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Biomedical subjects

T Salvatore

Publications and source records attributed to T Salvatore.

At least 37 records · Page 2Linked to original sources
PubMed1992

Decreased insulin clearance as a feature of essential hypertension.

Several studies report that essential hypertension is associated with hyperinsulinemia. This condition may depend on enhanced pancreatic insulin secretion and/or a decreased MCR of the circulating hormone. Twenty-five nonobese glucose-normotolerant patients with primary hypertension were divided into 5 groups, each consisting of 5 subjects. Each group was submitted to continuous 120-min double infusion of different doses of insulin (group I, 0.025; II, 0.05; III, 0.1; IV, 0.2; V, 0.4 U/kg.h) and glucose (I, 2; II, 3.5; III, 6; IV, 8; V, 10 mg/kg.min). The same procedures were applied to 25 healthy normotensive volunteers. Basal and steady state plasma levels of glucose, insulin, and C-peptide were significantly (P less than 0.05 or less) higher in hypertensive patients than in control subjects of all groups. The MCR of insulin (milliliters per kg/min) at all insulin-glucose infusion rates was significantly (P less than 0.05 or less) lower in hypertensive than normotensive subjects. Despite the significantly higher steady state plasma insulin levels in hypertensives, the MCR of glucose (milliliters per kg/min) was significantly (P less than 0.05 or less) lower in hypertensive than normotensive subjects. These results suggest that an altered insulin removal may contribute to the hyperinsulinemia found in the essential hypertensive subjects. In addition, a defect in insulin-stimulated glucose uptake which persists at supraphysiological insulin concentrations is confirmed in this population.

Blood Glucose↗
PubMed1991

Improvement of insulin-induced glucose disposal in obese patients with NIDDM after 1-wk treatment with d-fenfluramine.

OBJECTIVE: To study the short-term effects of the serotoninergic anorectic drug d-fenfluramine on insulin-induced glucose disposal. RESEARCH DESIGN AND METHODS: A randomized double-blind placebo-controlled crossover trial with 1-wk treatment periods (2 x 15 mg/day d-fenfluramine) was conducted. Twenty obese subjects, 10 with normal oral glucose tolerance and 10 with non-insulin-dependent diabetes mellitus (NIDDM), were all treated with a weight-maintaining diet. Euglycemic-hyperinsulinemic glucose clamps with measurement of glucose kinetics with D-[3-3H]glucose were performed at either two (patients without NIDDM, 0.05 and 0.10 U.kg-1.h-1) or three (patients with NIDDM, 0.05, 0.10, and 0.50 U.kg-1.h-1) insulin delivery rates. RESULTS: In the nondiabetic subjects, no significant changes in any metabolic or hormonal parameter were measured in the basal state or during the clamp despite a slight reduction in body weight (-1.2 +/- 0.5 kg, P less than 0.05). In the diabetic patients, no significant changes in body weight or basal plasma insulin levels were observed, but fasting blood glucose levels (8.0 +/- 0.8 vs. 9.4 +/- 1.1 mM, P less than 0.005) and plasma free fatty acid concentrations (1150 +/- 227 vs. 1640 +/- 184 microM, P less than 0.05) were significantly reduced after d-fenfluramine compared with placebo. During the clamp, insulin metabolic clearance rate (MCR) was similar after both placebo and d-fenfluramine; endogenous (hepatic) glucose production was similarly and almost completely suppressed, whereas glucose disposal was remarkably enhanced after d-fenfluramine (average increase of glucose MCR 35 +/- 12%, P less than 0.02). CONCLUSIONS: Whatever the mechanism(s) involved, a 1-wk treatment with d-fenfluramine induces better blood glucose control and improves insulin sensitivity in obese patients with NIDDM independent of significant weight reduction; this last effect is not present in obese subjects with normal oral glucose tolerance.

Adult↗
PubMed1990

Metabolic effects of pulsatile insulin infusion in the elderly.

The present study investigated the metabolic effects of pulsatile insulin delivery at a pulse rate of 2 + 11 and 2 + 18 min in 7 healthy, elderly subjects (71.4 +/- 2.1 years), submitted to 260 min controlled iv glucose infusion via the Biostator. The endogenous secretion of pancreatic hormones was inhibited by somatostain (3 micrograms/min) and glucagon was replaced (67 ng/min) to basal levels. The same total insulin dose was delivered on both occasions. Insulin infusion rate was 1.3 and 2.0 mIU. kg-1. min-1 during switching on/off of 2 + 11 and 2 + 18 min, respectively. Blood glucose levels and glucose infusion rate were monitored continuously by the Biostator; [D-3-3H]glucose infusion allowed determination of glucose turnover. During the last 60 min of the experiment, pulsatile insulin at a pulse rate of 2 + 11 vs 2 + 18 min produced a stronger inhibition of endogenous glucose production, whereas glucose disappearance rate and glucose metabolic clearance rate were similarly affected. Plasma triglycerides, apolipoprotein B, and free fatty acids levels were also more suppressed during insulin delivery at pulse rate of 2 + 11 than at 2 + 18 min.

Aged↗
PubMed1989

Low protein alimentation normalizes renal haemodynamic response to acute protein ingestion in type 1 diabetic children.

The effect of an acute protein load (2 g kg-1 bodyweight [BW]) was studied in nine type 1 diabetic children. Patients were maintained on two different dietary regimens. In study one, patients were on a high protein diet providing from 2.7 to 1.8 g of protein/kg of BW per day. In study two, patients were reevaluated after three weeks of a diet providing from 1.0 to 1.2 g kg-1 of BW per day of protein. In study one (High Protein Diet), we failed to observe any rise in GFR and RPF following the protein meal (137 +/- 21 basal vs. 110 +/- 14 and 472 +/- 93 basal vs. 494 +/- 93 ml/1.73 m2 of SA min-1 at 60 min. This is in contrast with results from seven age matched controls consuming a free diet, which showed a significant rise in both GFR and RPF. In study two (low protein diet), basal GFR was significantly reduced. However after the protein load, both GFR (92 +/- 11 vs. 126 +/- 18 ml/1.73 m2 of SA min-1) and RPF (467 +/- 83 vs. 705 +/- 102 ml/1.73 m2 min-1) rose significantly (P less than 0.05 vs. basal). The data indicate that: 1. short term protein restriction reduces significantly GFR in type 1 diabetic children; 2. diabetic children maintained on an high protein intake show an altered haemodynamic response to protein ingestion; 3. a normal response to protein ingestion can be restored by short term dietary protein restriction.

Adolescent↗
PubMed1989

Beta-endorphin and islet hormone release in humans: evidence for interference with cAMP.

The present studies were undertaken to characterize further the influence of synthetic human beta-endorphin (0.5 mg/h) on insulin and glucagon responses to intravenous glucose in humans. Infusion of beta-endorphin in 10 normal volunteers caused a clear-cut inhibition of the overall insulin responses to a glucose pulse (0.33 g/kg iv) with values of glucose disappearance rates in the diabetic range [0.89 +/- 0.09 (P less than 0.01) vs. saline 1.82 +/- 0.15%/min]. Glucose-induced glucagon suppression was significantly lower during beta-endorphin, a fact that could have contributed to the reduced glucose utilization rates. The infusion of theophylline (150 mg + 350 mg/h) to increase the intracellular cAMP activity by inhibiting phosphodiesterase completely reversed the inhibitory effect of beta-endorphin on glucose-induced insulin secretion. As a consequence, glucose disappearance rates rose to 1.77 +/- 0.18%/min. Theophylline did not influence significantly the glucagon-releasing effect of beta-endorphin as well as the reduced glucagon suppression. An infusion of exogenous calcium (100 mg as iv bolus + 5 mg/min) to raise serum calcium in the hypercalcemic range (15 mg/dl) and lysine acetylsalicylate (72 mg/min) to block the synthesis of endogenous prostaglandin E did not interfere with the inhibiting effect of beta-endorphin on insulin secretion. These data confirm that beta-endorphin stimulates glucagon and inhibits basal and glucose-stimulated insulin secretion and suggest that the opioid influences the intraislet adenylate cyclase activity.

Adult↗
PubMed1988

Altered metabolic and hormonal responses to epinephrine and beta-endorphin in human obesity.

Catecholamines and endogenous opioid peptides are released in response to stress. Exogenous infusions of epinephrine and beta-endorphin (both in doses of 15, 50, and 80 ng/kg.min sequentially, each dose lasting 30 min) were used to mimic short term stress in both normal weight (body mass index, less than 25 kg/m2) and obese (body mass index, greater than 30 kg/m2) subjects. Fasting plasma insulin, C-peptide, and beta-endorphin concentrations were significantly higher in the obese than in the normal subjects (P less than 0.01-0.005). In lean subjects epinephrine produced significant increases in plasma glucose levels, but no appreciable changes in plasma insulin, C-peptide, or glucagon. Infusion of beta-endorphin in the same subjects caused plasma glucose and glucagon to rise, but insulin and C-peptide levels did not change. The simultaneous infusion of epinephrine and beta-endorphin produced a glycemic response which, although greater, was not significantly different than the sum of the responses to the individual hormone infusions. However, the two hormones had a synergistic interaction on plasma glucagon levels [total glucagon response, 2275 +/- 370 pg/min.mL (ng/min.L); sum of single effects, 750 +/- 152 (+/- SE) pg/min.mL (ng/min.L); P less than 0.01]. The plasma epinephrine [207 +/- 21, 607 +/- 70, and 1205 +/- 134 pg/mL (1130 +/- 115, 3640 +/- 382, and 6577 +/- 691 pmol/L] and beta-endorphin [875 +/- 88, 1250 +/- 137, and 1562 +/- 165 pg/mL (250 +/- 25, 358 +/- 39, and 447 +/- 47 pmol/L] concentrations attained during the infusions of each single hormone were not different from those recorded during the combined hormonal infusion. In obese subjects epinephrine raised plasma glucose levels and caused dose-related increments of plasma glucagon concentrations. Plasma insulin and C-peptide concentrations remained low and rebounded at the end of the infusions. In the same subjects, beta-endorphin produced elevations of plasma glucose, insulin, C-peptide, and glucagon. When the combined hormonal infusion was given to obese subjects, the plasma epinephrine and beta-endorphin concentrations rose to values not significantly different from those in normal weight subjects. However, there was a dramatic increase in plasma glucose exceeding 200 mg/dL (11.1 mmol/L), which remained elevated 30 min after the infusion. The glucagon response was not greater than the sum of the single effects.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1988

Theophylline prevents the inhibitory effect of prostaglandin E2 on glucose-induced insulin secretion in man.

This study was undertaken to assess the mechanism by which prostaglandins of the E series inhibit glucose-induced insulin secretion in man. Acute insulin response (mean change 3-10 min) to iv glucose (0.33 g/kg) was decreased by 40% during the infusion of prostaglandin E2 (10 micrograms/min) and glucose disappearance rates were reduced (P less than 0.05). Insulin response to arginine (5 g iv) and tolbutamide (1 g iv) were not affected by the same rate of prostaglandin E2 infusion. The inhibitory effect of prostaglandin E2 on glucose-induced insulin secretion was prevented by theophylline (100 mg as a loading dose followed by a 5 mg/min infusion), a drug that increases the intracellular cAMP concentrations by inhibiting phosphodiesterase activity. Our data suggest the involvement of the adenylate cyclase system in the inhibitory action of prostaglandin E2 on glucose-induced insulin secretion in man.

Adult↗
PubMed1988

Beta-endorphin-induced inhibition and stimulation of insulin secretion in normal humans is glucose dependent.

This study evaluated the effect of human beta-endorphin on pancreatic hormone levels and their responses to nutrient challenges in normal subjects. Infusion of 0.5 mg/h beta-endorphin caused a significant rise in plasma glucose concentrations preceded by a significant increase in peripheral glucagon levels. No changes occurred in the plasma concentrations of insulin and C-peptide. Acute insulin and C-peptide responses to intravenous pulses of different glucose amounts (0.33 g/kg and 5 g) and arginine (3 g) were significantly reduced by beta-endorphin infusion (P less than .01). This effect was associated with a significant reduction of the glucose disappearance rates, suggesting that the inhibition of insulin was of biological relevance. beta-Endorphin also inhibited glucose suppression of glucagon levels and augmented the glucagon response to arginine. To verify whether the modification of prestimulus glucose level could be important in these hormonal responses to beta-endorphin, basal plasma glucose concentrations were raised by a primed (0.5 g/kg) continuous (20 mg kg-1.min-1) glucose infusion. After stabilization of plasma glucose levels (350 +/- 34 mg/dl, t = 120 min), beta-endorphin infusion caused an immediate and marked increase in plasma insulin level (peak response 61 +/- 9 microU/ml, P less than .01), which remained elevated even after the discontinuation of opioid infusion. Moreover, the acute insulin response to a glucose pulse (0.33 g/kg i.v.) given during beta-endorphin infusion during hyperglycemia was significantly higher than the response obtained during euglycemia (171 +/- 32 vs. 41 +/- 7 microU/ml, P less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Sensitivity to beta-endorphin as a cause of human obesity.

Naloxone, an opiate antagonist, was given as an intravenous bolus (5 mg) in both lean and obese healthy subjects. In lean people, there was a slight trend for insulin and C-peptide concentrations to decrease below baseline values with no glucose change. Obese subjects showed an exaggerated suppression of insulin and C-peptide and a slight decrease of glucose. Glucagon was suppressed in both groups. An infusion of human beta-endorphin (0.05 mg/h) produced only minor changes in plasma glucose, insulin, glucagon, and C-peptide concentrations in lean subjects, but caused marked increments in obese. Glucagon rose in both groups, but its response was greater in obese subjects. A ten-day treatment with naloxone (1.2 mg twice a day) did not change the metabolic and hormonal responses to an oral glucose load (75 g) in lean but significantly inhibited the insulin and C-peptide responses to glucose in obese people. These results suggest that an increased opiate drive to the pancreatic beta-cell and an increased responsiveness of insulin to beta-endorphin are present in human obesity.

Adult↗
PubMed1987

Beta-endorphin infusion restores acute insulin responses to glucose in type-2 diabetes mellitus.

To address the possibility that an abnormality in pancreatic beta-endorphin activity might contribute to abnormal insulin secretion in diabetes mellitus, we studied the effects of beta-endorphin infusion on islet function in diabetic patients. The iv infusion of human beta-endorphin at a dose of 0.5 mg/h for 2 h in type-2 non-insulin-dependent diabetic patients (n = 12) raised plasma insulin and glucagon levels and slightly but significantly lowered plasma glucose concentrations. beta-Endorphin infusion also resulted in reappearance of a clear-cut acute insulin response to glucose, while second phase insulin release was increased and glucose disposal accelerated. Acute insulin and glucagon responses to arginine were not increased by beta-endorphin, suggesting that the effect of the opioid on the B cells of the diabetic patients is specific for glucose. An intraislet abnormality of opioid peptides action and/or secretion may play a role in the disturbances of insulin secretion in patients with type-2 diabetes mellitus.

Arginine↗
PubMed1987

Hyperglycemia and obesity as determinants of glucose, insulin, and glucagon responses to beta-endorphin in human diabetes mellitus.

The effect of human beta-endorphin on plasma glucose, insulin, and glucagon concentrations was studied in patients with noninsulin-dependent diabetes mellitus and in normal subjects. The subjects were divided according to their body weight into lean (body mass index, less than 25) and obese (body mass index, greater than 29.5) groups. In lean subjects, infusion of 0.5 mg/h beta-endorphin caused significant increases in peripheral plasma glucose and glucagon levels, but no change in plasma insulin. In obese subjects, there was an immediate marked increase in both plasma insulin and glucagon concentrations during the beta-endorphin infusion, but the plasma glucose response was lower than that of lean subjects. In lean diabetic patients, beta-endorphin produced significant simultaneous increments in both insulin and glucagon concentrations and significantly decreased plasma glucose levels. These hormonal responses to beta-endorphin were amplified in the obese diabetic patients. There was a significant correlation (r = 0.61; P less than 0.01) between fasting plasma glucose levels and the integrated insulin area in response to beta-endorphin. The infusion of a lower dose of beta-endorphin (0.05 mg/h) in diabetic patients produced similar increments in both insulin and glucagon levels and also decreased plasma glucose concentration. These results indicate that beta-endorphin may have important glucoregulatory effects in man depending on the dose administered, the presence of obesity, and the prevailing plasma glucose concentration.

Adult↗
PubMed1985

Organizational adaptation in the VNA: paradigm change in voluntary sector.

The organizational history of the visiting nurse association (VNA) is reviewed from the perspective of paradigm change. A paradigm is a behavioral and structural model that comes to characterize a field because of its compatibility with environmental conditions. The concept is applied to interpreting adaptation among the VNA's. Four distinct paradigms are identified which comprise the overlapping but sequential course of VNA adaptation to changing circumstances. These paradigms are "public health nursing," "community nursing service," "the home health agency," and the "home care enterprise." The emergence of each is examined with emphasis on the continuity and discontinuity of elements. Particular focus is given to the durability to date of the voluntary auspice and its future prospects in light of ongoing paradigmatic change is discussed.

Community Health Nursing↗
PubMed1985

The private nonprofit home health agency: an exploratory essay.

Despite a history that coincides with the medicare-funded home health program the private nonprofit (PNP) home health agency does not appear to have been the focus of any extensive or objective examination. Herein that task is undertaken. First, the PNP is positioned within the context of the other four nonprofit provider forms comprising home health's "third sector." These are the voluntary nonprofit, the combination agency, the institution-based nonprofit, and the sectarian nonprofit. Second, the principal attributes characterizing the PNP ethos are described. Third, the criticism received by PNP's over the lat decade is briefly reviewed. Fourth, the major past and present trends in the growth and distribution of PNP's are charted. Fifth, the three pathways to PNP formation are looked at. These are incorporation, conversion, and transition of nonprofit auspice. Sixth, the major rationales for PNP development are considered. Lastly it is observed that the PNP may serve as an object lesson to other nonprofit providers endeavoring to reach an accord with a seemingly anti-nonprofit health care environment.

Home Care Services↗