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Biomedical subjects

Juan Soler

Publications and source records attributed to Juan Soler.

6 recordsLinked to original sources

Peripheral fibrinolytic markers, soluble adhesion molecules, inflammatory cytokines and endothelial function in hypopituitary adults with growth hormone deficiency.

BACKGROUND: Increased mortality due to cardiovascular disease has been described in adult patients with untreated GH deficiency (GHD). GH replacement has been demonstrate to improve vascular reactivity and reverse early atherosclerotic changes in adults with GHD. OBJECTIVE: Assessment of fibrinolytic markers, soluble adhesion molecules, inflammatory cytokines and endothelial function in hypopituitary adults with GHD at baseline and 1 year after GH replacement therapy. METHODS: We studied 10 patients with GHD (five men and five women; aged 45.6 +/- 10.4 years) at baseline and 1 year after GH replacement therapy compared with a control group (nine men and 16 women) matched for age and body mass index (BMI). All subjects, patients and controls, were life-long nonsmokers, normotensive and nondiabetic. The following variables were recorded: anthropometric and body composition variables, serum concentrations of glucose, insulin and C-peptide; thrombin anti-thrombin (TAT) fragments and fibrin degradation product D-dimer, which were determined by an enzyme-linked immunosorbent assay (ELISA); IGF-I by radioimmunoassay (RIA); C-reactive protein (CRP) by highly sensitive immunonephelometry; E-selectin, P-selectin, soluble intercellular cell adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1) by ELISA. The assessment of endothelial function in vivo was measured with a Doppler device. RESULTS: Patients with GHD without GH substitution had higher hip/waist ratio and body fat than controls. Insulin, C-peptide and triglyceride concentrations were also higher. Our results demonstrated no difference in fibrinogen and in TAT fragment concentrations among patients and controls. E-selectin concentrations were higher in patients than in controls (26.1 +/- 11 vs. 10.7 +/- 6.2 microg/l, P = 0.0001). P-selectin, sICAM-1, sVCAM-1, IL-6, MCP-1 and CRP were similar in the two groups. Vascular reactivity and carotid intima-media thickness (IMT) were also similar in patients and controls. After 1 year of GH treatment we found no changes in biochemical parameters, fibrinolytic markers, soluble adhesion molecules, inflammatory cytokines and endothelial function. CONCLUSION: Adults with GHD show some subtle changes in soluble adhesion molecules but our data suggest no beneficial effects of GH over these markers in relationship to endothelial function. Factors other than GH treatment, such as differences in age, degree of obesity, the presence of diabetes mellitus and arterial hypertension or tobacco consumption, could explain the observed increase in markers of vascular risk in GH-deficient patients.

Adult↗

Differential regulation of insulin action and tumor necrosis factor alpha system activity by metformin.

BACKGROUND: Tumor necrosis factor alpha has a key role in insulin resistance. We study the effects of metformin on glucose tolerance, insulin resistance, beta cell function, and soluble tumor necrosis factor receptor (sTNFR) levels. METHODS: We performed a double-blind, randomized metformin-placebo study. Twenty-three subjects with impaired glucose tolerance or impaired fasting glucose were studied. Oral glucose tolerance, homeostasis model assessment, and continuous infusion of glucose with model assessment tests were used to evaluate glucose tolerance, insulin sensitivity, and beta cell function, respectively. Soluble tumor necrosis factor receptor levels were measured before and after therapy. Repeated measures analysis of variance was used for statistical analysis. RESULTS: After 12-week treatment, fasting glucose (110.1 +/- 9.9 to 98.9 +/- 15.7 mg/dl, P < .001), fasting insulin (11.6 +/- 5.4 to 8.8 +/- 3.5 mU/L, P = .05), fasting C-peptide (2.5 +/- 0.7 to 1.8 +/- 0.5 ng/mL, P < .05), and achieved C-peptide (5.2 +/- 1.2 to 4.2 +/- 1 ng/mL, P < .05) levels decreased in the metformin group. In addition, there was an improvement in insulin sensitivity (37.4% +/- 15.2% to 50.4% +/- 23.2%, P < .05) with unchanged sTNFR1 (2.0 +/- 0.8 to 2.3 +/- 1.2 microg/L, P = NS) and sTNFR2 (4.8 +/- 1.7 to 4.4 +/- 1.2 microg/L, P = NS) levels. CONCLUSIONS: Metformin is able to reverse insulin resistance and hyperglycemia in high-risk subjects for type 2 diabetes mellitus independently of the effects on tumor necrosis factor alpha system activity.

Adult↗

The IGF-I system component concentrations that decrease with ageing are lower in obesity in relationship to body mass index and body fat.

The aim of this study was to investigate the GH-IGF-I axis in healthy adults and its relationship to obesity. We studied 268 subjects: 134 men and 134 women, and determined anthropometric and body composition variables. Serum total IGF-I was measured by radioimmunoassay, serum free IGF-I concentrations by enzyme linked immunosorbant assay and serum IGFBP3 concentrations by radioimmunoassay. In men, we observed a decrease in total IGF-I, free IGF-I and IGFBP-3 throughout decades. In women, the body mass index and fat mass were higher throughout decades, and we observed a similar decrease to that in men in total IGF-I, free IGF-I and IGFBP3. In men with obesity, as measured by body fat, free IGF-I concentrations were lower than those without obesity; in women with obesity, total IGF-I concentrations and free IGF-I concentrations were lower than in those with obesity. These changes were observed in relationship to obesity when the subjects were adjusted for differences in age. We showed that in controls randomly selected, the GH-IGF-I axis component concentrations that decrease with increasing age are lower in obesity, especially in women, and that this decrease is related to body mass index and body fat.

Adipose Tissue↗

Interactions between serum leptin, the insulin-like growth factor-I system, and sex, age, anthropometric and body composition variables in a healthy population randomly selected.

OBJECTIVE: Leptin secretion is influenced by many factors and the GH/IGF axis plays an important role in the regulation of body composition, but the physiological interactions between leptin and the IGF-I system remain unknown. In this study we investigated the relationship between leptin, the IGF-I system, and sex, age, anthropometric and body composition variables in a group of healthy adults randomly selected. DESIGN: A cross-sectional study. PATIENTS: The study included 268 subjects, representative of the whole population of the city of L'Hospitalet de Llobregat in sex and age distribution: 134 men aged 41.4 years, range 15-70 years; and 134 women, aged 40.7 years, range 15-70 years. MEASUREMENTS: Body mass index (BMI) was calculated, and body composition was determined by using a bioelectrical impedance analyser. Serum leptin concentrations were determined by using a radioimmunoassay (RIA). Serum total IGF-I concentrations, after acid-ethanol extraction, were also measured by RIA. Serum free IGF-I concentrations were determined by an enzymoimmunometric assay. Serum IGFBP3 concentrations were determined by RIA. Plasma basal TSH concentrations were determined by a specific electrochemiluminescence assay. RESULTS: In men the BMI was similar in all decades and waist/hip ratio increased in the last three decades. Fat-free mass decreased by decade. We observed an increase in leptin in the fourth decade with a decrease in IGF-I, free IGF-I and IGFBP3 throughout the decades. Basal TSH showed an increase in the last two decades. In women, BMI, waist/hip ratio and fat mass increased significantly in the last decades. Leptin concentrations increased in the last decades and total IGF-I, free IGF-I and IGFBP3 decreased by decade without changes in basal TSH concentration. In men, there was a positive correlation between leptin and BMI, waist/hip ratio, total body water, fat-free mass and fat mass, and these anthropometric and body composition variables showed a negative correlation with free IGF-I and IGFBP3, without any correlation with total IGF-I. In women, there was a positive correlation between leptin and BMI, waist/hip ratio, total body water, fat-free mass, and fat mass, which showed a negative correlation with total IGF-I and IGFBP3, without any correlation with free IGF-I. In men, total IGF-I was negatively correlated with waist/hip ratio without any correlation with the other variables and free IGF-I was negatively correlated with BMI and waist/hip ratio, and IGFBP3 did not show any correlation. In women, total IGF-I, free IGF-I and IGFBP3 were negatively correlated with BMI, waist/hip ratio and fat mass. The multiple linear regression analysis produced a model that explained 60.5% of leptin variability in men and 40% in women. Notably, only age, BMI, fat mass and waist/hip ratio brought an independent significant contribution to leptin variability. The final model also explained 28.2% and 60.4% of total IGF-I variability and 17.2% and 27.4% of free IGF-I variability in men and women, respectively. Age and leptin contributed to free IGF-I variability in men, and age and fat mass were significantly and independently associated with total IGF-I in women. CONCLUSIONS: In this well-characterized population of controls randomly selected without chronic disease or drug administration and with biochemically confirmed euthyroidism, we found that both men and women had a significant correlation between leptin levels and the IGF-I system, and anthropometric and body composition variables, but that leptin did not regulate the IGF-I system, and that the IGF-I system did not regulate leptin synthesis and secretion.

Adolescent↗

Insulin resistance, leptin and TNF-alpha system in morbidly obese women after gastric bypass.

UNLABELLED: Obesity is a complex disease associated with insulin resistance. Leptin and the TNF-alpha system could be involved in the pathogenesis of obesity and insulin resistance. Gastric bypass (GBP) is a surgical treatment for morbidly obese patients. We conducted a study after GBP to analyze the pattern of variation of anthropometric and body composition variables, leptin and sTNFR1 and 2. METHODS: 29 morbidly obese women were studied, at baseline and throughout 6 months after gastric bypass. RESULTS: At baseline, the BMI was 49 +/- 6 kg/m(2) and patients showed a higher fasting insulin resistance index (FIRI), leptin, leptin/fat mass and sTNFR1 and 2 than did controls. 6 months after GBP, BMI was 35+/-4, and FIRI, leptin and leptin/fat mass decreased significantly in the first months and throughout the follow-up. sTNFR1 and 2 showed an initial increase, but at 6 months their concentrations were similar to baseline (2.6+/-0.8 vs 3.1+/-0.95 ng/ml, P < 0.05; 4.6+/-1.4 vs 7+/-2.5 ng/ml, P < 0.05). At baseline, there was no correlation between leptin and BMI and body composition variables but there was a correlation with fat mass (r=0.42, P=0.004) and sTNFR1 (r=0.58, P=0.001). At 6 months, there was a correlation between leptin and BMI (r=0.53, P=0.004) and sTNFR1 (r=0.46, P=0.013). CONCLUSIONS: Morbidly obese women after GBP became less insulin resistant with lower leptin concentrations, but showed an initial increase of sTNFR1 and 2. This pattern of variation of the leptin TNF-alpha axis suggests a disregulation of the system after dramatic weight loss and also that insulin and leptin up-regulate TNF-alpha production irrespective of insulin resistance status.

Adult↗

Hypothalamic-pituitary sarcoidosis with hypopituitarism. Long-term remission with methylprednisolone pulse therapy.

A 29-year-old man presented with diplopia and decreased strength in the left arm. A magnetic resonance image (MRI) showed an extensive hypothalamic and pituitary gland mass, and hormonal studies showed partial hypopituitarism and mild hyperprolactinemia without diabetes insipidus. Biopsies of the hypothalamic lesion and of a mediastinal lymph node demonstrated noncaseating granulomas, and a Kveim-Siltzbach test was positive. He was successfully treated with a regimen of high-dose intravenous methylprednisolone pulse therapy for eight weeks along with a low dose of oral corticosteroids which was maintained indefinitely. An MRI obtained immediately after pulse therapy revealed a substantial reduction in the hypothalamic-pituitary mass, which was maintained in an MRI performed 3 years later. However, hormonal deficits persisted and indefinite hormonal substitutive therapy was required.

Adult↗