Biomedical subjects

Helena Schmid

Publications and source records attributed to Helena Schmid.

6 recordsLinked to original sources

PubMed2006

[Nationwide multicenter study on the prevalence of overweight and obesity in type 2 diabetes mellitus in the Brazilian population].

AIM: To evaluate the prevalence of overweight and obesity in type 2 diabetic (DM2) outpatients from different regions of Brazil. PATIENTS AND METHODS: We studied 2,519 randomly selected patients, from 11 hospitals, 2 endocrine and one general public care clinics from 10 cities. Overweight was defined as body-mass index (BMI) > 25 and obesity as BMI > 30 kg/m2. Glycemic control (GC) was evaluated by GC index (GCI = patient's HbA1 or HbA1c/upper limit of normal for the method x 100). RESULTS: 39% of the population studied was male, the mean age was 58.8 +/- 11.6 y, the duration from clinical diagnosis of DM2 was 9.0 +/- 7.3y, and BMI was 28.3 +/- 5.2 kg/m2. No measurements of BMI were recorded from 265 patients (10.5%). Patients from the Northeast presented lower BMI as compared with those from the Midwest, Southeast and South areas, respectively (26.4 +/- 4.7 vs. 27.9 +/- 4.8 vs. 29.2 +/- 5.1 vs. 29.4 +/- 5.4 kg/m2; p < 0.001). A greater prevalence of obesity was observed in the Southeast and South areas as compared to the Northeast (p < 0.001), as well as in the female group, respectively (69% vs. 31%; p < 0.001). Normal weight patients presented lower GCI. Patients being treated with two or more oral drugs and an association of insulin plus oral drug presented greater BMI values than those being treated with diet, oral hypoglycemic agents and insulin p < 0.001. The BMI of patients treated by a specialist did not differ from those treated by a generalist. CONCLUSIONS: 75% of our sample was out of adequate BMI and 30% was obese. The percentage of patients with overweight and obesity was comparable to those found in similar European studies but still lower than those found in the USA. The prevalence of obesity in diabetic patients was three times higher than in the overall Brazilian population according to data from the Brazilian Institute of Geography and Statistics (IBGE).

Adult↗

PubMed2006

Urinary TGF-beta1 reduction related to a decrease of systolic blood pressure in patients with type 2 diabetes and clinical diabetic nephropathy.

With the aim to determine the influence of reducing systolic blood pressure in urinary TGF-beta1 of type 2 diabetes (DM2) with diabetic nephropathy (DN), 21 subjects with type 2 diabetes and proteinuria >500 mg/24 h were studied. Amlodipine and ramipril were added to their previous antihypertensive treatment for 12 weeks. Urinary TGF-beta1 (UTGF-beta1) was determined at 0, 4, 8 and 12 weeks. Plasma TGF-beta1 was determined at 0 and 12 weeks. Subjects whose mean systolic blood pressure (SBP) during treatment were under 140 mmHg were grouped as the better SBP controlled group (n = 11) and those with SBP equal to or greater than 140 mHg were grouped in a moderate SBP controlled group (n = 10). Compared to baseline, mean log UTGF-beta1 at 4, 8 and 12 weeks decreased (-0.22 +/- 0.15 pg/mg; p = 0.04) in better SBP controlled group but not in the moderate SBP controlled group (-0.12 +/- 0.08 pg/mg, p = 0.82). Mean SBP correlated with UTGF-beta1 (r = 0.458, p = 0.0357), and this effect was independent of HbA1c (p = 0.042). By controlling SBP in DM2 subjects with DN we might decrease UTGF-beta1. We propose that reduction of UTGF-beta1 is due to a decrease in renal TGF-beta1 production.

Amlodipine↗

PubMed2005

Sympathetic modulation of the renal glucose transporter GLUT2 in diabetic rats.

We have previously shown that the abolition of renal sympathetic nervous activity (RSNA) can influence cortical GLUT1 expression in diabetic rats. However, no study has examined the effects of nervous activity on expression of GLUT2, the major glucose transporter in proximal renal tubules, which participates in renal glucose handling. The aim of this study was to determine whether sympathetic activity modulates renal GLUT2 content. We studied diabetic and nondiabetic rats with normal, low, or high RSNA. The low-RSNA experiment used four groups of Wistar male rats: Wistar sham-operated, Wistar renal-denervated, Diabetic sham-operated, and Diabetic renal-denervated. The high-RSNA experiment used four groups of Wistar-Kyoto male rats: WKY (control), WKY-Diabetic, SHR (spontaneously hypertensive rats), and SHR-Diabetic. Renal denervation was confirmed by a decrease in intrarenal norepinephrine levels and sympathetic hyperactivity, by measurement of RSNA. Western blotting was used to determine the renal cortical GLUT2 protein content, and 24-h urinary sodium and glucose levels were also evaluated. Compared with controls (Wistar and WKY), diabetes increased the GLUT2 protein content in normal-RSNA Diabetics (47%) and WKY-Diabetics (83%). The renal denervation-induced decrease in RSNA reduced the GLUT2 content in both normal and diabetic rats (-21% and -15%, respectively). Compared to WKY rats, SHR presented elevated RSNA and also showed an increase in renal GLUT2 content (17%). Diabetes caused a major increase in GLUT2 protein (52%) in the SHR. These results demonstrate a direct relationship between RSNA and GLUT2 levels; they also reveal an additive effect of sympathetic hyperactivity and diabetes on GLUT2 expression, suggesting a new mechanism for modulating protein expression in renal tissue.

Analysis of Variance↗

PubMed2004

Sympathetic dysfunction in type 1 diabetes: association with impaired myocardial blood flow reserve and diastolic dysfunction.

OBJECTIVES: This study was designed to explore the relationships of early diabetic microangiopathy to alterations of cardiac sympathetic tone and myocardial blood flow (MBF) regulation in subjects with stable type 1 diabetes. BACKGROUND: In diabetes, augmented cardiac sympathetic tone and abnormal MBF regulation may predispose to myocardial injury and enhanced cardiac risk. METHODS: Subject groups comprised healthy controls (C) (n = 10), healthy diabetic subjects (DC) (n = 12), and diabetic subjects with very early diabetic microangiopathy (DMA+) (n = 16). [(11)C]meta-hydroxyephedrine ([(11)C]HED) and positron emission tomography (PET) were used to explore left ventricular (LV) sympathetic integrity and [(13)N]ammonia-PET to assess MBF regulation in response to cold pressor testing (CPT) and adenosine infusion. RESULTS: Deficits of LV [(11)C]HED retention were extensive and global in the DMA+ subjects (36 +/- 31% vs. 1 +/- 1% in DC subjects; p < 0.01) despite preserved autonomic reflex tests. On CPT, plasma norepinephrine excursions were two-fold greater than in C and DC subjects (p < 0.05), and basal LV blood flow decreased (-12%, p < 0.05) in DMA+ but not in C or DC subjects (+45% and +51%, respectively). On adenosine infusion, compared with C subjects, MBF reserve decreased by approximately 45% (p < 0.05) in DMA+ subjects. Diastolic dysfunction was detected by two-dimensional echocardiography in 5 of 8 and 0 of 8 consecutively tested DMA+ and DC subjects, respectively. CONCLUSIONS: Augmented cardiac sympathetic tone and responsiveness and impaired myocardial perfusion may contribute to myocardial injury in diabetes.

Adenosine↗

PubMed2003

Impact of renal denervation on renal content of GLUT1, albuminuria and urinary TGF-beta1 in streptozotocin-induced diabetic rats.

In long-term diabetes mellitus, the progression of nephropathy has been related to the occurrence of autonomic neuropathy. This study was designed to evaluate the effects of bilateral denervation of the kidneys of streptozotocin-diabetic rats, an experimental model that presents diabetic nephropathy with increased abundance of cortical GLUT1 in the kidney and increased urinary excretion of albumin and transforming growth factor-beta1 (TGF-beta1). Twenty-four-hour urinary TGF-beta1 (ELISA), urinary albumin (electroimmunoassay) and GLUT1 protein levels (Western blotting) in the renal cortex and medulla were evaluated in diabetic (n=13) and control (n=13) rats 45 days after streptozotocin injection, submitted or not to surgical renal denervation. Evaluations were performed 15 days after the surgery. The effects of renal denervation were confirmed by intra-renal decrease of norepinephrine levels. Mean arterial pressure did not differ between diabetic and control rats, whether they underwent renal denervation or not. Renal denervation increased cortical (6905+/-287, 3506+/-193, 4144+/-246 and 5204+/-516 AU in renal-denervated controls, controls, renal-denervated diabetics and diabetics, respectively) and medullar GLUT1 protein in control rats, but reverted the cortical GLUT1 protein rise determined by diabetes. Although kidney denervation in diabetic rats induced a decrease in cortical GLUT1 abundance toward normal levels, these levels did not reach those of normal animals. However, renal denervation did not determine any changes in urinary albumin and urinary TGF-beta1 in both diabetic (127.3+/-12 microg/24 h and 111.8+/-24 ng mg(-1) creatinine, respectively) and control rats (45.9+/-3 microg/24 h and 13.4+/-4 ng mg(-1) creatinine, respectively). In conclusion, early-phase renal denervation in streptozotocin-diabetic rats produces a normalisation of previously elevated cortical GLUT1 protein content, but is not enough for reverting the increased urinary TGF-beta1 and albuminuria of diabetes.

Albuminuria↗

PubMedDate not supplied

Inhaled corticosteroid treatment and growth of asthmatic children seen at outpatient clinics.

OBJECTIVE: To ascertain the effect of inhaled corticosteroid use on gain in height and weight of asthmatic pediatric outpatients. METHODS: A one-year prospective cohort study was carried out with 124 asthmatic children aged 3 to 16 years who were prescribed inhaled corticosteroids for at least 12 months, evaluating z-scores for height/age, weight/age, body mass index and parental target height for current age. Exclusion criteria were: birth weight less than 2,500 g, malnutrition, chronic diseases and systemic corticoid use for more than 7 consecutive days. RESULTS: The mean +/- standard deviation for z-scores for initial and final height/age were 0.06+/-1.2 and 0.01+/-1.2 (95%CI 0.05-0.11), respectively; for initial and final weight/age z-scores they were 0.6+/-1.5 and 0.5+/-1.5 (95%CI 1.84-6.6), respectively. These figures did not differ significantly (p = 0.199 and p = 0.808). There was also no loss in stature when children were stratified into well and poorly controlled asthma or into pubescent and non-pubescent groups. CONCLUSIONS: In comparison with the NCHS (National Center for Health Statistics) growth curves, there was no compromise to the height or body weight of children/adolescents using inhaled corticosteroids for more than 1 year at the doses recommended for asthma prevention.

Administration, Inhalation↗