PubMed Health⌕ Search

Biomedical subjects

G Paolisso

Publications and source records attributed to G Paolisso.

At least 199 records · Page 11Linked to original sources
PubMedDate not supplied

Glycemic control with an artificial pancreas improves insulin responses to both oral and glucose in nonobese noninsulin-dependent diabetic subjects.

Insulin secretory responses to both oral and intravenous glucose were investigated in 12 nonobese noninsulin-dependent diabetic subjects before and after strict metabolic control of blood glucose levels without weight loss. Glycemic control was achieved by applying an artificial pancreas to all diabetics for 2 or 3 days, which led to restoration of normal fasting blood glucose levels and to significant reduction of fasting plasma insulin (p less than 0.01) and C-peptide (p less than 0.05) levels. Initially, the insulin response to oral glucose was weak and delayed, but increased significantly after treatment (p less than 0.01), although none of the diabetic subjects achieved completely normal glucose tolerance. The i.v. glucose tolerance test (0.33 g/kg) revealed that all diabetics lacked acute insulin response in the basal state with low glucose disappearance rates (0.37 +/- 0.07 %/min). After 48h of normoglycemia, these figures did not change significantly, although the insulinogenic index (insulin area/glucose area) was significantly increased (p less than 0.05). A marked increase in both phases of insulin secretion was evident when a larger intravenous glucose pulse (0.66 g/kg) was used in some diabetics in order to raise the blood glucose concentrations of the post-treatment test to those of the pre-treatment test. In absolute terms, the insulin responses of the post-treatment tests were not significantly different from those of sex-, age- and weight-matched control subjects, but were significantly lower if related to the corresponding plasma glucose responses (insulinogenic index lower than that of controls). These studies in nonobese noninsulin-dependent diabetic subjects indicate that glycemic control with an artificial pancreas improves insulin response to glucose, suggesting that chronic hyperglycemia may stress the impaired B-cell secretory capacity of diabetes.

Administration, Oral↗
PubMedDate not supplied

Sodium salicylate restores the impaired insulin response to glucose and improves glucose tolerance in heroin addicts.

Plasma glucose, insulin, C-peptide, glucagon and growth hormone responses to intravenous glucose were evaluated in 10 heroin addicts in the basal state and during an infusion of sodium salicylate, an inhibitor of endogenous prostaglandin synthesis. Ten normal subjects, matched for age, sex and weight served as controls. In the basal state, the heroin addicts had markedly reduced insulin responses to intravenous glucose and low glucose disappearance rates (p less than 0.01 vs controls). The infusion of sodium salicylate caused a striking increase of the acute insulin response to intravenous glucose (from 14.5 +/- 4 microU/ml to 88 +/- 11 microU/ml, p less than 0.001) and restored to normal the reduced glucose tolerance (KG from 1.10 +/- 0.1% min-1 to 2.04 +/- 0.19% min-1). Hypoglycemic values were found in all addicts at the end of the test during salicylate infusion. Indomethacin pretreatment in five additional addicts also caused normalization of the impaired insulin responses to the intravenous glucose challenge and restored to normal the reduced glucose disappearance rate. Plasma glucagon and growth hormone levels were normally suppressed by glucose in addicts in basal conditions; sodium salicylate infusion completely overturned these hormonal responses which became positive in the first 15 min following the glucose challenge. These results demonstrate that the two prostaglandin synthesis inhibitors can restore the impaired B-cell response to glucose in heroin addicts to normal, indicating that this response is not lost but is inhibited by heroin itself or by other substances, perhaps by the endogenous prostaglandins.

Adolescent↗
PubMedDate not supplied

Exaggerated orthostatic hypotension as first sign of diabetic autonomic neuropathy in the elderly.

Long-standing diabetic subjects have an impaired sympathetic nervous system activity as a consequence of autonomic neuropathy. Moreover, in this latter group of subjects the parasympathetic rather than the sympathetic nervous system seems firstly impaired by glucose metabolism derangements. In the present study we show that, in aged diabetic subjects with a short duration of the disease (less than 5 years), and who are free from diabetic complications, it is possible to evidence a primary compromise of sympathetic rather than parasympathetic nervous system activity since a greater rate of orthostatic hypotension occurred. In the light of the well-known age-related changes in the physiopathology of cardiovascular activity, we hypothesize that in aged diabetic patients, even after a short duration of disease, sympathetic compromise precedes the derangement of parasympathetic nervous system activity.

Adult↗
PubMedDate not supplied

Glucose intolerance in the elderly: an open debate.

The presence of glucose intolerance in aged people is a well known physio-pathological condition. Nevertheless, the mechanisms by which it takes place are still unclear. In the present report we have reviewed the possible mechanisms (impaired insulin secretion and action, role of the environmental factors) which may contribute to the impaired glucose handling of aging. Moreover, we have also pointed out that not all aged subjects are glucose intolerant; in fact it seems clear that only aged subjects who present more than one of the pathological findings reported above may develop impaired glucose handling.

Journal Article↗
PubMedDate not supplied

Changes in glucose turnover parameters during muscular exercise: role of age.

In a study of ten young and seven elderly healthy men we have performed an oral glucose tolerance test (75 g) and employed a euglycemic hyperinsulinemic (0.25 mUx kg/min) glucose clamp technique in order to determine insulin sensitivity. This latter experimental protocol consisted of 120 min of euglycemic clamp followed by 60 min in which the clamp and a mild muscular exercise (35% VO(2) (max)) were combined. D-[(3)H]glucose infusion allowed a determination of the glucose turnover parameters. Our results show that in elderly subjects glucose disappearance rate and glucose metabolic clearance rate are significantly lower during both clamp, and clamp + muscular exercise studies. On the contrary, hepatic glucose production was similar under both conditions and was independent of age.

Journal Article↗
PubMedDate not supplied

Insulin resistance as cause of increased blood pressure in the elderly: effects on intracellular ion contents.

Previous reports have evidenced a strong relationship between high plasma insulin levels and blood pressure in diabetic and obese subjects but not in the elderly. During aging many patho-physiological changes in cardiovascular functions and autonomic nervous system occur, so that aging per se might be a cause of a 'physiological' increase in blood pressure. Nevertheless, an insulin resistance also develops during aging. The present study investigates the possible role of age-dependent insulin resistance in the genesis of increased blood pressure. Our data show that insulin resistance calculated by the glucose infusion rate during a euglycemic hyperinsulinemic glucose clamp procedure is significantly correlated with the insulin-mediated net decrease in erythrocyte Na+ content (r = 0.58, P < 0.05), as well as with net increase in erythrocyte K+ (r = 0.64, P < 0.05) and Mg2+ (r = 0.67, P < 0.01) content and to basal diastolic blood pressure (r = -0.63, P < 0.05). We conclude that in elderly subjects the age-related and normally occurring insulin resistance might contribute to the increase of arterial blood pressure through its effect on cell cation content.

Journal Article↗
PubMedDate not supplied

Prevention of metabolic alterations by insulin supplements administered either before or after 2-h nocturnal interruption of CSII.

To evaluate the efficacy of a bolus insulin injection to prevent the metabolic alterations induced by a 2-h nocturnal interruption of a continuous subcutaneous insulin infusion (CSII), nine type I (insulin-dependent) C-peptide-negative diabetic patients were studied from 2200 to 0800 h during two randomized tests. An insulin bolus (2.1 +/- 0.2 U) was administered via the pump either at 2300 h, just before CSII interruption, or at 0100 h, after reactivating the pump at its usual basal rate (1.05 +/- 0.11 U/h). The insulin bolus at 2300 h induced a significant rise in plasma free-insulin levels at 2400 h (+6.9 +/- 1.8 mU/L, P less than .01), resulting in an early and marked fall in blood glucose concentrations between 2300 and 0100 h (-2.7 +/- 0.5 mM, P less than .001), with hypoglycemic values in five patients. The insulin bolus at 0100 h counteracted the fall in plasma free-insulin levels observed between 2300 and 0100 h and significantly increased plasma insulin at 0200 h (+3.2 +/- 0.8 mU/L, P less than .01). Blood glucose concentrations that remained stable during the 2-h arrest of the pump fell significantly between 0100 and 0400 h (-2.1 +/- 0.5 mM, P less than .005). This fall rate was significantly lower than that measured within the 3 h after the insulin bolus given before CSII interruption but significantly higher than that observed in a reference control group of patients whose pump was functioning normally throughout the night.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Metabolic effects of nitrendipine.

A randomized, double-blind, placebo-controlled study was conducted to evaluate the safety and clinical efficacy of nitrendipine in the treatment of isolated systolic hypertension in elderly patients. The subjects were 20 elderly patients with isolated systolic hypertension who received 20 mg of nitrendipine or placebo daily for 60 days. In the nitrendipine-treated patients, both systolic and diastolic blood pressures were reduced significantly during treatment (from a mean of 180 to 155 mmHg and 92 to 80 mmHg); heart rate did not change significantly. Standard laboratory test results did not change in either group during treatment and results of a posttreatment oral glucose tolerance test were similar in the two treatment groups.

Aged↗
PubMedDate not supplied

Sensorimotor evaluation of ano-rectal complex in diabetes mellitus.

To evaluate the status of ano-rectal complex in diabetic patients, 20 patients with no fecal incontinence and/or local ano-rectal disorders and 18 normal subjects underwent to: 1) ano-rectal manometry; 2) defecography; and 3) rectal sensation tests. In all subjects, the five classic cardiovascular reflexes tests were performed to detect autonomic neuropathy. No significant difference between diabetic patients and controls was found in length, maximum resting pressure and strength of phasic external anal sphincter or anal canal at ano-rectal manometry; similarly, no significant difference between diabetic and normal subjects was found by the same technique in threshold and amplitude of ano-rectal inhibitory reflex. Ano-rectal angle of diabetic patients was not significantly different from normals both at resting and during straining at defecographic study. By rectal sensation testing, it was possible to demonstrate a significant difference between diabetic and normal subjects in perception of rectal distension (87.5 +/- 27.5 vs 39.2 +/- 6.5 ml, p less than 0.05; mean +/- SEM) and of stimulus of defecation (147.0 +/- 56.3 vs 52.9 +/- 18.5 ml, p less than 0.001) but not in perception of maximum tolerable volume (343.5 +/- 69.9 vs 322.0 +/- 48.5 ml, p = NS). No relationship was found between these results and the score of autonomic neuropathy and/or duration of diabetic disease. These data suggest that an early involvement of only sensory parasympathetic fibers of ano-rectal complex occurs in diabetic patients without gastrointestinal symptoms.

Adolescent↗
PubMedDate not supplied

Characteristics of insulin resistance in Turner syndrome.

The characteristics of insulin resistance, in Turner syndrome are still unclear. For this purpose in 4 patients with Turner syndrome and in 8 control females we performed an euglycaemic hyperinsulinemic glucose clamp at the following insulin infusion rates (50 and 100 mU/Kg x h), each period lasting 120 min. A simultaneous infusion of D-3-H-glucose allowed us to determine in basal conditions and during the clamp hepatic glucose output and glucose disappearance rate (Rd). In basal conditions plasma glucose (4.8 +/- 0.1 vs 4.6 +/- 0.2 mmol/1 p = NS) and plasma glucagon (102 +/- 7.5 vs 112 +/- 11.3 ng/l p = NS) were similar in both groups despite higher plasma insulin (19 +/- 1.8 vs 7 +/- 2.2 mU/l p less than 0.05) and C-peptide (1.0 less than 0.1 vs 0.8 +/- 0.06 pmol/l p less than 0.05) levels in patients with Turner syndrome. In the last 60 min of the lower insulin infusion rate glucose infusion rate (4.1 +/- 0.3 vs 2.9 +/- 0.4 mg/Kg x min p less than 0.05) and glucose disappearance rate (3.89 +/- 0.12 vs 2.63 +/- 0.11 mg/Kg x min p less than 0.01) were significantly reduced in patients with Turner. On the contrary hepatic glucose output was similarly suppressed in both groups of subjects. Doubling the insulin infusion rate, we obtained similar results in patients and controls respectively. So we conclude that in Turner syndrome the insulin resistance state is mainly due to a muscular receptor defect.

Adolescent↗
PubMedDate not supplied

Impaired insulin-mediated erythrocyte magnesium accumulation is correlated to impaired insulin-mediated glucose diposal in aged non-diabetic obese patients.

Basal erythrocyte magnesium levels were significantly lower in obese than lean subjects. In vitro incubation in the presence of 100 mU/l insulin significantly increased magnesium erythrocyte levels in both groups of subjects. However, even in the presence of 100 mU/l, the erythrocyte magnesium content of obese patients was lower than that of control subjects. The in vitro dose-response curve of the effect of insulin on magnesium erythrocyte accumulation was shifted to the right when the red cells of obese were used, with a highly significant reduction of the maximal effect. Such reduction of the maximal effect of insulin suggests that the impairment of insulin-induced erythrocyte magnesium accumulation observed in obese patients results essentially from a post-receptor defect. In obese patients, net increase in erythrocyte magnesium levels (calculated as the difference between basal and 100 mU/l insulin-induced erythrocyte magnesium levels) was negatively correlated with basal plasma insulin levels (r = 0.79 p less than 0.01), and with body mass index (r = 0.81 p less than 0.01) while it was positively correlated with the glucose disappearance rate after glucose load (r = 0.67 p less than 0.05) and glucose metabolic clearance rate (r = 0.71 p less than 0.01). These results demonstrate that insulin-induced erythrocyte magnesium accumulation is impaired in patients with obesity and that such defect is correlated to impaired -- mediated glucosal disposal in the patients.

Aged↗
PubMedDate not supplied

Pulsatile rather than continuous glucagon infusion leads to greater metabolic derangements in insulin-dependent diabetic subjects.

The present study aimed at investigating the respective effects of continuous and pulsatile intravenous delivery of glucagon in insulin-dependent diabetic subjects. The study was performed in seven insulin-dependent diabetic subjects proven to have no residual insulin secretion. In random order and in different days each subject was submitted to glucagon delivery given continuously (58 ng/min) and in a pulsatile (377 ng/min during 2 min followed by 11 min during which no glucagon was infused) manner. In this conditions plasma glucose levels were significantly higher during pulsatile glucagon delivery. In particular in the last 65 min plasma glucose levels reached 10.8 +/- 0.3 vs 12.9 +/- 0.4 mmol/l (p less than 0.05) during continuous and pulsatile glucagon delivery respectively. Similarly plasma lipid changes also evidenced a greater effects of pulsatile rather than continuous hormone administration in producing the metabolic derangements classically encountered in insulin-dependent diabetic subjects. In conclusion, pulsatile glucagon delivery seem to produce greater metabolic effects than continuous hormone delivery.

3-Hydroxybutyric Acid↗
PubMedDate not supplied

Lack of diabetogenic action of calcitonin in subjects affected by insulinoma.

Calcitonin has been shown to affect calcium handling within cells thus impairing insulin secretion and glucose tolerance in healthy subjects. In the present study we investigate the effects of calcitonin on basal and nutrients-induced plasma glucose and insulin levels variations in healthy subjects (n = 10) and in patients affected by islet cell tumor (n = 6). In healthy subjects calcitonin markedly decreased basal and nutrients-induced plasma insulin levels while in patients with islet cell tumor this calcitonin-mediated effect was lost. So we conclude that the lack of calcitonin effect upon insulin secretion in patients with insulinoma is probably due to the autonomous insulin secretion characterizing islet cell tumor.

Adenoma, Islet Cell↗