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J Cabezas-Cerrato

Publications and source records attributed to J Cabezas-Cerrato.

At least 19 recordsLinked to original sources
PubMed2003

Comparison of several insulin sensitivity indices derived from basal plasma insulin and glucose levels with minimal model indices.

Some techniques for the evaluation of insulin resistance (IR), such as the clamp technique, are not viable for the study of large populations; and for this reason, alternative approaches based on fasting plasma glucose (FPG) and plasma insulin (FPI) have been proposed. The aim of this study was to compare the IR calculations obtained from FPI and FPG values with the insulin sensitivity (IS) index derived from the minimal model. Eighty-seven healthy subjects with a wide range of body mass index (18 - 44 kg x m -2) and 16 DM2 non-obese patients were included in the study. All of the patients underwent a frequently sampled intravenous glucose tolerance test (FSIGTT), and the minimal model of glucose was used for the estimation of insulin sensitivity (IS MINIMAL ). The HOMA-IR index, the Avignon index, and the quotient FPG/FPI were used to calculate basal steady-state IR. The basal IR value that best correlated with IS was Log (1/HOMA-IR) (r = 0.70, p < 0.001). All of the basal indices showed a high correlation with each other. In conclusions, insulin sensitivity indices as determined from the basal glycaemia and insulinemia values are not good estimators for metabolic reality from the perspective of the minimal model. Nevertheless, they might well have an IR screening value for epidemiological studies, as long as there is no pancreatic beta-cell dysfunction.

Adult↗
PubMed2003

Phenotypic gender differences in subjects with familial partial lipodystrophy (Dunnigan variety) due to a nuclear lamin A/C R482W mutation.

Phenotypic features appeared after puberty in female, but not male subjects with familial partial lipodystrophy (FPLD). We have studied anthropometrical, clinical, and metabolic gender differences in a Spanish family with FPLD resulting from a lamin A/C gene mutation, R482W. Genetic studies were carried out on 14 members of the family. In eleven heterozygous mutation carriers (6 men, 5 women), body composition was evaluated by bioelectric impedance analysis, skin-fold measurements were taken, and lipid profiles were drawn. Moreover, plasma glucose, insulin, and leptin were determined, and insulin resistance and beta cell response were evaluated using HOMA. Ten healthy women and 10 healthy men matched for age and body mass index were used as control group. Body composition was similar in these patients to normal people. However, skin-folds of extremities were thinner in FPLD women compared with those of control subjects, but not in men. The affected women, but not men, showed hypoleptinaemia, insulin resistance, and beta-cell hyperresponse compared with unaffected women. The lipid profile was normal in the young patients, irrespective of sex. Type 2 diabetes mellitus and hypertriglyceridaemia were detected in old and overweight patients only. In conclusion, molecular diagnosis allows us to demonstrate that women with FPLD present both adipose tissue and biochemical abnormalities early in life, and this did not happen in affected men.

Adolescent↗
PubMed2003

[Superior vena cava syndrome and insular thyroid carcinoma: the stent as a palliative therapeutic alternative].

The superior vena cava syndrome (SVCS) is a uncommon complication of thyroid cancers. It is produced as consequence of the mediastinal spread of the tumor or by intravascular invasion with thrombosis. We describe a case of insular thyroid carcinoma with an SVCS solved by putting an intravenous stent. The patient was a 73 year old male that consulted for aphonia and presence of a tumor in the right side of the neck of two months of evolution. The PAAF of thyroid suggested the diagnosis of "follicular tumor". A total thyroidectomy was performed on the patient and the sample histological study revealed the existence of a insular carcinoma. An ablative dosis of 131I was administered to him. One year after the patient developed the SVCS. A TAC detected a tumoral relapse consistent with clinical syntoms, and was confirmed by a high level of Tg (with TgAntibodies -). As the patient showed a slight response to radiotherapy (52Gy), a thoracic phlebography was realized demostrating an extense upper vena cava obstruction. After having accomplished an angioplasty, a long stent (20 mm wide) was put into the upper vena cava that was followed by a fast clinical and radiological improvement. A new phlebography practiced three month later showed a rapid venous flux through the stent, and near total disapperance of collateral circulation on thorax wall and mediastinum.

Adenocarcinoma, Follicular↗
PubMed1999

Maintenance of blood pressure control and left ventricular performance with small doses of enalapril.

Enalopril treatment (20 mg every 12 hours) of 24 patients with essential hypertension and left ventricular (LV) hypertrophy established normal blood pressure (BP) after 8 weeks, and after 7 years had reduced LV mass index by 39% from 148 +/- 34 to 90 +/- 16 g/m2, and had normalized LV structure and function and QT dispersion. Stepwise reduction of the enalapril dosage from 40 to 30, 20, 10, and 5 mg/day during the eighth year caused no significant changes in BP, LV structure, LV systolic function, or QT dispersion, which all likewise remained unaltered during a further year of the 5-mg/day regimen. We conclude that for hypertensive patients in whom prolonged treatment with standard doses of enalapril has normalized BP, LV structure and function, and QT dispersion, significantly smaller doses are sufficient to maintain these cardiovascular achievements.

Adult↗
PubMed1999

Insulin sensitivity, glucose effectiveness, and insulin secretion in nondiabetic offspring of patients with non-insulin-dependent diabetes mellitus: a cross-sectional study.

To evaluate the factors that determine the worsening of intravenous glucose tolerance in subjects at high risk for developing non-insulin-dependent diabetes mellitus (NIDDM), 15 glucose-tolerant offspring of NIDDM patients and 21 control subjects were studied. Each subject underwent a frequently sampled intravenous glucose tolerance (FSIGT) test. The intravenous glucose tolerance index (K(G) index) was calculated between minutes 10 and 40 of a FSIGT test. Insulin sensitivity (S(I)), glucose effectiveness at zero insulin (GEZI), and first- and second-phase insulin responsiveness (phi1 and phi2) were estimated using glucose and insulin kinetic minimal models. The acute insulin response to glucose (AIRg) was calculated as the area under the insulin curve above the basal level between 0 and 10 minutes, and the suprabasal insulin effect was determined by the product of S(I) times AIRg. Offspring had a lower S(I) than control subjects (14.1 +/- 7.5 v 9.25 +/- 4.20 x 10(-5) x min(-1)(pmol x L(-1))(-1), P < .01), and their AIRg was similar (3,284 +/- 2,280 v 3,105 +/- 1,499 pmol x L(-1), NS). Sample division according to the median K(G) value showed that control subjects with low tolerance had a lower AIRg (4,417 +/- 2,531 v 2,043 +/- 1,068 pmol x L(-1), P < .05) and a lower suprabasal insulin effect (0.057 +/- 0.03 v 0.023 +/- 0.009 min(-1), P < .05) than control subjects with high tolerance. Offspring with low tolerance had a lower AIRg (2,574 +/- 1,197 v 3,707 +/- 1,656 pmol x L(-1), P < .05) and a lower GEZI (0.101 +/- 0.05 v 0.212 +/- 0.08 x 10(-1) x min(-1), P < .05) than offspring with high tolerance. Offspring with high and low tolerance showed lower phi1 (375 +/- 155 v 272 +/- 181 v 698 +/- 336 (pmol x L(-1))min(mmol x L(-1)), NS) than control subjects with high tolerance. In conclusion, our data suggest that decreases in GEZI and AIRg are the main factors responsible for the worsening of intravenous glucose tolerance in the offspring of NIDDM patients.

Adolescent↗
PubMed1999

Differences between men and women as regards the effects of protein-energy malnutrition on the hypothalamic-pituitary-gonadal axis.

Although protein-energy malnutrition (PEM) affects 50% of hospitalized patients, its effects on the hypothalamic-pituitary-gonadal (HPG) axis have not been extensively investigated. To investigate the effects of PEM on the HPG axis in hospitalized patients, 62 inpatients ages 18-91 y (35 men and 27 women) had a nutritional and hormonal evaluation. Hormones were determined in blood samples obtained between 0700 and 1200 h. Patients were divided into two subgroups: those with body mass index (BMI) <18.5 kg/m2 (low body mass index [LBMI]; 16 men, 13 women) and those with BMI >20 kg/m2 (normal-high body mass index [NHBMI]; 19 men, 14 women). The nutritional parameters of LBMI patients were inferior to those of NHBMI patients. Total and free testosterone levels were subnormal, 31.4% and 17.2% respectively, in all men; free testosterone was subnormal in 31.25% of LBMI versus 5.3% of NHBMI male patients and total testosterone concentration was subnormal in 43.8% of LBMI versus 21.1% of NHBMI male patients. Luteinizing hormone (LH) level was higher in LBMI men than in NHBMI men, whereas the reverse was the case for women, for whom follicle-stimulating hormone (FSH) also was lower in the LBMI group than the NHBMI group. The HPG axis hormones which best discriminated between the LBMI and NHBMI groups were free testosterone for men and LH and FSH for women, which were all lower in the LBMI than in the NHBMI group. LH was correlated with BMI and midupper arm muscle circumference (AMC) (women positively and men negatively) but not with triceps skin-fold thickness (TSF). Total testosterone level was positively correlated with AMC and free testosterone with TSF. Hypogonadism is common among hospitalized patients with PEM. Men with PEM have low testosterone levels with normal or high gonadotropin levels, which suggests impairment of Leydig cell function. Women with PEM suffer hypogonadotropic hypogonadism. AMC correlates positively with total serum testosterone concentration in men and with LH levels in women, suggesting that satisfactory function of the HPG axis requires a functional (protein) reserve as well as an energy (fat) reserve.

Adult↗
PubMed1999

Step-down of enalapril treatment for arterial hypertension.

Enalapril treatment (20 mg every 12 hours) of 24 patients with essential hypertension and left ventricular (LV) hypertrophy established normal blood pressures after 8 weeks, and after 5 years, it had reduced LV mass index by 39% (from 148+/-34 to 90+/-16 g/m(2)) and had normalized LV structure and function and QT dispersion. Stepwise reduction of the enalapril dosage from 40 to 30, 20, 10, and 5 mg/d during the eighth year caused no significant change in blood pressure, LV structure, LV systolic function, or QT dispersion, which all likewise remained unaltered during an additional 2-year period of the 5-mg/d regimen. We conclude that for hypertensive patients in whom prolonged treatment with high doses of enalapril has normalized blood pressure, LV structure, LV function, and QT dispersion, the dose may be reduced as much as 8-fold without detriment to cardiovascular control. The use of smaller doses is evidently advantageous from the point of view of health costs.

Adult↗
PubMed1998

Reduction of QT and QTc dispersion during long-term treatment of systemic hypertension with enalapril.

We report, in conjunction with other findings, the evolution of the dispersion of QT and QTc in patients who for the last 7 years have been treated with enalapril for systemic hypertension with left ventricular (LV) hypertrophy. Twenty-four essential hypertensive patients who had received no previous treatment took enalapril (20 mg twice daily) for 7 years. In a pretreatment placebo phase and 8 weeks and 1, 3, 5, 6, and 7 years after the start of therapy, cardiovascular parameters were determined by two-dimensional guided M-mode echocardiography, and the QT interval and corrected QT interval (QTc) and their dispersions were obtained from amplified standard 12-lead electrocardiograms. Therapy rapidly reduced blood pressure (BP) from 156/105 mm Hg to normal values; at 7-year follow-up, BP was 130/84 mm Hg (p <0.001 with respect to the placebo phase). LV mass index decreased progressively until at 5-year follow-up the reduction had reached 39% (p <0.001), after which neither LV mass index nor any structural parameter underwent any further significant change. LV pump function was also significantly better after 7 years of treatment. During this time, QT and QTc decreased significantly, as did the dispersion of both QT (from 61+/-21 to 37+/-14 ms) and QTc (from 67+/-27 to 41+/-16 ms). We conclude that long-term enalapril treatment of hypertensive patients with LV hypertrophy not only induces marked regression of LV mass and improved LV systolic function, but also reduces the dispersions of QT and QTc, which probably reduces the likelihood of ventricular arrhythmias and improves prognosis.

Adult↗
PubMed1998

The prevalence of clinical diabetic polyneuropathy in Spain: a study in primary care and hospital clinic groups. Neuropathy Spanish Study Group of the Spanish Diabetes Society (SDS).

A multiregional cross-sectional study of clinical diabetic polyneuropathy (DPN) was carried out among Spanish diabetes patients using a standard system for scoring symptoms and signs of polyneuropathy. The main patient sample comprised 2644 patients (54.7% women) aged 15-74 years (mean 57.2 +/- 0.3 years), 86.9% of whom had Type II (non-insulin-dependent) diabetes mellitus and 29.4% were attending hospital clinics. Mean duration of diabetes since diagnosis was 10.2 +/- 0.2 years. The prevalence of DPN was 22.7% (95% confidence interval 21.2-24.3%) in the whole sample, 12.9% (9.4-16.5%) among patients with Type I (insulin-dependent) diabetes mellitus and 24.1% (22.4-25.9%) among patients with Type II diabetes; there was no significant difference in prevalence between men and women. Prevalence increased with age (from < 5% in the 15- to 19-year-old age group to 29.5% in the 70- to 74-year-old group) and with duration of diabetes since diagnosis (from 14.2% among those with duration < 5 years to 44.2% among those with duration > 30 years). In a supplementary sample of 161 diabetic patients aged 75 to 79 years (excluded from the main sample to prevent confusion between diabetes-induced and ageing-induced neuropathies), prevalence was 37.8%. Ninety-three patients (3.3%) had or had had foot ulcers and 21 of these 93 (0.7%) had undergone amputation; 90.8% of ulcerated patients had Type II diabetes, and 54% had DPN (in most cases with loss of perception of vibration), as against a prevalence of DPN of 19.9% among patients without ulcers. We conclude that nearly a quarter of Spanish diabetic patients have DPN; that over 90% of DPN patients have Type II diabetes; that the prevalence of DPN increases with age and with the duration of the disease, and that the risk of foot ulcers among DPN patients is about three times the risk among diabetic patients without DPN. We accordingly emphasize the responsibility of primary care physicians to try to prevent diabetic foot lesions by early diagnosis of DPN.

Adolescent↗
PubMed1998

Both a reduced acute insulin response to glucose and lower glucose effectiveness are responsible for the worsening of intravenous glucose tolerance in healthy subjects independently of the degree of obesity.

The effects of the acute insulin response to glucose (AIRg), insulin sensitivity (SI), and glucose effectiveness at zero insulin (GEZI) on intravenous glucose tolerance were studied in 94 non elderly healthy subjects with a wide range of body mass index (BMI). Conrad's coefficient of glucose assimilation (KG) was calculated between 10 and 19 minutes of an intravenous glucose tolerance test. Both SI and GEZI were estimated using Bergman's minimal model. AIRg was calculated as the area under the insulin curve above basal between 0 and 10 minutes, and the suprabasal insulin effect was determined by the product of SI x AIRg. Stepwise multiple regression showed that the combined effect of SI x AIRg and GEZI explained 67% of the KG index variance. Division of the sample into tertiles according to KG shows that subjects with the lowest KG (KG < 1.32 min[-1]) had the lowest AIRg (2,832 +/- 1,362 v 6,510 +/- 4,410 [pmol x L(-1)] min, P = .0005), the lowest GEZI (0.092 +/- 0.06 v 0.179 +/- 0.09 min(-1), P = .0004), and the lowest SI x AIRg (0.014 +/- 0.008 v 0.022 +/- 0.01 min(-1), P = .00001), and were the oldest (41 +/- 10 v 31 +/- 10 years, P = .002) compared with subjects with the highest KG (KG > 1.8 min[-1]). However, no differences in SI (4.86 +/- 4.6 v 6.5 +/- 3.7 min(-1) [pmol x L(-1)],(-1) NS) or BMI (29.6 +/- 5.0 v 26.6 +/- 5.9 kg x m(-2), NS) were observed. These results did not vary when lean and obese subjects were analyzed separately. Age correlated significantly only with SI x AIRg. In conclusion, although the main factors that determine intravenous glucose tolerance are the suprabasal insulin effect and GEZI, worsening of the KG index depends on inadequate insulin secretion for the degree of insulin sensitivity and lower non-insulin-mediated glucose uptake. Age seems to be another factor in the worsening of intravenous glucose tolerance through a lower suprabasal insulin effect.

Adult↗
PubMed1998

Non-insulin-mediated glucose uptake in several insulin-resistant states in the postabsortive period.

The aim of our work was to study non-insulin-mediated glucose uptake (NIMGU), in the postabsorptive state, in several pathologies characterized by peripheral insulin resistance, namely, obesity (n = 10), NIDDM (n = 7), acromegaly (n = 7) and Cushing's disease (n = 6). These groups were compared with a group of 16 healthy subjects. To estimate peripheral insulin sensitivity (SI) and glucose effectiveness (SG), we used the minimal model of glucose metabolism. Although all of these pathologies showed severe insulin resistance (control: 6.44 +/- 2.63, obesity: 2.84 +/- 1.57, NIDDM: 1.71 +/- 0.77, acromegaly: 1.88 +/- 1.23, Cushing's disease: 1.87 +/- 0.66 x 10(-4) min-1 (microU/ml)-1, P < 0.01), fasting insulin-mediated glucose uptake (IMGU) did not differ significantly among the five groups, because reactive hyperinsulinaemia was present in all of these states. The contribution of NIMGU to whole-body glucose uptake did not differ significantly among the five groups (control: 77 +/- 8%; obesity: 77 +/- 9%; acromegaly: 82 +/- 8%; Cushing's disease: 83 +/- 8%; NIDDM: 84 +/- 7%). In conclusion, our data show that, in the postabsorptive period, non-insulin mediated glucose uptake is a major determinant of glucose disposal and is similar in the different pathologies studied; on the other hand, although absolute rates of basal insulin-mediated glucose uptake are reduced in insulin-resistant states, they did not achieve statistical value compared with control subjects because of compensatory hyperinsulinaemia.

Acromegaly↗
PubMed1998

Minimal model of glucose metabolism: modified equations and its application in the study of insulin sensitivity in obese subjects.

As implemented in their program MINMOD, some of the parameters and variables of the equations representing Bergman and coworkers' minimal model of glucose metabolism have no simple rational relationship with the kinetic constants and constants of proportionality of the minimal model as such. In this work we implemented the original version of the minimal model, which does not suffer from this problem, and used it to investigate the source of insulin resistance among obese but otherwise healthy subjects. A fasting sampled intravenous glucose tolerance (FSIGT) test was performed in 38 healthy subjects of varying degrees of obesity (standard FSIGT test in 21 and tolbutamide FSIGT test in 17 subjects) in order to compare MINMOD and 'modified' equations (MI). Insulin sensitivity index (SI) in obese subjects was significantly lower than in lean subjects (4.58 +/- 3.5 vs. 11.7 +/- 4.3. 10(-5) min-1 (pmol.l-1)-1, P < 0.0001). The lower SI in obese subjects was a consequence P3 parameter (0.178 +/- 0.08 vs. 0.440 +/- 0.26.10(-5) min-2 (pmol.l-1)-1, P < 0.01), being p2 similar between obese and lean subjects (0.389 +/- 0.19 vs. 0.376 +/- 0.19.10(-1) min-1, NS). SI index correlated with p3 (r = 0.73, P < 0.0001), but not with p2 (r = 0.01, NS). Using these results and assuming that interstitial insulin is higher in obese subjects than in lean subjects, we have demonstrated that the proportionality constants of the model (k4 and k6) were lower in obese subjects than in lean subjects, but not the rate constant for insulin transfer across capillaries, k2. Our results suggest that the modified equations are a better theoretical approach to the minimal model method; and that low insulin sensitivity in obese subjects is due to receptor and/or post-receptor events rather than to slow transfer of insulin across capillary endothelium into the interstitial space.

Adult↗
PubMed1998

L-5-hydroxytryptophan does not stimulate LH secretion directly from the pituitary in patients with gonadotrophin releasing hormone deficiency.

OBJECTIVE: There is abundant histological and physiological evidence that serotonin plays a role in the regulation of LH secretion in rats. Studies in human subjects have been few, but their results include the finding that pulsatile administration of L-5-hydroxytryptophan (5-HTP, the immediate precursor of serotonin) amplifies LH secretion in women in the medium-late follicular phase, and that this effect is not due to 5-HTP directly inducing LH secretion by the pituitary. We have investigated whether 5-HTP amplifies LH secretion by enhancing the response of the pituitary to GnRH. PATIENTS: Seven patients aged 20-40 years with hypogonadotrophic hypogonadism (HH) of hypothalamic origin (3 men with Kallmann's syndrome, 2 women without anosmia and with GH deficiency, and 2 women with anorexia nervosa). DESIGN: To prime the pituitary, subcutaneous pulsatile GnRH was administered for 7 days at the rate of one 5-20 micrograms pulse every 90 min. The day before the investigation, this regimen was replaced by 1.5-3 micrograms intravenous pulses at the same frequency. On the day of the investigation, 3 ml blood samples were taken every 10 min from 0850 to 19:00 hours. After the first two samples, the intravenous GnRH pulse frequency was increased to one per hour and was maintained at this level throughout the rest of the study. The first 4 h of the study acted as a control phase allowing determination of the pituitary response to GnRH. At 1300 h, 75 mg of the aromatic-L-amino-acid decarboxylase inhibitor carbidopa was administered orally; carbidopa does not cross the blood-brain barrier, and prevents peripheral conversion of 5-HTP to serotonin. At 1600 h, another 75 mg dose of carbidopa was administered, and administration of 8-20 mg pulses of 5-HTP at a rate of one pulse per hour was begun. MEASUREMENTS: LH was determined in triplicate by an immunoradiometric assay (IRMA), and LH pulses identified by means of a program developed in our laboratory. RESULTS: When pulsatile administration of GnRH was accompanied by administration of carbidopa and 5-HTP, LH pulse amplitude (2.32 +/- 0.71 IU/I) did not differ significantly from its value in either the GnRH+ carbidopa phase (2.58 +/- 1.12 IU/I) or the unaccompanied GnRH phase (2.77 +/- 1.76 IU/I). CONCLUSIONS: L-5-hydroxytryptophan-induced amplification of LH secretion in humans is not due to enhancement of the pituitary response to GnRH. The effect of L-5-hydroxytryptophan must therefore be due to its action on the hypothalamus, where it may be hypothesized that it increases GnRH release.

5-Hydroxytryptophan↗
PubMed1997

[Relation between left ventricular hypertrophy and retinal vascular changes in mild hypertension].

BACKGROUND: To evaluate the possible relation between left ventricular hypertrophy and vascular changes in retine, in patients with mild hypertension. PATIENTS AND METHODS: We established a group with 51 hypertensives (27 males and 24 females), with essential mild hypertension, which had never been treated. An ambulatory monitoring blood pressure, 24 hours electrocardiographic monitoring, echocardiography and funduscopy were realized to all of them. RESULTS: Fifty-five per cent of the hypertensives had retinopathy grades I-II. We established two subgroups with and without retinopathy. The age, systolic, diastolic and mean blood pressures, so as body mass index higher in the group with retinovascular damage. No significant differences were observed in the ecographic parameters between two subgroups except the interventricular septal thickness (10.5 +/- 2.1 min in the subgroup without vs 11.1 +/- 2.3 mm in the subgroup with retinovascular damage) (p < 0.05). As 24-hour maximum and mean systolic and diastolic blood pressure, daytime mean systolic blood pressure (SBP) and diastolic blood pressure (DBP), daytime and night-time DBP load, as daytime SBP load were higher in the hypertensive patients with retinovascular changes. There was echocardiographic left ventricular hypertrophy in 51% of the hypertensive patients, without differences between both subgroups of hypertensive patients. Body mass index (g/m) correlated significantly (p < 0.01) with the retinovascular damage. In the multivariant analysis, male as well as female, the funduscopy correlated with left ventricular mass index (g/m2). We established a discriminant function to separate hypertensives with and without left ventricular hypertrophy and another to separate hypertensives with and without retinopathy. Both functions included body mass index and maximum SBP, so as daytime SBP load and nighttime mean DBP to the left ventricular hypertrophy function. CONCLUSIONS: Left ventricular hypertrophy and retinovascular damage appear early in the course of blood pressure elevation and both changes develop in parallel. Our results indicate that there exists a relation between both cardiac and vascular changes in the hypertension. Body mass index and maximum SBP, appear to be important determinants of structural adaptation in mild hypertension.

Body Mass Index↗