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Biomedical subjects

J Serrat

Publications and source records attributed to J Serrat.

11 recordsLinked to original sources
PubMed1997

Lipoprotein compositional abnormalities in type I diabetes: effect of improved glycaemic control.

Major lipoprotein mass and composition were assessed in 45 subjects with insulin dependent diabetes mellitus (IDDM), before and after 2 months of intensive insulin therapy (IIT) and in 40 healthy control subjects. As compared to the control group, diabetic subjects at baseline had higher low density lipoprotein (LDL) and lower high density lipoprotein (HDL) masses. Expressing each lipoprotein constituent as a percent of total lipoprotein mass, very low density lipoprotein (VLDL) of diabetic patients was enriched in cholesterol and phospholipid and depleted in triglyceride and protein; IDL had higher triglyceride and phospholipid and lower cholesterol and protein proportion; LDL was depleted in protein and enriched in triglyceride; HDL was depleted in protein and enriched in triglyceride, cholesterol and phospholipid. After 2 months of IIT, HbA1c fell from 10.3 +/- 2 to 7.5 +/- 2% (P < 0.0001) and so did VLDL mass, which was lower than in control subjects. In addition, LDL and HDL masses, as well as triglyceride and cholesterol proportion in IDL particles normalized. The other compositional abnormalities improved without complete normalization. Thus, intensive insulin therapy in IDDM subjects brought quantitative lipoprotein alterations to normal even subnormal range, while most of the composition abnormalities improved without reaching complete normalization.

Adolescent↗
PubMed1995

Failure of steroid replacement to consistently normalize pituitary function in congenital adrenal hyperplasia: hormonal and MRI data.

Exogenous glucocorticoid replacement in patients with congenital adrenal hyperplasia (CAH), who due to an adrenal 21-hydroxylase enzyme deficiency are unable to produce endogenous glucocorticoids, is aimed at normalizing hypothalamic-pituitary-adrenal function. Excess androgen production by the adrenals is thus decreased. Despite standard glucocorticoid replacement doses (12.5-40 mg, 10.5-27 mg/m2/day hydrocortisone equivalents) 4 of 7 patients ranging in age from 14 to 33 years had abnormalities of the pituitary on MRI. Three appeared to have microadenomas and 1 had an empty sella. Five (3 salt wasters, 2 simple virilizers) of these 7 patients had 60-min p.m. ovine corticotropin-releasing hormone (oCRH) stimulation studies. The mean (logarithm) area under the ACTH curve for 0-60 min after oCRH stimulation was significantly greater in patients than controls (p < 0.0001). Mean ACTH at each time point before and after oCRH stimulation was similarly greater in patients than controls (p < 0.05). Two of these patients had pituitary microadenomas, 1 had an empty sella; all 3 were salt wasters. Despite standard glucocorticoid replacement, adolescent and young adult patients with CAH tend to have high basal ACTH and ACTH hyperresponsiveness to oCRH, as well as structural abnormalities of the pituitary. The inevitable periods of under- and overexposure to glucocorticoids in CAH patients may over time cause abnormalities of the hypothalamic-pituitary-adrenal axis.

17-alpha-Hydroxyprogesterone↗
PubMed1993

Using mathematical morphology to determine left ventricular contours.

The aim of this study is to investigate the use of mathematical morphology for the determination of left ventricular contours in scintigraphic images using multigated radionuclide angiography. We have developed a completely automatic method that first restores the image with a Wiener filter, then finds the region where the left ventricle is contained, and finally segments the left ventricle contour and a background zone. The contours depend on the values of the parameters that appear in the mathematical morphology method, which are related to the height and the slope of the count distribution. Results obtained with this method are compared with the contours and the background zones outlined by experts on the basis of the number of counts. We study the values of the parameters with which the optimum correlation is obtained.

Humans↗
PubMed1992

Disease expression and molecular genotype in congenital adrenal hyperplasia due to 21-hydroxylase deficiency.

Genotyping for 10 mutations in the CYP21 gene was performed in 88 families with congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Southern blot analysis was used to detect CYP21 deletions or large gene conversions, and allele-specific hybridizations were performed with DNA amplified by the polymerase chain reaction to detect smaller mutations. Mutations were detected on 95% of chromosomes examined. The most common mutations were an A----G change in the second intron affecting pre-mRNA splicing (26%), large deletions (21%), Ile-172----Asn (16%), and Val-281----Leu (11%). Patients were classified into three mutation groups based on degree of predicted enzymatic compromise. Mutation groups were correlated with clinical diagnosis and specific measures of in vivo 21-hydroxylase activity, such as 17-hydroxyprogesterone, aldosterone, and sodium balance. Mutation group A (no enzymatic activity) consisted principally of salt-wasting (severely affected) patients, group B (2% activity) of simple virilizing patients, and group C (10-20% activity) of nonclassic (mildly affected) patients, but each group contained patients with phenotypes either more or less severe than predicted. These data suggest that most but not all of the phenotypic variability in 21-hydroxylase deficiency results from allelic variation in CYP21. Accurate prenatal diagnosis should be possible in most cases using the described strategy.

Adrenal Hyperplasia, Congenital↗
PubMed1992

Insulin insensitivity in adrenal hyperplasia due to nonclassical steroid 21-hydroxylase deficiency.

To determine whether hyperandrogenism caused by an inborn error of adrenal steroidogenesis could produce insulin resistance, we examined insulin sensitivity in females with 21-hydroxylase deficiency. Minimal modelling was used to analyze the results of tolbutamide-modified, frequently sampled, iv glucose tolerance testing. Insulin sensitivity [Si; (min-1) (microU/mL)-1] was plotted against body mass index (BMI; defined as kilograms per m2). Six patients with nonclassical 21-hydroxylase deficiency (mean age, 27 yr; mean BMI, 23.2) underwent testing. None of these patients was in active puberty, nor was any patient being treated with glucocorticoids at the time of the study. Twelve eumenorrheic nonhyperandrogenic young adult female control subjects (mean age, 27 yr; mean BMI, 22.4) were also tested. The basal 17-hydroxyprogesterone concentration, but not the total serum testosterone level, was significantly different in the two groups (mean +/- SEM, 11,987 +/- 2,761 vs. 4,059 +/- 802 pmol/L; P < 0.05). As a group the patients' Si values were significantly lower than those of the controls (mean +/- SEM, 4.1 +/- 0.6 vs. 9.7 +/- 1.2; P < 0.05). There was no correlation between Si and basal serum 17-hydroxyprogesterone, testosterone, delta 4-androstenedione, or dehydroepiandrosterone. We conclude that chronic hypersecretion of androgen precursors due to an inborn error of metabolism can induce a reduction in insulin sensitivity.

Adolescent↗
PubMed1989

Apolipoprotein C subtype distribution in type 2 diabetes mellitus.

Plasma lipid levels and apolipoprotein C (apo C) composition of VLDL were investigated in a group of Type 2 diabetic patients at first attendance at the outpatient clinic and before any therapeutic intervention. Patients were distributed into two groups of 26 individuals, normo- and hyperlipidaemic, respectively, and compared with two matched control groups. Normolipidaemic diabetic patients had higher serum triglycerides, VLDL cholesterol, and lower HDL cholesterol than matched normolipidaemic control subjects. While hyperlipidaemic non-diabetic individuals showed increased apo C II and decreased apo C III-1 percentages when compared with normolipidaemic non-diabetic individuals (12.1 +/- 4.9 vs 8.5 +/- 3.2% and 44.0 +/- 6.7 vs 48.1 +/- 7.0%, respectively, mean +/- SD, both with p less than 0.05), the relative distribution of apo C III isoforms and apo C II was similar in both normo- and hyperlipidaemic diabetic patients.

Apolipoproteins C↗
PubMed1988

Apolipoprotein E phenotypes, lipoprotein composition, and xanthelasmas.

The different types of serum lipoproteins, including apolipoprotein E phenotypes, were measured in 50 patients with xanthelasma. Half of them were found to be hyperlipemic. The normolipemic and hyperlipemic groups with xanthelasma were compared with two control groups (one a group of normolipemic patients and another a group of hyperlipemic patients without xanthelasma) selected as homogeneously as possible with regard to age, sex, degree of obesity, and hyperlipemic phenotype. The only significant differences found among the groups, regardless of the presence of hyperlipemia, were the increased levels of total and high-density lipoprotein phospholipids, and lower levels of apolipoprotein B, found in the group with xanthelasmas. The distribution of apolipoprotein E phenotypes was the same in both groups, with slight differences between the normolipemic and hyperlipemic groups. Patients with xanthelasmas showed slight deviations in the metabolism of lipoproteins that require further clarification.

Adult↗
PubMedDate not supplied

Plasma immunoreactive somatostatin is elevated in diabetic ketoacidosis and correlates with plasma non-esterified fatty acid concentration.

In experimental diabetes and after the administration of beta-hydroxybutyrate and non-esterified fatty acids (NEFA), an increase in circulating immunoreactive somatostatin (IRS) has been described. Both ketones and NEFA are raised in diabetic ketoacidosis. Therefore, we decided to investigate 10 patients in diabetic ketoacidosis by measuring, on admission and throughout the initial 24 hours of therapy, circulating levels of IRS, beta-hydroxybutyrate, acetoacetate, triglycerides, blood glucose, pH and NEFA. Fluids and insulin were administered IV following a previously established protocol. Nine patients showed abnormally high levels of circulating IRS. When compared with a group of controlled insulin-dependent diabetic patients, basal IRS was high (111 +/- 15 vs 28 +/- 3 pmol/l), and remained elevated for at least 24 h despite clear improvement of metabolic status. On admission we also found elevated levels of NEFA (1.04 +/- 0.2 mmol/l), triglycerides (4.7 +/- 1.1 mmol/l), beta-hydroxybutyrate (22.1 +/- 4mmol/l), and acetoacetate (4.8 +/- 1.1 mmol/l). A significant correlation was found initially between IRS and NEFA (p less than 0.01). We conclude that circulating IRS is high in most cases of diabetic ketoacidosis. The mechanism behind this hypersomatostatinaemia could be related to the abnormalities of lipid metabolism which occur in diabetic ketoacidosis.

3-Hydroxybutyric Acid↗