RESUMO
The metabolic syndrome (MS) has become the new epidemic of this century. Although its associated pathologies may vary, the most common are hypertension, central obesity, dyslipidemia, low High Density Lipoproteins (HDL), high Low Density Lipoproteins (LDL), and type-2 diabetes. Several others can be present, such as hypertriglyceridemia, cardiopathies, atherosclerosis, altered levels of sex hormones, hypogonadism in men and nephropathy. Several factors such as gender, age, race, lifestyle and diet may contribute to modify its prevalence: men develop cardiovascular diseases at an earlier age than pre-menopausal women, who seem to be protected by the antioxidant properties of estrogens. The present review offers information, mostly from 2008 to the present, as well as our own work on a rat model of MS, which was developed by the administration of sucrose in drinking water. Sex steroid hormones play an important role in the appearance and development of the MS and of cardiovascular diseases. Variations in the levels of sex hormones, whether normal or pathological, may have significant influence in the onset of several diseases, metabolic syndrome components included, as well as in the behavior of tissues and organs. These are just some of the non-reproductive actions of sex hormones.
Assuntos
Doenças Cardiovasculares/etiologia , Hormônios Esteroides Gonadais/metabolismo , Doenças Metabólicas/etiologia , Animais , Doenças Cardiovasculares/epidemiologia , Dieta , Modelos Animais de Doenças , Fatores Epidemiológicos , Feminino , Humanos , Estilo de Vida , Masculino , Doenças Metabólicas/epidemiologia , Ratos , Fatores de Risco , Caracteres SexuaisRESUMO
This study was undertaken with the aim of investigating the effect of sucrose addition to the drinking water of rats who were fed with the same diet as a control group, on Delta9- and Delta5-desaturase activities and on the fatty acid composition of serum and liver microsomes. Weanling male Wistar rats had 30% sucrose in their drinking water for 20 weeks. An increase in total calories consumed, visceral fat accumulation, insulin, triglycerides and blood pressure and a decrease in the food intake were observed in the sucrose-fed group as compared with the control group. A decrease in linoleic and alpha-linolenic acid (essential fatty acids) in all serum lipid fractions of sucrose-fed rats was found. This observation correlated with a low food intake by sucrose-fed rats. The conversion of [1 (14)C]-palmitic to [1 (14)C]-palmitoleic acid by Delta9-desaturase activity was increased in sucrose-fed compared with control rats, while the conversion of [1 (14)C]-dihomo-gamma-linolenic acids by Delta5-desaturase activity was depressed. In sucrose-fed as compared to control rats, the proportion of palmitoleic and oleic fatty acids was increased. Arachidonic acid was decreased in sucrose-fed rats. The 1,6-diphenylhexatriene fluorescence polarization of the microsomal membranes was significantly lower in the sucrose-fed group compared to the control group. These results indicate that the sucrose addition to the drinking water of the rats increased microsomal Delta9-desaturase activity and membrane disorder and decreased the activity of the Delta5-desaturase, a key enzyme in the biosynthesis of arachidonic acid, implicated in hypertension.
RESUMO
OBJECTIVE: In a model of hypertriglyceridemia and hypertension in rats (HTG), induced by adding refined sugar to the animals' drinking water, we investigated the response to an acute stress, such as ischemia and reperfusion. In addition, we examined the contribution of calcium overload and free radical release to the injury caused by the post-ischemic reperfusion in a pathological state compared with the normal state. METHODS: Ischemia was induced in the whole anaesthetized animal, by occlusion of the left coronary artery for 4 min, followed by reperfusion for 6 min. To prevent either calcium overload or lipid oxidative processes during reperfusion, either Ketorolac (KET), a calcium ionophore-like drug, or alpha-Phenyl-N-ter-butyl nitrone (PBN), a spin-trapping agent, was administered beforehand. RESULTS: Ketorolac failed to protect the HTG animals from heart damage, as seen by the incidence of reperfusion dysrhythmias, release of lactate dehydrogenase and creatine kinase to the plasma, and non-recovery of the sinus rhythm. On the other hand, PBN was able to prevent these harmful events in the HTG heart by diminishing lipoperoxidation. CONCLUSIONS: The results suggest that, in HTG animals, the oxidative processes make a major contribution to the reperfusion injury and that the sole protection from calcium overload provided by KET is not sufficient to avoid damage compared with control rats.
Assuntos
Hipertensão/complicações , Hipertrigliceridemia/complicações , Isquemia Miocárdica/complicações , Isquemia Miocárdica/patologia , Traumatismo por Reperfusão Miocárdica/patologia , Miocárdio/patologia , Animais , Arritmias Cardíacas/etiologia , Arritmias Cardíacas/prevenção & controle , Cálcio/metabolismo , Creatina Quinase/sangue , Óxidos N-Cíclicos , Radicais Livres/metabolismo , Frequência Cardíaca , Hipertrigliceridemia/prevenção & controle , Incidência , Ionóforos/farmacologia , Cetorolaco/farmacologia , L-Lactato Desidrogenase/sangue , Peróxidos Lipídicos/metabolismo , Masculino , Traumatismo por Reperfusão Miocárdica/complicações , Óxidos de Nitrogênio/farmacologia , Oxirredução/efeitos dos fármacos , Ratos , Ratos EndogâmicosRESUMO
Insulin-elicited endothelin release in hypertriglyceridemic, hypertensive, hyperinsulinemic (HTG) rats was shown. Weanling male Wistar rats were given 30% sucrose in their drinking water for 20-24 wk. In vitro contractions of aorta and femoral arteries were elicited with 40 mM KCl. Endothelin release induced with KCl plus 50 microU/ml insulin resulted in increases in contractile responses: 41 +/- 5.9 and 57 +/- 6% for control and 65.5 +/- 6 and 95 +/- 9% for HTG aortas and femoral arteries, respectively. The endothelin ET(B)-receptor blocker BQ-788 decreased responses to KCl + insulin by 39 +/- 8 and 53 +/- 5% in control and 48 +/- 13 and 79 +/- 3.5% in HTG aortas and femoral arteries, respectively. The ET(A)-receptor antagonist PD-151242 inhibited these responses by 12 +/- 10 and 1 +/- 9% in control and by 51.5 +/- 9 and 58.5 +/- 1% in HTG aortas and femoral arteries, respectively. These results suggest that endothelin may contribute to the hypertension in this model.