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Biomedical subjects

P P Foà

Publications and source records attributed to P P Foà.

At least 19 recordsLinked to original sources
PubMed1985

Effect of insulin on the activity of amino acid transport systems in cultured human fibroblasts.

The regulation of amino acid transport by insulin has been studied in cultured human fibroblasts. Among the six amino acid transport systems operating in cultured human fibroblasts, two systems (A and X-C) are strongly stimulated by insulin and four (ASC, X-AG, y+ and L) are essentially not sensitive to the presence of the hormone in the incubation medium. The hormonal stimulation of system A and system X-C became significant after 3 h of incubation and increased up to 12 h. The stimulatory effect was related to insulin concentration, with a half-maximal stimulation at 10(-9) M hormone concentration. Insulin enhanced transport activity by increasing the maximal velocity (Vmax) of transport, without significant changes in Km values.

Amino Acids↗
PubMed1980

Reactive hypoglycemia and A-cell ('pancreatic') glucagon deficiency in the adult.

Serum glucose, A-cell (IRGA) and total glucagon (IRGT), insulin, growth hormone, cortisol, triiodothyronine, and thyroxine values were measured in the fasting state and in response to oral glucose, intravenously administered arginine, and a meal of pan-broiled ground beef in 31 symptomatic patients and 11 normal subjects. Twenty-four patients and 11 control subjects had normal glucose tolerance (group 1); seven patients had reactive hypoglycemia (group 2). Under all conditions, serum IRGA value was significantly lower in group 2 than in group 1. Glucose, arginine, or meat increased serum IRGT levels. This response did not differ significantly in the two groups, nor did the secretion of the other measured hormones. We conclude that A-cell insufficiency can contribute to reactive hypoglycemia in the adult.

Adolescent↗
PubMed1979

Somatostatin-induced changes in the hemostasis of rats.

Somatostatin (SRIF) given intravenously, either as a single bolus or as a 2 hr infusion caused a significant prolongation of partial thromboplastin time (PTT) and depressed platelet counts and platelet aggregation in the rat. Following daily injections of protamin-zinc SRIF for 2 weeks the platelet count returned to normal, PTT remained prolonged and platelet aggregation was enhanced. The doses of SRIF used in this work were adequate to suppress the secretion of insulin and glucagon by the isolated pancreatic islets of treated animals.

Animals↗
PubMed1979

Insulin and glucagon secretion by islets isolated from fetal and neonatal rats.

Islets were isolated by mild collagenase digestion and microdissection from rat fetuses 2 days before term and pups 1 or 2 days after birth and their insulin and glucagon secretion studied in vitro. Fetal B cells were stimulated by 16.7 mmol/l glucose, 20 mmol/l leucine or 20 mmol/l arginine. Fetal A cells were not affected by glucose or leucine, but were significantly stimulated by arginine. Somatostatin abolished the effect or arginine on both IRI and IRG output. Neonatal islets proportionally released more insulin and glucagon than their fetal counterparts, but reacted to the tested agents in a similar fashion. During the perinatal period, pancreatic insulin storage increased at a higher rate than that of glucagon. It is concluded that fetal B cells are equipped with sensors to a variety of agents and able to modulate their secretory rate according to the concentration of these agents. A cells are reactive to arginine 2 days before term but do not become glucose reactive until several days after birth.

Animals↗
PubMed1979

Effects of histamine, of histidine and of anti-histaminic agents on the release of glucagon and insulin from the rat pancreas.

We have studied the effect of histamine (HA) and histidine (HIS) on the release of immunoreactive glucagon (IRG) and insulin (IRI) by isolated rat islets and pieces of pancreas. In isolated islets, HA and HIS stimulated IRG release at a glucose concentration of 3.0 mg/ml and IRI release at a glucose concentration of 0.5 mg/ml. In pieces of pancreas incubated in the presence of glucose (3.0 mg/ml), HA at a 2mM concentration stimulated IRG release and had no effect on the release of IRI; however, when the concentration of HA was doubled (4 mM), an inhibition of IRI release could also be demonstrated. HIS was ineffective. Perphenazine and dexchlorpheniramine, two anti-histaminic agents, inhibited IRG and stimulated IRI release. These results indicate that histamine, whether endogenous or exogenous, directly stimulated IRG and inhibits IRI release and suggest that some of the in vivo effects of histamine, such as hyperglycemia and lipid mobilization, may be mediated, at least in part, by these endocrinologic effects.

Animals↗
PubMed1979

Secretion of glucagon and insulin in hypophysectomized rats: effect of tolbutamide.

Normal and hypophysectomized (hypox) rats, fed ad libitum, received intraperitoneal injections of tolbutamide (75 mg/kg/day) or of saline for 6 weeks. 24 h after the last injection, blood samples were taken for glucose, insulin and glucagon determinations. In normal rats, tolbutamide treatment did not alter serum glucose, insulin and glucagon, although it suppressed the secretion of insulin and glucagon by the pancreatic islets. In hypox rats, tolbutamide decreased serum glucose and insulin, elevated serum glucagon and stimulated the secretion of glucagon, but not that of insulin by the pancreatic islets. In addition, tolbutamide treatment increased the glucagon response to arginine in normal, but not in hypox rats. The serum glucose response to arginine was decreased by tolbutamide treatment and by hypophysectomy and, thus, appeared independent of the glucagon rise or preexisting glucagon level. We conclude that tolbutamide treatment decreased the secretion of glucagon and insulin in normal rats and stimulated that of glucagon in hypox rats, perhaps because of the low levels of insulin in the serum and in the pancreas of the latter. Our results are compatible with the hypothesis that the pancreatic action of tolbutamide is influenced by the pituitary.

Animals↗
PubMed1979

A-Cell and gut glucagon in normal and depancreatized dogs. Inhibition by somatostatin and insulin.

The effect of somatostatin (SRIF) and of insulin on the plasma levels of immunoreactive glucagon (IRG) and glucose was examined in normal (N) and depancreatized (PX) dogs. The infusion of SRIF (3 microgram/min for 15 min) caused a rapid decrease of the total IRG measured by means of an antiglucanon serum (AGS 10) which cross reacts with extracts of intestinal mucosa. This decrease was due primarily to a fall in the IRG fraction measured by an antiserum (AGS 18) specific for the carboxyl terminus of pancreatic or A-cell IRG. When the dose of SRIF was increased to 10 microgram/min for 90 min, the difference between total and A-cell IRG in the systemic blood also decreased, indicating that other IRG fractions, such as gut IRG, had also been suppressed. The introduction of 50 ml of a 5% glucose solution into a loop of ileum was followed by an increase of gut IRG measured in the regional mesenteric blood. This response was suppressed by the infusion of SRIF (3 microgram/min). Insulin suppressed the basal level of total IRG, but did not alter the gut IRG response to glucose. The SRIF- and insulin-induced reduction in plasma IRG was not associated with a reduction in plasma glucose, suggesting that the high levels of total and A-cell IRG observed in depancreatized dogs were not essential for the maintenance of hyperglycemia.

Animals↗
PubMed1978

The serum glucose response to glucagon suppression with somatostatin, insulin or antiglucagon serum in depancreatized rats.

Total immunoreactive glucagon (IRG) and immunoreactive glucagon of A cell origin (IRGa) were measured in the serum of normal, sham-operated and depancreatized rats, after the administration of three glucagon antagonists: insulin (5--200 mU/rat/h), somatostatin (SRIF; 100 microgram/kg/h) and antiglucagon serum (AGS, enough to bind three times the calculated total amount of circulating IRG). Since no differences were noted between the responses of normal and sham-operated animals, the values were pooled and used as controls. Pancreatectomy caused a significant increase in serum glucose, IRGa and total IRG and a significant decrease in serum insulin. AGS and SRIF significantly decreased serum glucose in control, but not in depancreatized rats, even though SRIF caused a significant decrease of IRGa in all animals. SRIF significantly decreased plasma insulin in control rats, but did not modify total IRG secretion in either groups. In control rats the minimum effective hypoglycaemic dose of insulin (5 mU/rat/h) may have decreased serum IRGa, but not total IRG. At higher doses (20 mU/rat/h) insulin stimulated glucagon secretion. In depancreatized animals, higher doses of insulin (200 mU/rat/h) were needed to lower serum glucose. On the other hand, a dose of 100 muU/rat/h was sufficient to lower the serum IRG. We conclude that although hyperglucagonaemia may contribute to the hyperglycaemia of the untreated depancreatized rats, the excessive secretion of glucagon is secondary to insulin insufficiency and that, at least in this animal model, the hypoglycaemic action of insulin is only minimally dependent upon its ability to suppress glucagon secretion.

Animals↗
PubMed1978

Aspirin stimulates insulin and glucagon secretion and increases glucose tolerance in normal and diabetic subjects.

Normal subjects and patients with adult-onset diabetes received 10 gm. of aspirin in four days. On the fourth day, the fasting serum glucose and the glucose response to oral glucose were decreased in both groups. These changes were associated with increased levels of serum insulin and pancreatic glucagon, although the glucagon responses to oral glucose were unchanged. In the diabetic patients, aspirin therapy was followed by a decreased glucose response to I.V. glucose and by the appearance of an early insulin peak, which could not be demonstrated before treatment. Aspirin did not affect the I.V. glucose tolerance in normal subjects, although it did enhance the early insulin peak. A decrease in the fasting levels of free fatty acids was noted in both groups, whereas the fasting level of triglycerides decreased only in the diabetic patients. Cholesterolemia did not change in either group. A few preliminary observations indicate that, in normal subjects, ibuprofen and ketoprofen, two other presumed prostaglandin inhibitors, did not affect fasting glycemia, glucose tolerance, or the insulin response to glucose. No changes were noted after the administration of placebo.

Adult↗
PubMed1976

Insulin secretion and glucose uptake by isolated islets of the hamster. Effect of insulin, proinsulin and C-peptide.

Isolated pancreatic islets of normal hamsters were perifused either in a closed or in a open system. When the buffer was recirculated and the endogenous insulin was allowed to accumulate, the islets secreted significantly less insulin than when the system was open and the endogenous insulin was washed away. The addition of monocomponent insulin or of proinsulin to the perifusion buffer significantly decreased insulin secretion. The inhibitory action of proinsulin was significantly greater than that of monocomponent insulin. C peptide had no effect. When pancreatic islets were incubated in a fixed volume of stationary buffer containing unlabeled glucose (1.0 mg or 3.0 mg/ml) and glucose-U-14C (1.0 muC/ml), the amount of insulin secreted and the 14CO2 produced by each islet decreased progressively as the number of islets in the sample increased. Under these conditions, the concentration of insulin required to inhibit insulin secretion increased with the concentration of glucose in the medium. Proinsulin did not alter the incorporation of leucine-4.5(-3). H into total extractable insulin (insulin + proinsulin). Thus, insulin and proinsulin appear to inhibit insulin release, but not insulin synthesis.

Animals↗
PubMed1975

Glucose, insulin, pancreatic glucagon and glucagon-like immunoreactive materials in the plasma of normal and diabetic children. Effect of the initial insulin treatment.

Pancreatic glucagon (PG) and other glucagon-like immunoreactive materials (GLI) were measured in the plasma of normal and of newly diagnosed untreated diabetic children, using an antiglucagon serum (AGS) highly specific for pancreatic glucagon (AGS 18) and an AGS which crossreacts with extracts of intestinal mucosa (AGS 10). Gut GLI was considered to be the difference between "total" GLI (AGS 10) and PG (AGS 18). Glucose and immunoreactive insulin (IRI) were also measured. PG, total GLI and gut GLI were significantly elevated in children with severe insulin insufficiency and were reduced to normal by insulin treatment, even though a significant fasting hyperglycemia was still present. In three diabetic children who had high initial plasma IRI levels the three glucagon fractions were normal. We conclude that insulin insufficiency is characterized not only by high plasma levels of PG as previously reported, but also of gut GLI. These abnormalities can be corrected by the administration of insulin.

Adolescent↗
PubMed1975

Gastric operations and glucose homeostasis. II. glucagon and secretin.

Alimentary hyperglycemia in patients who have undergone gastric operations may be due, in part, to altered intestinal signals for glucose disposition. We measured glucose, immunoreactive insulin (IRI) pancreatic glucagon (IRG), and glucagon-like immunoreactivity (GLI) after oral glucose in patients with prior antrectomy or vagotomy and pyloroplasty and in normal individuals. All subjects had normal assimilation coefficients for intravenous glucose, which suggests that the responsiveness of the pancreatic beta-cells had not been altered by the surgical procedures. The early hyperglycemic response to oral glucose and the associated elevation of plasma GLI were much greater and the IRI levels slightly higher in both experimental groups in comparison to normal subjects. A decrease in the level of IRG, albeit not statistically significant, was noted in all groups after the ingestion of glucose. In gastrectomy patients, secretin infusion during repeated oral glucose tolerance tests partially corrected the hyperglycemia and lowered plasma GLI and IRI levels. The responses of the vagotomy and pyloroplasty patients and of the normal subjects were not altered by secretin infusion. We conclude that the intolerance or oral glucose after gastric surgery may be related to elevated GLI levels, and that the beneficial effect of secretin may be due to its ability to decrease these levels.

Adult↗