In search of an adequate model for the human metabolic syndrome, the metabolic characteristics of Wistar rats were analysed after being submitted to different protocols of high fructose ingestion. First, two adult rat groups (aged 90 d) were studied: a control group (C1; n 6) received regular rodent chow (Labina, Purina) and a fructose group (F1; n 6) was fed on regular rodent chow. Fructose was administered as a 10 % solution in drinking water. Second, two adult rat groups (aged 90 d) were evaluated: a control group (C2; n 6) was fed on a balanced diet (AIN-93G) and a fructose group (F2; n 6) was fed on a purified 60 % fructose diet. Finally, two young rat groups (aged 28 d) were analysed: a control group (C3; n 6) was fed on the AIN-93G diet and a fructose group (F3; n 6) was fed on a 60 % fructose diet. After 4-8 weeks, the animals were evaluated. Glucose tolerance, peripheral insulin sensitivity, blood lipid profile and body fat were analysed. In the fructose groups F2 and F3 glucose tolerance and insulin sensitivity were lower, while triacylglycerolaemia was higher than the respective controls C2 and C3 (P,0·05). Blood total cholesterol, HDL and LDL as well as body fat showed change only in the second protocol. In conclusion, high fructose intake is more effective at producing the signs of the metabolic syndrome in adult than in young Wistar rats. Additionally, diet seems to be a more effective way of fructose administration than drinking water.Fructose: Metabolic syndrome: Insulin sensitivity: Body fat Clinically, the metabolic syndrome involves a cluster of disturbances in which glucose intolerance represents an important symptom. Metabolic syndrome diagnosis implies in positive results to at least three metabolic alterations including insulin resistance, hypertension, obesity, endothelial dysfunction and blood lipid profile alterations (1,2) . These multiple risk factors accelerate the incidence of CVD in a cooperative way (1 -4) . Obesity prevalence has quadrupled in the past 25 years in the USA; 16 % of children and 30 % of adults are now affected and many of these obese individuals suffer from the metabolic syndrome (5)
In recent decades, metabolic syndrome has become a public health problem throughout the world. Longitudinal studies in humans have several limitations due to the invasive nature of certain analyses and the size and randomness of the study populations. Thus, animal models that are able to mimic human physiological responses could aid in investigating metabolic disease. Thus, the present study was designed to analyze metabolic syndrome markers in albino Wistar rats (Rattus norvegicus) of different ages. The following parameters were assessed at two (young), four ( adult), six (adult), and twelve (mature) months of age: glucose tolerance (glucose tolerance test); insulin sensitivity (insulin tolerance test); fasting serum glucose, triglycerides, total cholesterol, HDL cholestero, and LDL cholesterol concentrations; glucose uptake in isolated soleus muscle; and total lipid concentration in subcutaneous, mesenteric, and retroperitoneal adipose tissue. We found that aging triggered signs of metabolic syndrome in Wistar rats. For example, mature rats showed a significant increase in body weight that was associated. In addition, mature rats showed an increase in the serum concentration of triglycerides, total cholesterol, and LDL cholesterol, which is characteristic of dyslipidemia. There was also an increase in serum glucose compared with the younger groups of animals. Therefore, aging Wistar rats appear to be an interesting model to study the changes related to metabolic syndrome.
The present study investigated the role of swimming training on cerebral metabolism and hippocampus concentrations of insulin and IGF-1 in diabetic rats. Wistar rats were divided in sedentary control (SC), trained control (TC), sedentary diabetic (SD), and trained diabetic (TD). Diabetes was induced by Alloxan (35 mg kg(-1) b.w.). Training program consisted in swimming 5 days/week, 1 h/day, 8 weeks, supporting a load corresponding to 90% of maximal lactate steady state (MLSS). For MLSS determination, rats were submitted to three sessions of 25-min supporting loads of 4, 5, or 6% of body wt, with intervals of 1 week. Blood samples were collected every 5 min for lactate determination. An acute exercise test (25 min to 90% of MLSS) was done in 7th week to confirm the efficacy of training. All dependent variables were analyzed by one-way analysis of variance (ANOVA) and a significance level of P < 0.05 was used for all comparisons. The Bonferroni test was used for post hoc comparisons. At the end of the training period, rats were sacrificed and sample blood was collected for determinations of serum glucose, insulin, GH, and IGF-1. Samples of gastrocnemius muscle and liver were removed to evaluate glycogen content. Hippocampus was extracted to determinate glycogen, insulin, and IGF-1 contents. Diabetes decreased serum GH, IGF-1, and liver glycogen stores in SD. Diabetes also increased hippocampus glycogen and reduced hippocampus IGF-1 content. Physical training recovered liver and hippocampus glycogen stores and promoted increases in serum IGF-1 in TD group. Physical training restored hippocampus IGF-1 content in diabetic group. It was concluded that in diabetic rats, physical training induces important metabolic and hormonal alterations that are associated with an improvement in glucose homeostasis and with an increased activity in the systemic and hippocampus IGF-1 peptide.
There is evidence suggesting an association between fructose consumption and the development of metabolic syndrome. In turn, protein malnutrition in utero is proposed to "program" the fetal tissues, making them more susceptible to nutritional associated disorders. To test this hypothesis, the present study was designed to analyze body growth and metabolic aspects of rats subjected to fetal protein malnutrition and subsequently fed a fructose-rich diet. Wistar rats were distributed into 4 groups: balanced (B) diet-B diet offered the entire experimental period; balanced diet/fructose-B diet until birth and fructose-rich diet (F-60% fructose) until adulthood; low-protein (L) diet/balanced-L diet until birth and B diet until adulthood; low-protein diet/fructose (F)-L diet until birth and F diet until adulthood. After nutritional recovery, there was a restoration of serum glucose, total protein, and albumin concentrations, which were reduced by fetal malnutrition, and a restoration of the liver glycogen and lipids contents, which were increased by fetal malnutrition. This restoration was independent of the diet adopted after birth. It was verified that the high fructose diet arrested body growth of the rats independently of the nutritional state during fetal life and was associated with weight reduction and decrease of the adipose in some regions of the body (P < .05). Moreover, the serum concentrations of triglycerides and total cholesterol, which are indicators of metabolic syndrome, rose in the rats that ingested the fructose-rich diet (P < .05). In summary, high consumption of fructose impairs body growth and alters the circulating lipids independently of the protein nutrition in utero.
BackgroundAn increase in the prevalence of obesity entails great expenditure for governments. Physical exercise is a powerful tool in the combat against obesity and obesity-associated diseases. This study sought to determine the effect of three different exercise protocols on metabolic syndrome and lipid peroxidation markers and the activity of antioxidant enzymes in adult Wistar rats (120 days old).MethodsAnimals were randomly divided into four groups: the control (C) group was kept sedentary throughout the study; the aerobic group (A) swam1 h per day, 5 days per week, at 80% lactate threshold intensity; the strength group (S) performed strength training with four series of 10 jumps, 5 days per week; and the Concurrent group (AS) was trained using the aerobic protocol three days per week and the strength protocol two days per week.ResultsGroups A and S exhibited a reduction in body weight compared to group C. All exercised animals showed a reduction in triglyceride concentrations in fatty tissues and the liver. Exercised animals also exhibited a reduction in lipid peroxidation markers (TBARS) and an increase in serum superoxide dismutase activity. Animals in group A had increased levels of liver catalase and superoxide dismutase activities.ConclusionsWe concluded that all physical activity protocols improved the antioxidant systems of the animals and decreased the storage of triglycerides in the investigated tissues.
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