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Biomedical subjects

A Lala

Publications and source records attributed to A Lala.

At least 37 records · Page 2Linked to original sources
PubMed1989

Intravenous dexamethasone and subsequent ACTH test in comparison with dexamethasone oral test in the diagnosis of Cushing's syndrome: a report of 20 cases.

Dexamethasone inhibits ACTH secretion in the pituitary corticotropic cells of normal subjects; this ability is variously affected in Cushing's syndrome. The iv infusion of dexamethasone is not time consuming, nor it is influenced by the variability of intestinal absorption or hepatic metabolism, as occurs with oral administration. Iv dexamethasone (1.5 mg/h) over 7 h and an ACTH bolus at the 6th h were administered to 17 patients with Cushing's disease, 3 patients with Cushing's syndrome (2 with adrenal adenoma, 1 with ectopic ACTH secretion) and 13 normal subjects. After 4 days the 20 patients were also given the standard oral low-dose and high-dose dexamethasone test. Two h after starting the drug infusion, cortisol concentrations were inhibited by more than 50% in each control subject. In contrast, in all but one patient they remained higher than 50% over the baseline. At the 6th heach control subject and 15 of the 17 patients with Cushing's disease showed an inhibition of plasma cortisol concentration which was greater than 50%. Inhibition was less than 50% in 2 patients with Cushing's disease and in the 3 patients with non-pituitary dependent Cushing's syndrome. The sensitivity and specificity of this test are comparable with those of the dexamethasone oral test. Although statistically significant, results obtained from ACTH bolus were not sufficiently discriminating. If studies conducted on a larger population confirm these preliminary data, the rapidity and reliability of the dexamethasone infusion test could make it an important new tool in diagnosing Cushing's syndrome.

Administration, Oral↗
PubMed1989

Increased insulin sensitivity in patients with idiopathic reactive hypoglycemia.

We performed a euglycemic hyperinsulinemic glucose clamp in 20 patients selected from a large number of subjects referred to our clinic with symptoms suggesting reactive hypoglycemia. Diagnosis was made on the basis of blood glucose measurements during symptoms in their daily life and confirmed by a 5-h oral glucose tolerance test. The patients were divided into the following groups: 8 patients with idiopathic reactive hypoglycemia (IRH), i.e. biochemical hypoglycemia associated with symptoms and plasma insulin concentrations in the normal range; 6 patients with nonhypoglycemia (NH), i.e. patients experiencing the symptoms evoking hypoglycemia at essentially normal plasma glucose levels; and 6 patients with alimentary hypoglycemia secondary to previous gastric surgery (GS). Eight normal volunteers formed the control group (N). Hypoglycemia in this study was considered to be present when plasma glucose concentrations were below 2.5 mmol/L. The peak cortisol levels after glycemic nadir were higher (2P less than 0.05) in IRH compared to GS and N. In the same group, a partially deficient glucagon response to hypoglycemia was noted. During the euglycemic clamp, the glucose uptake appeared to be significantly greater in the IRH group than in NH, GS, and N groups (8.13 +/- 0.49 vs. 7.02 +/- 0.35, 6.48 +/- 0.22, and 6.66 +/- 0.42 mg/kg.min, respectively; 2P less than 0.05). Therefore, our data suggest that increased insulin sensitivity represents a feature of idiopathic reactive hypoglycemia.

Adult↗
PubMed1988

Electroencephalography and visually evoked potentials during moderate hypoglycemia.

The effects of hypoglycemia per se on the electroencephalogram (EEG) and visually evoked potentials (VEPs) were studied in eight normal young adults. The EEG and VEPs were recorded before and during hypoglycemic clamp studies, carried out at plasma insulin and glucose concentrations of about 287 pmol/L and 2.38 mmol/L, respectively. From the mean power EEG spectra obtained during each testing condition, several parameters in each frequency band considered were compared statistically. During the eyes closed recording, the mean frequency of the alpha-band (8-13 Hz) decreased from 10.1 +/- 0.2 (+/- SE) Hz in both the right and left frontal leads during euglycemia to 8.8 +/- 0.2 and 8.8 +/- 0.1 Hz (left and right frontal leads, respectively; P less than 0.05) during hypoglycemia. In the same leads, the peak frequency decreased from 10.6 +/- 0.4 and 10.3 +/- 0.4 Hz to 9.6 +/- 0.4 and 9.5 +/- 0.3 Hz, respectively (P less than 0.05). A similar pattern of variation was found during the eyes open recording. In contrast, mean VEP latencies did not vary significantly; they were 118 +/- 3 ms (smallest image size; square wave signals subtending 30 min of arc) and 116 +/- 3 ms (largest image size; square wave signals subtending 60 min of arc) during euglycemia to 121 +/- 3 and 119 +/- 3 ms, respectively, during hypoglycemia. This study demonstrates that the earliest hypoglycemia-induced EEG alterations occur in the frontal regions and can be quantified in terms of decreased mean and peak frequencies of the alpha-band. VEP latency is less sensitive. If confirmed in diabetic patients, these data may provide a theoretical basis for developing a portable device to detect early hypoglycemia in those patients who lack warning symptoms.

Adult↗
PubMed1984

Glucose-induced GIP levels in patients with insulinoma.

Gastric inhibitory polypeptide (GIP) levels during an oral glucose tolerance test (OGTT) have been determined in eight patients suffering from a single benign beta-cell adenoma. GIP hypersecretion and an absent correlation between the insulin: glucose ratio and plasma GIP concentration have been observed. Our data show that the insulinotropic effect of GIP is almost abolished in insulinoma patients. This finding may help explain blood glucose levels and the inappropriate plasma insulin response to oral glucose often observed in these patients.

Adenoma, Islet Cell↗
PubMed1983

Diazoxide infusion test in patients with single benign insulinoma.

The diazoxide infusion test (600 mg i.v. over a 1-hour period) was performed in 12 patients bearing single benign islet B-cell adenoma and in 6 normal subjects. Blood glucose, plasma insulin and glucagon concentrations were measured every 15 min during the infusion and thereafter up to 150 min. In insulinoma patients, blood glucose levels failed to increase significantly while in the control group a significant rise starting from 30 min persisted throughout the test (p less than 0.05 or less). Plasma insulin mean levels decreased significantly in normal subjects from 30 to 60 min (p less than 0.05), while they were significantly suppressed in hypoglycemic patients from 15 to 120 min (p less than 0.02). Diazoxide administration induced in the normal group a significant decrease in glucagon levels (p less than 0.02 from 30 to 150 min) whereas no such suppression occurred in patients. In our experience, insulin response to diazoxide infusion in patients with insulinoma may provide additional information for diagnosis.

Adenoma, Islet Cell↗
PubMed1983

Effect of bombesin on plasma insulin, pancreatic glucagon, and gut glucagon in man.

The effect of bombesin on insulin, pancreatic glucagon, and gut glucagon was investigated in eight healthy volunteers and two pancreatectomized patients. Bombesin, infused iv at the constant rate of 5 ng kg-1 min-1, produced a sharp and statistically significant rise in the plasma insulin concentration. The peak was reached at 5 min (26 +/- 2.17 microU/ml; P less than 0.005 vs. basal values), followed by a prolonged and statistically significant (P less than 0.05) decrease in blood glucose. Pancreatic glucagon rapidly rose to a maximal value of 80.5 +/- 7.6 pmol/liter (P less than 0.005 vs. basal values). In contrast with the prompt increase in insulin and glucagon plasma levels, the peak in gut glucagon concentration (55.8 +/- 4.6 pmol/liter; P less than 0.005 vs. basal values) was reached 30 min after bombesin infusion was discontinued. In the two pancreatectomized patients, bombesin induced an increase in gut glucagon concentrations only. The results presented indicate that bombesin acts directly on the A and B cells of the pancreas, influencing glucose homeostasis; however, more complex mechanisms seem to be involved in gut glucagon secretion.

Adult↗
PubMed1982

Plasma levels of glucagon-like polypeptides in gastrectomized patients transformed from Billroth II into Billroth I.

An oral glucose tolerance test (OGTT) has been performed in a group of patients with partial gastrectomy before and after transforming the anastomosis from Billroth type II (B II) into Billroth type I (B I). Glucose tolerance was normal in both groups. The statistically significant differences in blood glucose (BG) values observed at 30 min between B I and normals and at 30, 60 and 90 min between B II and normals occur without concomitant changes in insulin (IRI) plasma levels. In the course of the test a marked rise (statistically significant from 30 to 180 min) in glucagon-like immunoreactants (GLI) plasma levels was noted in B II patients and has been attributed to the rapid intestinal transit. Otherwise, the restoration of duodenal passage induced a clear decrease of GLI levels which returned to normal values. Increased immunoreactive glucagon (IRG) plasma levels in B II group do not seem to be due to cross-reactivity with GLI. The raised BG levels occurring in B II cannot be attributed either to a reduced insulin secretion or to an increase in biologically active components of glucagon.

Blood Glucose↗
PubMed1978

[Effect of sodium fluoride on the metabolism of the rat kidney cortex and medulla].

Tissue sections of cortex and outer and inner medulla of rat kidneys were examined in the Warburg apparatus with and without addition of NaF. It was shown that the O2 consumption was not significantly reduced in the presence of 0.05 mM F (=0.95 ppm F!) or smaller amounts. The respiratory quotient was not changed by NaF. Lactate formation in sections from the inner medulla was reduced to the same degree as O2 consumption. Maximal concentrations of plasma fluoride which are met in doses of fluoride used for the prophylaxis of caries, do not impair renal metabolism.

Animals↗
PubMedDate not supplied

Plasma levels of glucagon-like polypeptides in patients with esophagoplasty.

Seven patients with interposition of a jejunal tract between the esophagus and stomach or duodenum (EP group) and ten healthy normal volunteers have been submitted to an oral glucose load (OGTT) to clarify the significance of glucagon-like polypeptides (GLI) induced by glucose in carbohydrate metabolism. Blood glucose (BG) and GLI plasma levels were significantly higher in the EP group than in the normal one (p less than 0.01), respectively 30, 60, 90 min for BG and during all the test for GLI. The fasting immunoreactive glucagon (IRG) plasma levels were significantly lower in patients than in normals (p less than 0.05) whereas a marked and significant increase was observed in the EP group (p less than 0.01) from 90 to 240 min. The precocious stimulation of jejunal mucosa and the rapid intestinal transit which occur in these patients may explain the elevated GLI (probably glicentin) plasma levels. The rise in IRG plasma levels might be due to the enzymatic transformation of glicentin. The role of these types of glucagon on carbohydrate metabolism is still to be fully clarified.

Aged↗
PubMedDate not supplied

Chemotactic-like receptors and Abeta peptide induced responses in Alzheimer's disease.

Evidence suggests that beta-amyloid (Abeta) has chemokine-like properties and may act through formyl chemotactic receptors (FPR) to induce pathophysiologically important functional changes in Alzheimer's disease (AD) microglia. We have shown that Abeta 1-42, fibrillar Abeta 1-40, and Abeta 25-35 potentiate the release of interleukin-1beta (IL-1beta) from LPS activated human THP-1 monocytes [26] and LPS primed rat microglia. Moreover, Abeta-stimulated IL-1beta secretion seems to be receptor mediated because it is calcium dependent and requires activation of specific G-proteins [27]. Thus, we have evaluated the ability of Abeta 1-42 to mimic formyl chemotactic peptides in stimulating IL-1beta release from THP-1 monocytes. Several of the formyl chemotactic peptides and Abeta 1-42 significantly enhanced IL-1beta production in THP-1 monocytes. In contrast, a formyl chemotactic receptor antagonist inhibited Abeta 1-42-induced IL-1beta release from both human THP-1 monocytes and primary rat microglia. Further, primary rat microglia grown in culture expressed FPR as demonstrated by immunocytochemistry. Given the multiple pathophysiologic roles IL-1beta may play in AD, agents that block Abeta interactions with formyl chemotactic receptors on microglia might be important antiinflammatory therapeutic targets.

Alzheimer Disease↗