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Biomedical subjects

R Assan

Publications and source records attributed to R Assan.

At least 37 records · Page 2Linked to original sources
PubMed1990

Glucagon secretion is essential for aminoacid-induced hyperfiltration in man.

The role of glucagon as a mediator of aminoacid-induced alteration of renal haemodynamics was evaluated in man in three different protocols. In the first it was shown that the increase in glomerular filtration rate (GFR) and renal plasma flow (RPF) observed during an aminoacid infusion was prevented by the additional infusion of somatostatin (SRIF), but reproduced by a glucagon infusion in the presence of SRIF. In the second protocol it was shown that, at variance with normal subjects, six totally pancreatectomised patients, thus deprived of pancreatic glucagon secretion, did not increase their GFR and RPF when infused with amino-acids, whereas they exhibited the expected hyperfiltration when infused with glucagon. In the third protocol it was shown that glucagon infusion in a renal artery did not alter the homolateral renal haemodynamics. It is concluded that glucagon secretion is a mandatory step in the cascade of events linking the infusion of aminoacids to the renal hyperfiltration. Other steps beyond glucagon secretion are necessarily involved because glucagon has no direct renal effect.

Adult↗
PubMed1990

Hypoglycaemia and diabetes mellitus following parenteral pentamidine mesylate treatment in AIDS patients.

Of 18 AIDS patients with Pneumocystis carinii pneumonia treated with pentamidine mesylate parenterally, four developed serious to severe hypoglycaemia, three hypoglycaemia followed by insulin-requiring diabetes, and two others diabetes alone. Hypoglycaemia (blood glucose 2.1 +/- 0.2 (+/- SE) mmol l-1) occurred 9 (2-22) days after starting treatment, and diabetes (initial blood glucose 30 +/- 6 mmol l-1) after 60 (20-90) days. The other patients remained euglycaemic. The dysglycaemic patients (hypo- and hyper-glycaemic) had a higher pentamidine dosage (p less than 0.01), and higher serum creatinine levels at end of treatment (p less than 0.001), consistent with drug accumulation and dose-dependent toxicity. Plasma C-peptide levels were low in the diabetic patients, in the basal state (0.25-0.28 nmol l-1) and following stimulation by IV glucagon (0.35-0.40 nmol l-1), vs 0.80 +/- 0.06 nmol l-1 (basal) and 1.83 +/- 0.16 nmol l-1 (stimulated) in 23 healthy control subjects (mean +/- SE). Islet cell or insulin antibodies were not detected. Serum amylase levels rose abnormally in the dysglycaemic group, and pancreatitis was proved in one, and suspected in another patient. None of 28 similar AIDS patients whose P. carinii pneumonia was treated with cotrimoxazole showed blood glucose disturbance.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Plasma C-peptide levels and clinical remissions in recent-onset type I diabetic patients treated with cyclosporin A and insulin.

Remission from insulin dependency in insulin-treated recent-onset type I (insulin-dependent) diabetic patients can result from a partial recovery of insulin secretion, an improvement in tissue sensitivity to insulin, or both. The same hypothesis must be analyzed when remission occurs in cyclosporin A (CsA)-treated patients. In this study, plasma C-peptide levels were serially measured in the basal state and after stimulation in 219 recent-onset type I diabetic patients; 129 received CsA, and all patients were similarly monitored and insulin treated. The results were analyzed in view of the occurrence of remission. Remission was defined as good metabolic control in the absence of hypoglycemic treatment for greater than or equal to 1 mo. Remission occurred in 44% of the CsA-treated group and lasted for mean +/- SE 10.0 +/- 0.9 mo vs. 21.6% in the non-CsA-treated group with a duration of 4.4 +/- 0.8 mo. Plasma C-peptide levels were initially dramatically lower than normal in both groups in the basal and stimulated states. C-peptide levels increased significantly later, at 3 and 6 mo, in both groups. C-peptide values were proportional to the rates of remission in both groups. In the non-CsA-treated group, C-peptide levels later decreased, and these patients inexorably relapsed to insulin dependency. In contrast, in the CsA-treated group, the initial recovery in insulin secretory capacity was maintained over the 18-24 mo of the study. Furthermore, higher remission rates and longer-lasting remission were obtained in patients who reached higher C-peptide levels at the 3rd mo of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Hypertension induced by cyclosporin A in insulin-dependent diabetic patients. A one-year follow-up].

UNLABELLED: Forty-five recent insulin-dependent diabetics (IDD) were treated with cyclosporine A (CsA) 7.5 mg/kg b.i.d. as single immunosuppressive therapy to achieve remission of diabetes. Measurements of mean arterial pressure (MAP), glomerular filtration rate (GFR:inulin clearance), renal vascular resistance (RVR: MAP x [1-haematocrit] divided by PAH clearance), absolute (UNa.V) and fractional (FENa) urinary sodium excretion, were performed initially (M0) and after 3 (M3) and 12 (M12) months of treatment. Results were (mean +/- SD): [table: see text] Prevalence of hypertension defined as MAP greater than or equal to 107 mmHg was 12% at M3 and 24% at M12. Whereas the maximal changes in GFR and RVR occurred at M3, MAP increased further and sodium excretion decreased at M12. IN CONCLUSION: 1) CyA-induced increase in blood pressure paralleled that in RVR at M3 and decreased sodium excretion at M12. 2) There was a dissociation between MAP and GFR changes after 12 months of treatment with CyA.

Adult↗
PubMed1989

Short tertatolol treatment does not impair the hormone and metabolic responses to exercise and hypoglycemia in diabetics.

Beta-blockers can precipitate hypoglycemia and mask its warning signs. Ten male insulin-dependent, otherwise healthy diabetic patients underwent two submaximal exercise tests and two insulin-induced hypoglycemic events (0.2 u/Kg short-acting insulin IV) after six days administration of placebo followed by tertatolol, a non selective beta-blocker (5 mg once daily). Tertatolol modified neither the exercise-induced changes in blood glucose, lactate and plasma unesterified fatty acid levels, nor those of counter regulatory hormones (glucagon, growth hormone, cortisol), while blood pressure, heart rate and plasma renin activity were significantly reduced, proving that tertatolol had actually been ingested, and was active. During the insulin-induced hypoglycemia, similarly tertatolol did not modify the course of the plasma fuels and hormones. Particularly, hypoglycemia was neither deeper nor more prolonged in the presence than in the absence of tertatolol. Warning symptoms were not affected except for palpitations which were not perceived. These results suggest that tertatolol did not precipitate hypoglycemia following exercise, and did not aggravate insulin-induced hypoglycemia in short term administration, and in otherwise healthy diabetic patients.

Adrenergic beta-Antagonists↗
PubMed1989

[Effects of bombesin on gastrin, somatostatin, glucagon and acid secretion from isolated rat stomach in vitro].

Effects of bombesin on the secretion of gastric acid and gastro-intestinal hormones were investigated in isolated perfused rat stomach. Bombesin (intra-arterial, 2 x 10(-10) mol/L, 0.3 ml/min) stimulated gastric acid secretion from basal 2.50 +/- 0.05 x 10(-1) to 8.40 +/- 1.50 x 10(-1) mEq/min (P less than 0.001). Exogenous addition of pentagastrin did not potentiate this effect of bombesin. Bombesin induced twice releasing of gastrin and somatostatin in portal effluent but inhibited glucagon secretion. The basal releasing rates of these three hormones were 62 +/- 8 pg, 5.9 +/- 1.1 ng, and 0.40 +/- 0.03 ng/min respectively. The peak values of gastrin and somatostatin during bombesin stimulation were 1000 +/- 20 pg and 12.2 +/- 2.0 ng/min respectively, while the nadir value of glucagon was 0.17 +/- 0.05 ng/min. All three responses were dose-dependent. These three hormones were all detectable, albeit at much lower concentrations in the pyloric effluent perfusate than they were in the portal effluent.

Animals↗
PubMed1988

A simple strategy to amplify specifically the HLA-DQ beta gene region with genomic DNA as template.

The nature of codon 57 in the HLA-DQ beta gene was recently reported as a potential marker of genetic susceptibility to insulin-dependent diabetes mellitus. When exploring the relevance of this marker by using genomic DNA amplification, we encountered difficulties resulting from the coamplification of the homologous DX beta region. A simple strategy is proposed to amplify the DQ beta region exclusively. It involves the preliminary digestion of genomic DNA with a restriction enzyme which cleaves DX beta specifically, leaving intact the DQ beta sequence. The amplified material is suitable for dot blot analysis and restriction enzyme digestion. This strategy is of general interest when homologous sequences impair the specificity of enzymatic DNA amplification.

DNA↗
PubMed1988

MHC classes I, II, III antigens study in 70 insulin-dependent diabetics with associated auto-immune diseases.

Seventy IDDM patients (insulin-dependent diabetics), 48 females and 22 males, most of them adults at the onset of diabetes, and suffering from at least one other associated autoimmune manifestation (AAM) were studied for HLA A,B,C, DR markers and Bf, C4 complement components. Comparisons were made with 108 normal controls and a series of 287 IDDM patients with juvenile onset (under 25 years) and no patent other autoimmune disease. The increase in frequency of HLA-B8 among IDDM patients with AAM was confirmed (36% versus 20% in controls) (p less than 0.04). The frequency of DR4 among diabetics with AAM (33%) was not significantly different from the normal frequency (27%), and the allelic combination DR3/4 was found in only 13% of IDDM with AAM. Corresponding frequencies in patients with IDDM alone were 66% for DR4 and 34% for DR3/4 (p less than 10(-6) and 10(-3) respectively). These results confirm the heterogeneity of IDDM and support, by genetic arguments, the concept of overlapping entities. The hypothesis of a common background of autoimmunity associated with B8 DR3 can be postulated, while the organ specific target process should be associated with various DR alleles.

Adolescent↗
PubMed1988

Glucagon inhibits urinary acidification in the rat.

The effects on urinary acidification of an acute infusion of glucagon (GLU) were studied by paired experiments in plasma-replete rats whose endogenous GLU secretion was restrained by a 0.7 ng.min-1.g body wt-1 somatostatin infusion. GLU did not affect the glomerular filtration rate in any of the plasma-replete rats studied. In 10 thyroparathyroidectomized (TPTX) rats and five intact rats subjected to hypotonic volume expansion, a low-dose (0.02 ng.min-1.g body wt-1) GLU infusion that raised the plasma GLU concentration from 302 +/- 63 to 1,010 +/- 140 pg/ml significantly increased the urinary bicarbonate excretion and decreased the urinary net acid excretion; a high-dose (0.05 ng.min-1.g body wt-1) glucagon infusion in the intact rats, that increased the plasma GLU concentration to 1,609 +/- 307 pg/ml, further enhanced the urinary bicarbonate excretion rate. In intact plasma-replete rats that were not subjected to a hypotonic volume expansion, low- and high-dose GLU infusions failed to affect the urinary bicarbonate excretion rate. Finally, no change in urinary excretion rates was noted in TPTX volume-expanded time control rats. We conclude that 1) physiological increments in plasma GLU concentration decrease urinary acidification by affecting the tubular H+/bicarbonate transport; 2) the bicarbonaturic effect of GLU may be blunted by the renal effects of high circulating antidiuretic hormone levels, or may be facilitated in an undetermined manner by hypotonic volume expansion.

Animals↗
PubMed1987

Measurement of glycated albumin in diabetic patients by biospecific affinity chromatography.

The percentage of glycated plasma albumin was measured by a procedure involving ammonium sulphate precipitation and Affi-Gel-Blue and phenylboronate chromatographies. The value correlates well with the amount of ketoamine-bound sugars determined by colorimetric assay (r = 0.98, n = 39). The normal mean value is 3.9 +/- 0.3% (mean +/- S.D., coefficient of variation = 7.7%, n = 32) and varies from 3.9 to 21% in diabetics (n = 54). A good correlation is found with the mean blood glucose value of the preceding twenty days (r = 0.92, n = 57). Because of its relative ease of determination, glycated albumin constitutes a good short-term glycemic index and an alternative to glycated haemoglobin in some specific cases.

Blood Glucose↗