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Biomedical subjects

G Federspil

Publications and source records attributed to G Federspil.

At least 19 recordsLinked to original sources
PubMed1994

Effect of naltrexone treatment on insulin secretion, insulin action and postprandial thermogenesis in obesity.

For many years a series of studies has been carried out to evaluate the role of endogenous opioid peptides on glucose metabolism. In this work we studied the influence of endogenous opioid peptides on insulin response to OGTT and glucose-induced thermogenesis before and after a prolonged oral treatment with Naltrexone (50 mg/daily for 6 days), an opioid receptor antagonist, in a group of 9 obese subjects. Moreover in obese patients we evaluated the effect of this anti-opioid drug on insulin secretion and insulin sensitivity during an IVGTT using the minimal model approach. We compared the pre-treatment results with data coming from a group of 5 normal-weight subjects. We measured blood glucose, plasma insulin and C-peptide concentrations and evaluated the following parameters: first (phi 1) and second (phi 2) phase of beta-cell sensitivity, insulin sensitivity and glucose effectiveness. Obese subjects displayed an increased insulin response to oral and i.v. glucose load, due to an increased first phase of insulin secretion (phi 1), a reduced insulin sensitivity (Si) and glucose effectiveness (Sg) in respect to normal-weight subjects. They showed no difference in glucose and insulin area during oral load and in their profiles during i.v. glucose load after naltrexone treatment. Similarly no significant variation in insulin sensitivity and glucose effectiveness was observed. The glucose-induced thermogenesis, measured by indirect calorimetry, was not modified by naltrexone. Therefore our study demonstrates that endogenous opioids do not play any role in the impairment of peripheral insulin sensitivity and energy expenditure in human obesity.

Adult↗
PubMed1994

Effect of endogenous organic hyperinsulinaemia on blood pressure and serum triglycerides.

Hyperinsulinaemia and insulin resistance have been hypothesized to be the common pathophysiological factor of hypertension, NIDDM and obesity. To evaluate the possible role of hyperinsulinaemia and insulin resistance on hypertension, we studied a group of 37 patients with insulinoma who were admitted to our department in the period from 1966 to 1990. We recorded blood pressure and assayed blood glucose, plasma insulin, plasma triglycerides and serum uric acid levels, before and after surgery, in these patients and in a 37-subject control group. No significant increase in blood pressure and triglyceride plasma levels was recorded in the chronic hyperinsulinaemic hypoglycaemic patients, suggesting the lack of a direct role of hyperinsulinaemia on hypertension.

Adult↗
PubMed1994

The nature of life in the history of medical and philosophic thinking.

The vitalistic doctrine of Aristotle and Galen, in which the soul is an indissoluble part of the body, was undisputed throughout most of the Middle Ages. The first radical change came with Telesio, who developed philosophic naturalism in which the soul has a reality of its own, though it is connected to the body. The definitive change came with Descartes, who believed that all biologic phenomena can be explained by the laws of mechanics, and only man is distinguished by the possession of a soul. For the next 300 years, this mechanistic view would be challenged by a new vitalism, in which the 'vital force' has an existence in its own right.

Europe↗
PubMed1993

Acromegalic cardiopathy: a left ventricular scintigraphic study.

In order to study "acromegalic cardiomyopathy", cardiac function was examined, using gated radionuclide ventriculography, in 18 acromegalic patients and 21 control subjects with no clinical evidence of cardiac involvement. In these acromegalic subjects, while the Ejection Fraction (EF) did not appear to be significantly different, the Peak Filling Rate (PFR) was reduced while the Time to Peak Filling Rate (TPFR) resulted significantly greater than in control subjects. These findings indicate that chronic growth hormone (GH) hypersecretion, as observed in acromegaly, deteriorate the cardiac ventricular relaxation (diastolic phase) while it has no influence on contractility (systolic phase).

Acromegaly↗
PubMed1993

Lipolytic effect of beta-endorphin in human fat cells.

Recently, a role of beta-Endorphin on peripheral tissue metabolism has been suggested. A lipolytic effect of beta-Endorphin has been observed both in vivo and in vitro in animals but, at present, there is no evidence for a similar effect in humans. In this study, we investigated the lipolytic effect of beta-Endorphin in isolated human adipocytes. beta-Endorphin induced a significant increase in glycerol release in isolated human fat cells. Naloxone was able to inhibit the beta-Endorphin-induced lipolysis. The opioid antagonist alone had no effect on basal lipolysis and on Epinephrine-stimulated lipolysis when administered together with this hormone. Our results suggest that beta-Endorphin may play a role on lipolysis also in human fat cells and that this effect may be mediated by a specific opiate receptor.

Adipose Tissue↗
PubMed1991

Endocrine pancreatic function in pheochromocytoma.

In six patients with pheochromocytoma oral glucose tolerance test (OGTT) and arginine test were carried out. Blood insulin and glucagon response were investigated. In subjects with adrenal tumor glycemic curve pattern was typical: a rapid and exaggerated increase of glycemia followed by an abrupt drop. Absolute insulinemic response to oral glucose was normal, but inappropriate to glycemic stimulus. Arginine infusion provoked a slightly above normal increase in blood glucose and a normal increase in blood glucagon. In three of the patients studied postoperatively, reduced glycemic response to glucose was observed, whereas there were no evident variations in blood insulin and glucagon response. These data suggest that in pheochromocytoma impaired glucose tolerance is partly due to the reduced insulin response to oral glucose load.

Adrenal Gland Neoplasms↗
PubMed1991

A study on the hyperinsulinism of late pregnancy.

Much research has demonstrated that in late pregnancy glucose administration causes a marked increase of peripheral insulin levels. To ascertain whether this particular increase is due to increased insulin secretion and/or to reduced hepatic insulin removal, we measured blood glucose, plasma C-peptide and plasma insulin during OGTT in 7 nonpregnant women and in 20 nondiabetic women at third trimester of gestation and 60-90 days after delivery. The C-peptide/insulin molar ratio was calculated for all subjects. Data obtained showed that both plasma insulin and C-peptide response to oral glucose is considerably higher in women at third trimester of pregnancy as compared with that observed in the same subjects after delivery and in nonpregnant women. The basal (overnight fasting) C-peptide/insulin molar ratio did not differ significantly between pregnant and nonpregnant women. After the oral glucose load the molar ratio was sharply reduced in all groups of subjects, but the overall decrease in the pregnant women in the three hours following oral glucose was considerably greater than in postpartum and in nonpregnant women. The increased plasma C-peptide response clearly indicates that in pregnancy oral glucose-induced hyperinsulinism is caused by increased insulin release from pancreatic B-cells. Moreover, the marked overall decrease of the C-peptide/insulin molar ratio suggests, even if it does not definitely prove, that hyperinsulinism after glucose in late pregnancy may be a consequence not only of increased insulin secretion, but also of decreased hepatic extraction of insulin.

Adult↗
PubMed1991

[Giacomo Andrea Giacomini: a Padua clinician between metaphysics and science].

As Professor of Theoretical Medicine for Surgeons at Padua University between 1824 and 1849, Giacomini achieved a position of great academic professionalism and prestige, not only in Padua, but throughout Italy and Europe. His fundamental medical thesis became part of the established field of medical practice that existed into the first decades of the 19th century. This thesis, derived directly from a vitalistic concept of biological phenomena, was based on the existence of a 'life force' that is distinct from the forces of physical-chemistry, having its own specific laws, contrary to those of physical-chemistry. Using this concept Giacomini was able to distinguish two causes of death: mechanical illness and dynamic illness. The nosographic and therapeutic beliefs of Giacomini were based on his distinction between the 'mechanical' or 'dynamic' effects of drugs. Giacomini's medical philosophy is the result of an interweaving of scientific theories and metaphysical ideas. The merits and limits of this philosophy must be analysed in the light of modern epistemology to explain why Giacomini was unable to develop fully clinical anatomy.

Europe↗
PubMed1989

Possible involvement of endogenous opioids in beta-cell hyperresponsiveness in human obesity.

Since increased opiate production in obesity has been reported, the effects of naloxone in obese subjects were studied in order to ascertain whether endogenous opioid peptides play a role in the abundant insulin secretion of obesity. The results obtained showed that intravenous administration of naloxone considerably reduced insulin of obese subjects to a mixed meal, whereas it did not modify the blood insulin response to arginine or glucose infusion. Glucagon secretion to ingestion of a mixed meal and to arginine infusion was not modified by the opioid receptor blocking agent. This study seems to indicate that hyperproduction of endogenous opioid peptides in obesity increases insulin secretion stimulated by food intake, whereas it does not appreciably affect insulin production stimulated by circulating glucose or aminoacids.

Adolescent↗
PubMed1989

[Study of diet-induced thermogenesis using telethermography in normal and obese subjects].

It is well established that food ingestion induces increased thermogenesis, but the site in man of this increased heat production is still not known. Recent data suggest that brown adipose tissue or the liver may have an important role in this phenomenon. Since recent research provides some evidence to suggest that activation of thermogenesis in a specific organ or tissue may determine increased skin temperature in the surrounding region, we have studied skin temperature in the dorsal interscapular and in the liver regions using infra-red thermography in groups of normal and obese subjects before and after administration of oral glucose. In a separate group of normal subjects we studied oxygen consumption before and after glucose administration. While oral glucose produced a clear increase in thermogenesis, no ascertainable variation was observed in body temperature and, therefore, of heat dispersion in any of the regions studied in either normal or obese subjects.

Adult↗
PubMed1988

Acromegalic cardiomyopathy. An echocardiographic study.

Eighteen acromegalic patients (A) and 18 controls without clinical evidence of cardiac involvement and/or endocrine disease (C), matched for sex, age, body surface area, and blood pressure (BP), were investigated by M-mode (2-D derived) echocardiography, to clarify the prevalence and the possible determinants of left ventricular hypertrophy (LVH). Seven patients in each group were hypertensive (BP greater than 160/95 mmHg). Left ventricular mass (LVM) was 183.1 +/- 60.0 g/m2 in A and 130 +/- 25.9 g/m2 in C. A LVM above 140 g/m2 (that is the upper normal range in our laboratory) was found in 15/18 A and 2/18 C. The LVH was concentric (h/r greater than 0.45) in 12/15 A and 1/2 C. Systolic function indexes (% FS, end-systolic stress/end-systolic volume), cardiac index and total peripheral resistance index (as determined by echo) were within the normal range and similar in both groups. No correlation was found between LVM and BP, LVM and GH plasma levels, LVM and Sm-C levels. A significant correlation was found between LVM and duration of the disease (r 0.44; p less than 0.05). Our data confirm that LVH is an early and frequent finding in acromegaly. Its prevalence is not entirely accounted for by such factors as body size, BP or increased cardiac output. Metabolic factors may play a major role, and a long lasting exposition to increased GH levels seems the most relevant determinant of LVH.

Acromegaly↗
PubMed1987

Effect of prolonged physical exercise on muscular phospholipase A2 activity in rats.

Prolonged muscular exercise stimulates glucose uptake by the working muscles themselves. The mechanism of this phenomenon is at present unclear. It has been proposed that the kallikrein-kinin-prostaglandin system plays a role in the physiological regulation of muscular glucose metabolism during exercise. Since bradykinin can stimulate phospholipase A2, a key enzymatic step in prostaglandin synthesis, phospholipase A2 activity was assayed in rats at rest and in rats compelled to swim for 60 minutes. The physiological significance of an increase in muscular phospholipase A2 activity is not clear. Since bradykinin can stimulate both muscular glucose uptake and phospholipase A2 activity, it is possible that the increased activity of this enzyme is involved in the exercise-induced increase of muscular glucose uptake. Phospholipase A2 activity was strongly increased in the exercising rat muscles. A small but significant increase in phospholipase A2 activity was observed in the heart, whereas no variation in activity was demonstrated in either the kidney or the liver of exercising rats. These findings strongly indicate that prolonged exercise increases muscular phospholipase A2 activity only in the muscle and heart. This phenomenon appears to be strongly related to muscular contraction, since other stress situations such as cold exposure did not modify phospholipase A2 activity. Our data are in agreement with the hypothesis of a possible involvement of prostaglandins in the priming action of insulin on glucose uptake during muscular work.

Animals↗
PubMed1986

Effect of exercise on plasma kallikrein and muscular phospholipase A2 activity in rats.

Many experimental observations show that prolonged physical exercise produces an increase of muscular glucose uptake. Recent findings suggest that the kallikrein-kinin-prostaglandin system may be related to this phenomenon, but so far, no direct evidence of quantitative alteration in this system has been observed during exercise. We measured plasma kallikrein and muscular phospholipase A2 activity, respectively the first and the last steps of reactions leading to prostaglandin synthesis. We demonstrated, for the first time, that during exercise plasma kallikrein activity increases in rats. We also observed an increase of muscular phospholipase A2 activity after exercise and a positive correlation between these parameters. Our findings demonstrate, under physiological conditions of enhanced muscular glucose uptake, a concomitant significant increase of plasma kallikrein and muscular phospholipase A2 activity, supporting the hypothesis that activation of the kallikrein-kinin-prostaglandin system may play some part in the enhanced muscular glucose uptake during physical activity.

Animals↗
PubMed1985

Role of antecedent mumps and reovirus infections on the development of type 1 (insulin-dependent) diabetes.

Type 1 diabetes mellitus is thought to derive from organ-specific autoimmune reactions, probably triggered by environmental factors. In view of the possible involvement of mumps virus and reoviruses in the pathogenesis of autoimmune endocrine disease, serum antibody levels to these viruses were measured in newly-diagnosed diabetic patients aged 5 to 25 years and in matched control subjects. Diabetic patients showed a significantly lower prevalence and reduced titers of antibodies to mumps and reoviruses. By contrast, the antibody response to measles virus (a non-diabetogenic agent) was remarkably similar in the two groups. It is suggested that individuals with an impaired humoral response to some viral agents are at increased risk of developing diabetes when exposed to pancreotropic viruses.

Adolescent↗
PubMed1985

Dopamine is not involved in the opioid control of luteinizing hormone secretion in man.

The aim of this study was to examine the role of the central dopaminergic system in the mechanisms by which opioid peptides exert their influence on luteinizing hormone (LH) secretion in man. The effects of sulpiride and naloxone on the changes in LH secretion induced by a metenkephalin analog (D-Ala2-MePhe4-Met-(o)-ol-Enkephalin, FK 33824, Sandoz, Basel, Switzerland) (DAMME) and dopamine infusion in four castrated men (21 to 25 years of age) were studied. In these patients, sulpiride pretreatment counteracted the inhibitory effect of dopamine but did not alter the fall of LH plasma levels that DAMME induced. Moreover, in these subjects naloxone reduced the inhibitory effects induced by DAMME but did not change the inhibitory effect of dopamine on LH secretion. These findings confirm that central dopaminergic and opiatergic systems play a role in the control of LH secretion; the data also exclude any interaction between these systems in regulating LH secretion.

Adult↗
PubMed1985

Naloxone reduces the fenfluramine-induced prolactin release in man.

In order to ascertain whether there is a relation between opioids and the serotoninergic system in prolactin (PRL) secretion increase, we investigated in seven healthy men (21 to 26 years of age) the effect of naloxone, a specific opioid antagonist, on PRL secretion induced by fenfluramine, a drug that stimulates serotonin release and inhibits its re-uptake. We observed that subjects receiving fenfluramine (60 mg orally) had a significantly (P less than 0.001) higher increase in PRL plasma levels than the controls receiving placebo. In all subjects naloxone infusion at a dose of 15 mg caused a significant reduction (P less than 0.0005) in the PRL response to fenfluramine. Higher doses of naloxone (30 mg) do not further inhibit the PRL secretion induced by fenfluramine. These results suggest that naloxone may interact with opiate receptors on serotonin neurons thereby reducing the synthesis and release of serotonin. It seems that in man, therefore, there is an interplay between opiates and the serotoninergic system in the facilitatory influence on PRL release.

Adult↗