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Biomedical subjects

M Sekso

Publications and source records attributed to M Sekso.

At least 37 records · Page 2Linked to original sources
PubMed1983

Effect of fasting on posthyperglycemic glucose homeostasis in obesity--experimental model for reactive hypoglycemia.

The relationship between altered glucose-insulin interaction in the hyperglycemic period of oral glucose tolerance test (oGTT) and impaired posthyperglycemic glucose homeostasis was studied in 9 obese females. They underwent 6-hour oGTT following 72-96 hour total fast, and the results of blood glucose, insulin, growth hormone, cortisol, glucagon and free fatty acids were compared to those of the control test. Blood glucose values in the hyperglycemic period of oGTT were higher during the post-fasting than in the control study. Posthyperglycemic glucose levels following fast dropped below the control values and four patients showed subjective symptoms of reactive hypoglycemia. Mean maximum blood glucose irrespective of time was significantly higher, mean glucose nadir lower after fast than in the control experiment (138.4 +/- 7.1 mg/dl vs. 112.4 +/- 5.2 and 47.3 +/- 1.4 vs. 61.3 +/- 3.0, respectively). Insulin response following fast was significantly reduced in 0-2 h period with delayed maximum value obtained at 123.3 +/- 14.5 min vs. 60.0 +/- 10.0 min in the basal experiment. Post-fasting counter-regulatory cortisol response was higher when compared to control, but there was no difference in growth hormone and glucagon secretion. Basal and post-glucose values of free fatty acids were significantly higher after fast than in the control study. The data suggest that fasting-induced impairment of glucose-insulin interaction in the hyperglycemic period of oGTT decreases the ability of obese subjects to maintain posthyperglycemic glucose homeostasis and provokes reactive hypoglycemia in some of them. Examination of glucose metabolism in fasted subjects is a convenient experimental model for the investigation of reactive hypoglycemia.

Blood Glucose↗
PubMed1983

Effect of l-dopa on growth hormone, glucose, insulin, and cortisol response in obese subjects.

Plasma growth hormone, glucose, insulin and cortisol response to oral administration of L-dopa and in insulin-tolerance test were investigated in 18 obese subjects. The results were compared with the results obtained in 10 normal subjects. The obese subjects displayed a lack of growth hormone responsiveness to L-dopa and a diminished GH responsiveness to hypoglycemia. There was no significant difference in glucose response to hypoglycemia in normal and obese subjects. Obese subjects showed normal increments of plasma cortisol following induction of hypoglycemia although there was no consistent cortisol response after L-dopa administration. A blood glucose response following L-dopa administration was seen in most of normal subjects while no increment of blood glucose was noticed in obese subjects.

Adult↗
PubMed1983

Increased serum reverse triiodothyronine in patients with hyperemesis gravidarum.

Thyroid function and pituitary responsiveness to TRH were studied in patients with hyperemesis gravidarum. Serum T3 and T4 concentrations were normal. Serum TBG levels in hyperemesis were normal for gestation, and the T4:TBG ratio was in the euthyroid range. In all patients a normal TSH response to TRH was found. Mean serum rT3 concentration was increased by 31% as compared to a control group of normal pregnant women (P less than 0.001). The data suggest that in patients with hyperemesis gravidarum there is: (a) normal function of the thyroid gland and pituitary-thyroid axis, (b) an enhanced peripheral conversion of T4 to rT3.

Adult↗
PubMed1982

Estimation of systolic time intervals and timing of arterial sounds in hyperthyroidism during antithyroid medication.

During antithyroid drug therapy hyperthyroid patients with border-line elevated serum T3 had shortening of pre-ejection period (PEP) and QKd interval (period between the onset of QRS complex and the onset of the Korotkoff arterial sound). There was a significant relationship between PEP and QKd interval with serum T3 concentration in a group of patients under medical therapy; PEP and QKd were normalized later than serum thyroid hormone concentration in such patients. Propranolol induced a prolongation of PEP and QKd interval in hyperthyroid patients. PEP and QKd are sensitive measures of metabolic status in thyrotoxic patients during antithyroid treatment.

Heart Auscultation↗
PubMed1981

Absence of thyroid-stimulating antibody and long acting thyroid stimulator in relatives of Graves' disease patients.

None of the 76 euthyroid relatives of patients with Graves' disease had detectable LATS in their serum nor was thyroid-stimulating antibody (TSAb), assessed by an increment of cAMP in human thyroid slices, detected in any of the 60 sera tested. Seven of 41 were slightly positive for TSH binding-inhibiting immunoglobulin (TBII). Nineteen of 73 sera were positive (greater than 1:1600) for antibody to thyroid antimicrosomal antigen, of which 4 were also positive (greater than 1:400) for antibody to thyroglobulin; 3 of the 19 had a slightly elevated basal TSH which rose excessively after TRH. Thus, although these euthyroid relatives had evidence of thyroid immunological defects, a thyroid-stimulating antibody was not found.

Antibodies↗
PubMed1981

Serum thyroid hormones in two Yugoslav districts with different iodine intake.

Serum thyroid hormones were measured in two areas of Yugoslavia, one with relatively low iodine intake, Zagreb (urinary iodide 111 +/- 36 microgram/g creatinine), and the island of Brac with higher iodine intake (247 +/- 76 microgram/g creatinine). The serum concentration of T4 and T3 in two groups were not different. These data confirm previous findings that iodine intake within accepted normal range, is not a factor in determining serum thyroid hormone levels.

Adult↗
PubMed1980

Conversion of thyroxine to triiodothyronine and reverse triiodothyronine in human placenta and fetal membranes.

Conversion of thyroxine (T4) to 3,5,3'-triiodothyronine (T3) and reverse 3,3',5'-triiodothyronine (rT3) was measured in vitro in human placenta and fetal membranes. T4 (5 micrograms/ml) was incubated in 0.15 mol/l phosphate buffer with tissue homogenates for 2 h at 37 degrees C, and the T3 and rT3 generated were determined in ethanol extract using RIA methods. The placenta and chorion homogenates converted more T4 to T3 than to rT3; the placenta was more active than the chorion. In both tissues the highest converting activity was found in microsomal fractions.

Chorion↗
PubMed1980

Secretion of growth hormone and cortisol in obese subjects with asymptomatic reactive hypoglycemia.

Secretion of growth hormone and cortisol during 6-hour glucose tolerance test was investigated in obese subjects with asymptomatic reactive hypoglycemia (n = 27), obese controls (n = 22) and nonobese individuals (n = 18). Asymptomatic reactive hypoglycemia was defined as the presence of blood glucose value(s) of 40 mg/dl and below in the posthyperglycemic period of the test with no related symptoms. Growth hormone and cortisol levels following glucose nadir were significantly higher in obese asymptomatic hypoglycemics than in obese controls. Specific post-nadir increment (delta growth hormone) was higher in hypoglycemic (6.41 +/- 0.48/Mean +/- SE/) than in nonhypoglycemic obese subjects (1.04 +/- 0.28 ng/ml). Similar difference was found for delta cortisol (8.48 +/- 1.1 vs. -0.81 +/- 0.63 microgram/dl). In contrast to growth hormone, significant inverse proportion was found between delta cortisol and blood glucose nadir (i.e. the lower glucose nadintrols. Cortisol response seems to be more important in the diagnosis of previous hypoglycemic condition. Results suggest that obese subjects with asymptomatic reactive hypoglycemia are similar to manifest reactive hypoglycemics.

Glucose Tolerance Test↗
PubMed1979

Competitive ligand - binding assay for thyroxine binding globulin. Comparison with TBG radioimmunoassay and T3 uptake test.

A simple and reproducible competitive ligand binding assay has been utilized to measure serum TBG concentration. In euthyroid subjects TBG concentration (mean +/- SD, mg/l) was 33.7 +/- 4; hyperthyroid 24 -/+ 6; T3-thyrotoxicosis 20 +/- 7; hypothyroid 37 -/+ 7; pregnant 67 -/+ 18; post-partum period 59.8 -/+ 17; oral contraceptives 45 -/+ 7. The correlation of CLBA with RIA measurement of TBG was significant (p less than 0.001). The estimations of serum TBG by CLBA correlated significantly with T3 uptake test (p less than 0.001), but at higher concentration of TBG correlation was non-linear. T4 : TBG ration according to serum T4 and TBG concentration provided a reliable index in the assessment of thyroid function.

Contraceptives, Oral↗
PubMed1979

Similar serum concentrations of thyroid hormones in two geographically separate populations on disparate iodine intake.

Serum thyroid hormones were measured in Montreal, Canada (urinary iodine 446 +/- 164 micrograms/day) and Zagreb, Yugoslavia (urinary iodine 108 +/- 32 microgram/day). The serum concentrations of thyroxine and triiodothyronine in the two populations were almost identical. We conclude that dietary iodine, within accepted normal limits, is not a factor in determining serum thyroid hormone levels. The wide differences in reported serum triiodothyronine concentrations are related to methodological problems.

Adolescent↗