ABSTRACT
Considering the similarity between structural, hemodynamic, and functional changes of obesity-related renal disease and diabetic nephropathy, we hypothesized that renal glucose transporter changes occur in obesity as in diabetes. The aim of the work was to evaluate GLUT1 and GLUT2 in kidneys of an animal model of metabolic syndrome. Neonate spontaneously hypertensive rats (SHR), n=15/group, were treated with monosodium glutamate (5 mg/g) (MetS) for 9 days and compared with saline-treated Wistar-Kyoto (C) and SHR (H) rats. Lee index, systolic arterial pressure (SAP), glycemia, insulin resistance, triglycerides, and HDL cholesterol were evaluated at 3 and 6 months. Medullar GLUT1 and cortical GLUT2 were analyzed by Western blot. MetS vs. C and H rats had the highest Lee index (p<0.001) and insulin resistance (3-months C: 4.3±0.7, H: 3.9±0.9, MetS: 2.7±0.6; 6-months C: 4.2±0.6, H: 3.8±0.5, MetS: 2.4±0.6% · min⻹, p<0.001), similar glycemia, and the lowest HDL-cholesterol at 6-months (p<0.001). In the MetS and H rats, SAP was higher vs. C at 3-months (p<0.001) and 6-months (C: 151±15, H: 190±11, MetS: 185±13 mm Hg, p<0.001) of age. GLUT1 was Ì´ 13× lower (p<0.001) at 3-months, reestablishing its content at 6-months in MetS group, while GLUT2 was 2× higher (p<0.001) in this group at 6-months of age. Renal GLUT1 and GLUT2 are modulated in kidney of rats with metabolic syndrome, where obesity, insulin resistance and hypertension coexist, despite normoglycemia. Like in diabetes, cortical GLUT2 overexpression may contribute to the development of kidney disease.
Subject(s)
Glucose Transporter Type 1/metabolism , Glucose Transporter Type 2/metabolism , Kidney/metabolism , Metabolic Syndrome/metabolism , Animals , Disease Models, Animal , Male , Rats , Rats, Inbred SHRABSTRACT
The effects of exercise training on systolic blood pressure (BP), insulin sensitivity, and plasma membrane GLUT4 protein content in spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats were compared. 16 SHR and 16 WKY male rats, aged 6 months, were randomized into sedentary and trained (treadmill running, 5 days/week, 60 min/day for 10 weeks) groups (n=8/group). At baseline, SHR had lower insulin sensitivity than WKY rats, however, there were no differences between WKY and SHR GLUT4 expression. The 10-week training reduced BP by â¼19% in SHR, improved insulin sensitivity by â¼24% in SHR, but not in WKY, and increased GLUT4 expression in both animal models. Compared to the sedentary group, there was an increase of GLUT4 in WKY rats by â¼25% in the heart, by â¼23% in the gastrocnemius, and by â¼15% in the fat tissue. Trained SHR presented an increase in GLUT4 of â¼21%, â¼20%, and â¼14%, in the same tissues, respectively. There were no differences between SHR and WKY rats in post-training GLUT4 expression. We conclude that training determined BP and insulin resistance reduction in SHR, and increased GLUT4 expression in both normotensive and hypertensive rats. However, considering the similar rise in GLUT4-induced training in SHR and WKY, it is possible that GLUT4 levels in plasma membrane fraction do not have a pivotal role in the exercise-induced improvement of insulin sensitivity in SHR.
Subject(s)
Exercise Therapy , Glucose Transporter Type 4/genetics , Hypertension/genetics , Animals , Blood Pressure , Disease Models, Animal , Glucose Transporter Type 4/metabolism , Humans , Hypertension/metabolism , Hypertension/physiopathology , Hypertension/therapy , Male , Random Allocation , Rats , Rats, Inbred SHR , Rats, Inbred WKYABSTRACT
We report a 44-year-old man with chronic chagasic cardiomyopathy who underwent latissimus dorsi dynamic cardiomyoplasty and died 4 months later. The clinicopathological findings are discussed, and the literature is reviewed.
Subject(s)
Chagas Cardiomyopathy/surgery , Adult , Atrophy , Chagas Cardiomyopathy/pathology , Chronic Disease , Fibrosis , Heart Failure/etiology , Humans , Male , NecrosisSubject(s)
Antibodies, Viral/analysis , Arbovirus Infections/immunology , Arboviruses/immunology , Adolescent , Brazil , Child , HumansABSTRACT
In April, 1975, an outbreak of human encephalitis caused by Rocio virus, a new flavivirus, occurred in the coastal region of southern São Paulo, Brazil. The epidemic started during the second half of March, 1975, and ended in June, 1975. A total of 465 cases with 61 deaths were recorded, and the overall attack rate was 15 per thousand population. The mortality rate was two per thousand inhabitants and the overall case-fatality rate was 13%. However, the case-fatality rate was markedly decreased when adequate hospital care was provided. The number of cases in the 15--30 years age group was higher than in the other age groups and the rate was higher in males than in females. Lack of evidence of person-to-person transmission, based on a study of families involved in the epidemic and on the antigenic relationship to other mosquito-borne flaviviruses, suggested that the virus was transmitted by a vector and that wild animals were involved in the virus cycle.
