forearm blood flow (4.8 +/- 0.3 vs. 4.4 +/- 0.3 ml x 100 ml(-1) tissue x min(-1); NS), mean blood pressure (100 +/- 4 vs. 92 +/- 4 mmHg; NS), and vascular resistance (21 +/- 1 vs. 21 +/- 1 units; NS), as well as their increments during ACh and SNP, infusion were similar in both groups. No difference existed in baseline NO2-/NO3- concentrations (4.09 +/- 0.33 [NIDDM patients] vs. 5.00 +/- 0.48 micromol/l [control subjects]; NS), their forearm net balance (0.31 +/- 0.08 [NIDDM patients] vs. 0.26 +/- 0.08 micromol/l x 100 ml(-1) tissue x min(-1); NS), and baseline forearm glucose uptake. During ACh infusion, both NO2- and NO3- concentrations and net balance significantly increased in both groups, whereas glucose uptake increased only in control subjects. When data from NIDDM and control groups were pooled together, a correlation was found between the forearm AV NO2- and NO3- differences and blood flow (r = 0.494, P = 0.024). On the contrary, no correlation was evident between NO2- and NO3- concentrations or net balance and insulin sensitivity. In summary, 1) no difference existed in basal and ACh-stimulated NO generation and endothelium-dependent relaxation between uncomplicated NIDDM patients and control subjects; 2) in both NIDDM and control groups, forearm NO2- and NO3- net balance following ACh stimulation was related to changes in the forearm blood flow; and 3) ACh-induced increase in forearm blood flow was associated with an increase in glucose uptake only in control subjects but not in NIDDM patients. In conclusion, our results argue against a role of impaired NO generation and blood flow regulation in determining the insulin resistance of uncomplicated NIDDM patients; rather, it supports an independent insulin regulation of hemodynamic and metabolic effects.

Acetylcholine↗
PubMed1996

Short-term diabetic ketosis alters n-6 polyunsaturated fatty acid content in plasma phospholipids.

At present, no information is available about the possibility that acute loss of metabolic control might be able to modify fatty acid composition in IDDM patients. Therefore, the aim of this study was to determine whether a short-term period of ketosis has any effect on the composition of fatty acid of plasma phospholipids in a group of insulin-dependent diabetes mellitus (IDDM) patients. Eleven IDDM patients and nine healthy volunteers were studied. Patients were studied over a 2-day period; each 2-day period consisted of initial baseline measurements followed by a day of hyperglycemia and mild ketosis, which was promptly alleviated by insulin infusion. No significant difference in baseline percent fatty acid composition was observed between normal controls and IDDM patients. In IDDM patients, ketosis induced a significant decrease in percent arachidonic acid (20:4 n-6) content, with a significant parallel decline in n-6 total polyunsaturated fatty acids. A significant inverse correlation between the prevailing plasma glucose and the relative content of arachidonic acid in plasma phospholipids was observed (r = -0.35; P = 0.0488). A highly significant inverse correlation was observed between the change from baseline condition to ketosis of the ratio C20:4/C20:3, the product/precursor ratio for the reaction catalyzed by delta5-desaturase, and the values of hemoglobin A1c,(r = -0.855; P = 0.0015). In conclusion, short term diabetic ketosis is associated with a significant decrease in n-6 polyunsaturated fatty acid content in plasma phospholipids, especially arachidonic acid. This decrease in arachidonic acid appears to be related to the degree of metabolic derangement, whereas the influence of short-term diabetic ketosis on the ratio of C20:4 to C20:3 seems to be due to the degree of long-term metabolic control.

Adult↗
PubMed1996

Ethanol impairs insulin-mediated glucose uptake by an indirect mechanism.

The effect of ethanol (ETOH) on muscle metabolism was assessed in both normal (NC) and noninsulin-dependent (NIDDM) subjects in the basal state and during isoglycemic hyperinsulinemia (450 pmol/L) clamp studies carried out either with systemic (NC, n = 5; NIDDM, n = 5) or intrabrachially (NC, n = 5; NIDDM, n = 5)ETOH infusion. On a repeat study, each subject underwent the same experimental procedures, except that saline was infused instead of ETOH. Systemic ETOH significantly decreased whole body glucose disposal in both NC and NIDDM patients. In NC, ETOH infusion decreased basal forearm glucose uptake (FGU) from 1.22 +/- 0.20 to 0.32 +/- 0.04 mumol/min.100 mL tissue (P < 0.01), whereas in NIDDM, this decrement was not significant (from 0.95 +/- 0.31 to 0.66 +/- 0.23). With saline infusion, hyperinsulinemia significantly stimulated FGU to 4.09 +/- 0.46 mumol/min.100 mL tissue in NC and to 2.50 +/- 0.76 in NIDDM. During ETOH, FGU was depressed by 81% in NC (delta = 3.32 mumol/min.100 mL tissue) and by 48% (P < 0.05) in NIDDM (delta = 1.21 mumol/min.100 mL tissue). Local ETOH infusion did not affect FGU in either NC (1.18 +/- 0.23 vs. 1.1 +/= 0.11 mumol/min.100 mL tissue in the baseline condition and 4.12 +/- 0.65 vs. 3.97 +/- 0.35 in insulin-stimulated conditions) or NIDDM (1.05 +/- 0.29 vs. 1.1 +/- 0.19 mumol/min.100 mL tissue in baseline condition and 2.72 +/- 0.82 vs. 2.83 +/- 0.51 in insulin-stimulated conditions) subjects. With systemic ETOH, but not local infusion, there was a reduction in baseline plasma free fatty acid level and an increase in blood lactate concentration during isoglycemic hyperinsulinemia. In summary, systemic ETOH infusion impairs both whole body and forearm glucose uptake in NC and NIDDM subjects; this effect was more apparent in NC than in NIDDM at both the whole body and forearm level. On the contrary, intrabrachial ETOH infusion did not affect forearm glucose balance in either group. These results suggest that the reduction in muscle glucose disposal associated with increased systemic ETOH concentrations is not caused by a direct ETOH effect on muscle glucose metabolism.

Adult↗
PubMed1996

The hemodynamic abnormalities in short-term insulin deficiency: the role of prostaglandin inhibition.

It has been suggested that the hemodynamic derangements present in diabetic ketoacidosis are the results not only of profound volume depletion but also of the effects of increased production of vasodilating prostaglandins (PGs), principally PGI2, released by adipose tissue. In animal and in vitro models, prostaglandin synthesis is increased during insulin deficiency. We assessed the effects of short-term ketosis on the metabolic and hemodynamic variables of 10 IDDM patients free from long-term complications and of 9 normal control subjects after a 7-day randomized double-blind indomethacin (INDO) (50 mg q.i.d.) or placebo treatment period. Calf blood flow (CBF), postocclusive reactive hyperemia (PORH), and recovery half-time (an index of overall perfusion) after PORH were measured by plethysmography. Left ventricular and myocardial functions were also studied in each different condition during placebo and INDO treatment in IDDM patients. During placebo treatment, the increase in CBF during ketosis was higher (1.75 +/- 0.29 ml / min / 100 ml muscle) than during INDO (0.85 +/- 0.17 ml / min) / 100 ml muscle; P = 0.007). PORH was similar in baseline conditions, during ketosis, and in recovery in both the placebo and INDO arms. Recovery half-time significantly increased during placebo (10 +/- 2; 200%; P < 0.01) but not during INDO (1 +/- 1; 106%; NS) treatment. In normal control subjects, insulin deficiency did not induce any significant effect on hemodynamic variables. In IDDM patients, during placebo treatment, ketosis increased both the cardiac index (from 3.4 +/- 0.7 to 4.1 +/- 0.81 / min / m; P < 0.01) and the stroke index (from 42 +/- 8 to 49 +/- 7 ml/m2; P < 0.01) without changes in left ventricular ejection fraction but with a significant increase in both left and right ventricular end-diastolic volumes. Metabolic recovery induced a normalization of these parameters. INDO treatment significantly blunted these alterations. In summary, we showed that during acute insulin deficiency, INDO-sensitive mechanisms mediate vascular disturbances. Moreover, INDO treatment was capable of completely preventing the cardiac venous return and the left ventricular alterations. INDO does not interfere with the overall ketogenetic process or with insulin-induced metabolic recovery.

3-Hydroxybutyric Acid↗
PubMed1991

Clodronate treatment increases serum osteocalcin in normocalcemic osteolytic bone metastases.

28 consecutive patients with multiple osteolytic bone metastases due to various types of cancer were treated with 300 mg/day of sodium clodronate given intravenously as a 3-hour infusion, 16 patients were treated for 10 days and 12 for 20 days. Our findings showed that clodronate administration causes an increase in serum osteocalcin (sBGP) in the group of patients treated for 20 days (p less than 0.05), a reduction in serum Ca in both groups of patients (p less than 0.01), an increase in serum alkaline phosphatase (p less than 0.05 and p less than 0.01), a reduction in urinary Ca (p less than 0.01) and a reduction in uOHP (p less than 0.05). The raise in sBGP may be attributed to the reduction of sCa and to the consequent secondary hyperparathyroidism. The increase in sBGP can be considered as the expression of osteoblasts stimulation following an adequate period of therapy with sodium clodronate.

Adult↗
PubMed1984

Calcitonin in hepatoma and cirrhosis.

Plasma immunoreactive calcitonin (iCT) is elevated in primary liver cancer and its measurement has been proposed as a tumour marker. Since iCT is also frequently raised in alcoholic liver cirrhosis, it would be of practical relevance to distinguish this condition from primary hepatoma by measuring the plasma level of iCT. We measured plasma iCT levels in 23 subjects with primary liver cancer, in 27 with hepatic cirrhosis and in 42 healthy subjects who served as normal controls. A gel-chromatography analysis was carried out on the plasma of two cases of hepatoma, two of cancer and cirrhosis, and two of alcoholic liver cirrhosis. The subjects with primary liver cancer had values of plasma iCT (pg/ml; mean +/- SE) of 342 +/- 41; those with liver cirrhosis 159 +/- 22, and normal controls 73 +/- 3. The increase in primary liver cancer was significant in comparison both healthy subjects (P less than 0.001) and with cirrhotic patients (P less than 0.001). Twenty-two out of 23 patients with primary liver cancer and 13 out of 27 with liver cirrhosis had elevated iCT values (upper normal limit 113 pg/ml). There was no significant difference between plasma iCT values of patients with cancer and those with cirrhosis. However, we measured iCT values higher than 400 pg/ml only in patients with primary liver cancer. The gel-filtration analysis showed 3 or 4 peaks of iCT with a molecular weight higher than synthetic human calcitonin. The results suggest that plasma iCT levels can be considered a reliable marker of liver cancer, whereas its discriminating power between liver cancer and cirrhosis was not entirely satisfactory.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗