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J Marco

Publications and source records attributed to J Marco.

At least 253 records · Page 14Linked to original sources
PubMed1977

Effect of food ingestion on intestinal glucagon-like immunoreactivity (GLI) secretion in normal and gastrectomized subjects.

This work was undertaken to compare the intestinal GLI responses to oral glucose (1.75 g/kg, 25% sol.), to a carbohydrate-rich meal (carbohydrate content about 1.75 g/kg) and to a protein meal (250-400 g grilled lean beef) in normal (n = 6) and gastrectomized (n = 6) subjects. As expected, after glucose administration the elevation of plasma GLI was more pronounced in the gastrectomy group (approximately 500% above baseline) than in the controls (approximately 75% above baseline). However, the gastrectomized patients responded to the carbohydrate meal with a very slight elevation of circulating GLI (approximately 45% above baseline), similar to that found in the controls (approximately 70% above baseline). After the protein meal, a small increase of GLI was also observed in both groups. In conclusion, in gastrectomized subjects the ingestion of natural foodstuffs is followed by a normal elevation of plasma GLI, thereby suggesting the exclusion of this factor from involvement in the constellation of postgastrectomy syndrome. In these patients, the exaggerated rise in GLI after oral glucose is not representative of increments after physiological stimuli.

Adult↗
PubMed1977

Inhibition of glucagon release by serotonin in mouse pancreatic islets.

In this work we have investigated the effect of serotonin on glucagon release in mouse pancreatic islets isolated by the collagenase technique. Incubation of the islets with serotonin (4 X10(-3)mol/l) was associated with an inhibition of glucagon output both in the basal medium (3.3 mmol/l glucose) and in the presence of arginine (10 mmol/l). The inhibitory effect of serotonin on basal glucagon release was also apparent at concentrations of 2 X10(-3) mol/l, 10(-3)mol/l and 5 X 10(-4) mol/l. Addition of 5-hydroxytrypophan (4 X10(-3) mol/l) to the incubation medium was without effect on basal glucagon output while it significantly reduced arginine-induced glucagon release. In contrast, tryptophan (4 X10(-3) mol/l) provoked glucagon secretion. As inferred from our previous human studies, the present data indicate that serotonin is able to inhibit glucagon secretion. These findings provide further support for the participation of a serotoninergic mechanism in the control of A-cell function.

5-Hydroxytryptophan↗
PubMed1977

Elevation of plasma glucose and glucagon after tryptophan ingestion in man.

To evaluate the effect of tryptophan on blood sugar in man, we have orally administered 10 g of this amino acid to 14 normal subjects and determined their plasma levels of glucose, insulin, glucagon, and growth hormone for 4 hr after the load. Seven of the subjects also received a placebo. Tryptophan intake was followed by a slight but significant elevation of glycemia (maximum increment: 11% above basal values at 180 min, p = 0.02). This elevation of plasma glucose was accompanied by a clear rise of glucagon levels (peak: 60% at 140 min, p = 0.0007) and by increased concentrations of circulating insulin and growth hormone. Placebo administration did not significantly modify blood glucose or any of the hormones measured. In contrast to the reported hypoglycemic effect of tryptophan in rats, our data indicate that this amino acid increases plasma glucose in man. Given that tryptophan appears to possess the capability of eliciting glucagon secretion, its effect on blood glucose can be reasonably attributed to an enhanced glycogenolysis and/or gluconeogenesis provoked by its release of this hormone.

Blood Glucose↗
PubMed1977

Inhibition of intestinal glucagon-like immunoreactivity (GLI) secretion by somatostatin in man.

This work was undertaken to investigate the effect of somatostatin on intestinal glucagon-like immunoreactivity (GLI) secretion in man. In normal subjects GLI release is slightly stimulated by oral glucose while this sugar evokes a much greater GLI response in gastrectomized patients. Therefore, our study was performed in a group of such patients (N = 6). As expected, in the control experiments glucose ingestion elicited a clear-cut elevation of GLI plasma levels as measured with two antisera, 78J and R-8 (maximal peaks: 340% and 150% above basal values, respectively). Somatostatin infusion did not modify fasting GLI concentrations but completely abolished GLI response to glucose. Termination of the infusion was followed by a rebound of circulating GLI. The well-known suppressor effect of somatostatin on glucagon and insulin secretion was also detected. Finally, during somatostatin infusion the initial elevation of blood sugar after oral glucose, in the absence of insulin response, appeared considerably delayed. Our data demonstrate that somatostatin behaves as a potent inhibitory agent of GLI secretion in man. A retarding effect of somatostatin on glucose absorption is also compatible with our results.

Adult↗
PubMed1977

[Oral contraceptives and myocardial infarct].

In the light of four proven cases of myocardial infarction in patients under treatment with hormonal contraceptives, the authors point out: the sudden 'inaugural' appearance of the infarction during a therapeutic course; the appearances of the lesions on coronary arteriography; on 2 occasions a lacunar form on the proximal segment of a main coronary trunk, in one case lesions more redolent of atheroma, and in one case a completely normal vascular tree. These appearances had not changed at follow-up arteriography; the existance in 3 cases of multiple associated risk factors, especially of a mixed type of hyperlipoproteinaemia associated with tobacco consumption. The current relative frequency of coronary episodes in patients with multiple risk factors would seem to point towards caution in prescribing hormonal contraceptive treatment, especially for females of over 35 years of age.

Adult↗
PubMed1977

[Exercise electrocardiogram coupled with right cardiac microcatheterization after myocardial infarct. Correlations with ventriculo-coronarography].

This work is based on the results of a systematic scheme of investigation consisting of an exercise test on the bicycle ergometer with analysis of the ECG and of the pulmonary arterial pressure measured by cardiac micro-catheterisation, and of ventricular and coronary arteriography; 60 patients were investigated in this way after the third month following a myocardial infarction. After an anterior infarction, there is no significant correlation between the ECG changes and the coronary arteriogram. An elevation of the tracing is often (but not always) indicative of akinesia or dykinesia of the ventricle. After a posterior infarction, depression of the trace in leads which were initially normal indicates extension of the coronary lesions in 9 cases out of 10. It, is, however, possible for a tight stenosis on the anterior descending artery to exist with no changes on the ECG. A highly significant (p less than 0.001) and strong (r=0.83) correlation between an index of haemodynamic severity as defined by variations in the pulmonary arterial pressure on exercise and by the score on coronary arteriography, allows us to define certain indications for coronary arteriography and ventriculography after infarction.

Adult↗
PubMed1977

[Are stenoses of the common trunk of the left coronary artery at the root of unstable angina?].

In a series of 200 cases of unstable angina who have had coronary arteriography carried out, a stenosis of more than 60% of the trunk of the left coronary artery was noted in 40 cases (20%). This sinister site of arteriosclerosis may be suspected in patients presenting with long-standing angina (mean for the group 44 months), an angina which has recently become worse, one which is not responding rapidly to rest and beta-blockers, and in particular one where there has been a previous infarction (50% of cases). Coronary arteriography shows that the lesions were more diffuse and more severe in the group with stenosis of the main trunk. Surgical prognosis becomes worse (31% mortality) because of the risk of vascular complications. Treatment by large doses of Propranolol improves the classically gloomy prognosis of these patients when treated medically.

Adult↗
PubMed1976

Enhanced glucagon secretion by pancreatic islets from prednisolone-treated mice.

This work was undertaken to study the effect of prednisolone on glucagon release in mouse pancreatic islets isolated by the collagenase technique. Pretreatment of the donors with prednisolone (0.2--0.3 mg daily) induced an increase in glucagon release both in the absence (1005+/-75, SEM, vs. 796+/-46 pg/10 islets/60 min, p=0.019) and in the presence of 7.5 mM arginine (1500+/-119 vs. 1236+/-61 pg/10 islets/60 min, p=0.05). The glucagon content of the islets was not modified by the treatment (28.6+/-1.1 vs. 28.0+/-1.1 ng/50 islets). The addition of prednisolone (5 - 10(-5) M) into the medium, failed to affect significantly glucagon secretion. In agreement with previous human studies, our data indicate that chronic glucocorticoid administration augments the secretory activity of the A-cell. This does not seem to be a result of increased glucagon synthesis nor a direct effect of glucocorticoids on the glucagon-releasing mechanism. Rather, environmental changes induced by these hormones could be responsible for A-cell hyperfunction.

Animals↗
PubMed1976

Plasma glucagon immunoreactivity in a totally pancreatectomized patient.

Analysis of the plasma from a totally pancreatectomized patient, with antiserum 30 K, has demonstrated basal glucagon immunoreactivity (GIR) levels in the normal range (80-110 pg/ml). Neither i. v. arginine nor oral glucose affected these GIR values, thus indicating the absence of functioning pancreatic or gastrointestinal A-cells. Furthermore, filtration of whole plasma on Bio Gel P-30 showed no GIR in the 3500 MW elution volume. GIR was found to be distributed in two peaks. One peak eluted in the protein region, similarly to "big plasma glucagon" (BPG), and the second peak appeared after the glucagon-I125 marker. The protein-sized moiety was not absorbable by charcoal, and on Sephadex G-100 it eluted within the globulin region. When subjected to trypsin treatment, it yielded smaller GIR fractions. According to these criteria, it can be assumed that this component is identical to BPG. Therefore, an extrapancreatic source for BPG is suggested. On the other hand, the presence of fasting hyperglycaemia in this patient indicates that insulin deficiency by itself suffices to raise blood sugar to diabetic levels.

Chromatography, Gel↗
PubMed1976

Potentiation of glucagon secretion by serotonin antagonists in man.

To study the possible implication of endogenous serotonin in the control of glucagon secretion in man, normal volunteers were subjected to alpha-cell stimulation before and after oral treatment with serotonin antagonists (cyproheptadine and methysergide) and with an inhibitor of serotonin synthesis (para-chlorophenylalanine, PCPA). After administration of cyproheptadine (16 mg daily, for two days) the glucagon responses to arginine (N=12) and to insulin-induced hypoglycemia (N=9) were more marked than in the control experiments (differences between maximal elevations: +165 pg/ml, P less than 0.0001, and +197 pg/ml, P less than 0.02, respectively). After methysergide treatment (9 mg daily, for two days), a potentiation of arginine-provoked glucagon secretion was also observed (+260 pg/ml, P less than 0.002; N=7). Similarly, after PCPA administration (2 g daily, for four days) the alpha-cell responsiveness to both aminogenic (N=12) and hypoglycemic (N=7) stimuli was enhanced (+108 pg/ml, P less than 0.05, and +164 pg/ml, P less than 0.05, respectively). Since glucagon secretion is potentiated by treatment with drugs which either antagonize serotonin action or inhibit its synthesis, the suggestion can be made that endogenous serotonin modulates alpha-cell function in man by acting as an inhibitor.

Arginine↗