Metabolic syndrome represents one of the major health, social and economic issues nowadays, and affects more than 25% people worldwide. Being a multifactorial health problem, metabolic syndrome clusters various features, such as obesity, dyslipidemia, hyperglycemia and hypertension. Each of these disturbances represents a risk factor for developing cardiovascular disease. Moreover, patients with metabolic syndrome are more likely to suffer from depression, thus treatment with antidepressants (e.g. venlafaxine) is often neccessary. However, many of the antidepressants themselves may contribute to worsening or even development of the metabolic syndrome, thus creating a “vicious circle”. The aim of this work was to investigate on the animal model of metabolic syndrome, i.e. on hypertriacylglycerolemic rats fed high-fat-fructose diet (HFFD): 1) the effect of a change in diet from HFFD to a standard diet (SD) and the effect of venlafaxine treatment, 2) during HFFD, 3) as well as during a changed diet to SD. We focused on biometric parameters, blood pressure and selected ECG parameters. We observed the reversibility of the present metabolic and cardiovascular changes by switching the HFFD to SD in the last 3 weeks of the experiment. Switch to the standard diet led to decrease of body weight, even in the presence of venlafaxine. Administration of venlafaxine caused the decrease of heart weight/body weight index in rats fed with HFFD compared to the untreated group fed with HFFD for 8 weeks. Blood pressure, which was increased in the HFFD group showed a tendency to decrease to control values after switching to the standard diet. Administration of venlafaxine led to significant increase in all parameters of blood pressure when rats were fed with HFFD throughout the whole experiment. In untreated rats fed with HFFD for 8 weeks, we observed a shorter PQ interval and prolonged QRS complex as well as QTc interval compared to untreated rats with diet switched to SD. This effect was potentiated by venlafaxine administered not only during HFFD but even after switch to SD. Our results point to the fact that metabolic syndrome is clearly affecting the function of the cardiovascular system by modifying blood pressure and electrical activity of the heart. Moreover, administration of venlafaxine may lead to worsening of the observed changes, especially in the presence of high-fat-fructose diet.
Decreasing high fat and high carbohydrate intake, together with the administration of natural bioactive drugs is assumed to have a protective effect in the prevention and amelioration of metabolic syndrome (MetS). The aim of the study was to evaluate effects of diet improvement and/or a phenolic compound - rosmarinic acid (RA) administration (100 mg/kg/day) on metabolic as well as functional changes of vessels and hippocampus caused by MetS-like conditions. MetS-like conditions were induced by high-fat-fructose diet (HFFD) in Prague hereditary hypertriacylglycerolemic rats. The effect of diet improvement and RA administration was studied using biochemical and functional measurements. Consumption of HFFD by hypertriacylglycerolemic rats resulted in the development of conditions like MetS. The fat and fructose restriction from the diet led to amelioration of basic indicators of metabolic state in rats fed HFFD and to amendment parameters of glucose-tolerance test and reduction of the IL-1β serum levels. Moreover, aortic endothelial function was improved with an impact on blood pressure. The functional measurement of electrophysiology of the hippocampus showed that long-term potentiation of neuronal transmission course deteriorated after HFFD was improved by caloric restriction. Oral administration of RA had a supporting effect not only on lipid and glucose metabolism but also on the vascular endothelium. Combination of both types of therapy induced beneficial effect on glucose tolerance and lipid peroxidation. Thus, combined improvement of diet habits and treatment with natural bioactive drugs is assumed to have protective effect in prevention and amelioration of MetS.
A number of pregnant women all over the world suffer from depression and are treated during gestation with antidepressants, mostly with selective serotonin reuptake inhibitors or selective serotonin and norepinephrine reuptake inhibitors. Exposure to prenatal stress is also a great risk factor for a developing fetus and could be responsible for altered fetal development or various neurobehavioral disturbances of a child. Administration of selective serotonin and norepinephrine reuptake inhibitor venlafaxine is associated with various cardiovascular adverse effects, such as tachycardia, increased blood pressure, arrhythmias and hypertensive crisis. The aim of this study was to focus on the effect of pre-gestational chronic mild unpredictable stress and/or administration of antidepressant venlafaxine (10 mg/kg/day, p. o.) on specific parameters, determining the function of the cardiovascular system of male and female rat offspring. Blood pressure and standard ECG were recorded in the offspring. Exposure to pre-gestational stress did not cause significant changes in the systolic, diastolic blood pressure and pulse frequency either in males or in females, compared to the unexposed control animals. Pre-gestational stress caused the shortening of QT interval and prolongation of QRS complex duration in males. On the other hand, in females, the effects of pre-gestational stress were potentiated by the administration of venlafaxine and resulted in elevated systolic and diastolic blood pressure, prolonged QT interval and shortened QRS complex duration, compared to the control. In conclusion, the female rat offspring are more sensitive to exposure to pre-gestational, to chronic mild unpredictable stress and venlafaxine.
The aim of our study was to evaluate the possibility of influencing the risk factors of metabolic syndrome (MetS) and metabolic cognitive syndrome. As a model of MetS, we used high-fat-fructose diet (HFFD) fed hypertriacylglycerolemic (HTG) rats. Control group included HTG rats fed with HFFD during 8 weeks (HFFD8). Furthermore, we tested the effect of pharmacological and non-pharmacological therapies. Non-pharmacological therapy, which we chose, was a change in diet from HFFD (5 weeks) to standard one (3 weeks) and thus caloric restriction (HFFD5+3). The drug we used was rosmarinic acid (RA; 100mg/kg), which we administered to rats after 5 weeks of HFFD once a day for consecutive 3 weeks with current change in diet to standard one (HFFD5+3+RA) or during lasting last 3 weeks of HFFD (HFFD8+RA). After 8 weeks of experiment, lipid peroxidation markers, lipid profile of blood serum, and neuronal transmission and synaptic plasticity (long-term potentiation [LTP]) in hippocampal sections were evaluated in vitro. We observed a significant effect of dietary change in lipid profile (decreased total cholesterol and low-density lipoprotein cholesterol [LDL-cholesterol] and increased high-density lipoprotein cholesterol [HDL-cholesterol]). The combination of pharmacological and non-pharmacological treatments caused a decrease in total cholesterol, LDL-cholesterol, and lipid peroxidation in blood serum. Change in HFFD to standard diet without treatment resulted in slight improvement in neuronal transmission in the hippocampus and caloric restriction alone also had positive effect on LTP maintenance. Our results suggest that combination of pharmacological and non-pharmacological approaches had better impact on the biochemical parameters of MetS in blood serum, but weak impact on neuronal functions in the hippocampus, where the expected positive effect was achieved only by caloric restriction.
Metabolic syndrome (MetS) belongs to the serious health complications expanding in cardiovascular diseases, obesity, insulin resistance, and hyperglycemia. In this study, hypertriacylglycerolemic rats fed a high-fat-fructose diet (HFFD) were used as an experimental model of MetS to explore the effect of tested compounds. Effects of a new prospective pyridoindole derivative coded SMe1EC2 and the natural polyphenol rutin were tested. Endothelial nitric oxide synthase (NOS3) and nuclear factor kappa B (NF-κB) expression were assessed in the left ventricle immunohistochemically and left ventricle activity was monitored in isolated perfused rat hearts. NOS3 activity in the left ventricle decreased markedly as a result of a HFFD. NOS3 expression was upregulated by both substances. NF-κB expression was increased in the MetS group in comparison to control rats and the expression further increased in the SMe1EC2 treatment. This compound significantly improved the coronary flow in comparison to the control group during reperfusion of the heart followed after ischemia. Further, it tended to increase left ventricular systolic pressure, heart product, rate of maximal contraction and relaxation, and coronary flow during baseline assessment. Moreover, the compound SMe1EC2 decreased the sensitivity of hearts to electrically induced ventricular fibrillation. Contrary to this rutin decreased coronary flow in reperfusion. Present results suggest that despite upregulation of NOS3 by both substances tested, pyridoindole SMe1EC2 rather than rutin could be suitable in treatment strategies of cardiovascular disorders in MetS-like conditions.
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