Impact of early fructose intake on metabolic profile and aerobic capacity of rats.

BACKGROUND: Metabolic syndrome is a disease that today affects millions of people around the world. Therefore, it is of great interest to implement more effective procedures for preventing and treating this disease. In search of a suitable experimental model to study the role of exercise in prevention and treatment of metabolic syndrome, this study examined the metabolic profile and the aerobic capacity of rats kept early in life on a fructose-rich diet, a substrate that has been associated with metabolic syndrome. METHODS: We used adult female Wistar rats fed during pregnancy and lactation with two diets: balanced or fructose-rich 60%. During breastfeeding, the pups were distributed in small (4/mother) or adequate (8/mother) litters. At 90 days of age, they were analyzed with respect to: glucose tolerance, peripheral insulin sensitivity, aerobic capacity and serum glucose, insulin, triglycerides, total cholesterol, LDL cholesterol and HDL cholesterol concentrations as well as measures of glycogen synthesis and glucose oxidation by the soleus muscle. RESULTS: It was found that the fructose rich diet led the animals to insulin resistance. The fructose fed rats kept in small litters also showed dyslipidemia, with increased serum concentrations of total cholesterol and triglycerides. CONCLUSION: Neither the aerobic capacity nor the glucose oxidation rates by the skeletal muscle were altered by fructose-rich diet, indicating that the animal model evaluated is potentially interesting for the study of the role of exercise in metabolic syndrome.

Metabolic responses to acute physical exercise in young rats recovered from fetal protein malnutrition with a fructose-rich diet.

BACKGROUND: Malnutrition in utero can "program" the fetal tissues, making them more vulnerable to metabolic disturbances. Also there is association between excessive consumption of fructose and the development of metabolic syndrome. However, there is little information regarding the acute effect of physical exercise on subjects recovered from malnutrition and/or fed with a fructose-rich diet. The objective of this study was to evaluate the metabolic aspects and the response to acute physical exercise in rats recovered from fetal protein malnutrition with a fructose-rich diet. METHODS: Pregnant Wistar rats were fed with a balanced (B) diet or a low-protein (L) diet. After birth and until 60 days of age, the offspring were distributed into four groups according to the diet received: B: B diet during the whole experiment; balanced/fructose (BF): B diet until birth and fructose-rich (F) diet afterwards; low protein/balanced (LB): L diet until birth and B diet afterwards; low protein/fructose (LF): L diet until birth and F diet afterwards. RESULTS: The excess fructose intake reduced the body weight gain, especially in the BF group. Furthermore, the serum total cholesterol and the LDL cholesterol were elevated in this group. In the LF group, the serum total cholesterol and the muscle glycogen increased. Acute physical exercise increased the serum concentrations of glucose, triglycerides, HDL cholesterol and liver lipids and reduced the concentrations of muscle glycogen in all groups. CONCLUSION: An excess fructose intake induced some signs of metabolic syndrome. However, protein malnutrition appeared to protect against the short term effects of fructose. In other hand, most responses to acute physical exercise were not influenced by early malnutrition and/or by the fructose overload.

Exercise counteracts fatty liver disease in rats fed on fructose-rich diet.

BACKGROUND: This study aimed to analyze the effects of exercise at the aerobic/anaerobic transition on the markers of non-alcoholic fatty liver disease (NAFLD), insulin sensitivity and the blood chemistry of rats kept on a fructose-rich diet. METHODS: We separated 48 Wistar rats into two groups according to diet: a control group (balanced diet AIN-93 G) and a fructose-rich diet group (60% fructose). The animals were tested for maximal lactate-steady state (MLSS) in order to identify the aerobic/anaerobic metabolic transition during swimming exercises at 28 and 90 days of age. One third of the animals of each group were submitted to swimming training at an intensity equivalent to the individual MLSS for 1 hours/day, 5 days/week from 28 to 120 days (early protocol). Another third were submitted to the training from 90 to 120 days (late protocol), and the others remained sedentary. The main assays performed included an insulin tolerance test (ITT) and tests of serum alanine aminotransferase [ALT] and aspartate aminotransferase [AST] activities, serum triglyceride concentrations [TG] and liver total lipid concentrations. RESULTS: The fructose-fed rats showed decreased insulin sensitivity, and the late-exercise training protocol counteracted this alteration. There was no difference between the groups in levels of serum ALT, whereas AST and liver lipids increased in the fructose-fed sedentary group when compared with the other groups. Serum triglycerides concentrations were higher in the fructose-fed trained groups when compared with the corresponding control group. CONCLUSIONS: The late-training protocol was effective in restoring insulin sensitivity to acceptable standards. Considering the markers here evaluated, both training protocols were successful in preventing the emergence of non-alcoholic fatty liver status disease.

Strength Training Prevents Hyperinsulinemia, Insulin Resistance, and Inflammation Independent of Weight Loss in Fructose-Fed Animals.

The aim of this study was to compare the effects of aerobic, strength, and combined training on metabolic disorders induced by a fructose-rich diet. Wistar rats (120 days old) were randomized into five groups (n = 8-14): C (control diet and sedentary), F (fed the fructose-rich diet and sedentary), FA (fed the fructose-rich diet and subject to aerobic exercise), FS (fed the fructose-rich diet and subject to strength exercise), and FAS (fed the fructose-rich diet and subject to combined aerobic and strength exercises). After the 8-week experiment, glucose homeostasis, blood biochemistry, tissue triglycerides, and inflammation were evaluated and analyzed. The strength protocol exerted greater effects on glucose homeostasis, insulin sensitivity, and liver lipid contents than other protocols (all P < 0.05). All three exercise protocols induced a remarkable reduction in inflammation, tissue triglyceride content, and inflammatory pathways, which was achieved through c-Jun NH2-terminal kinase (JNK) phosphorylation and factor nuclear kappa B (NFkB) activation in both the liver and the muscle. Our data suggest that strength training reduced the severity of most of the metabolic disorders induced by a fructose-rich diet and could be the most effective strategy to prevent or treat fructose-induced metabolic diseases.

Muscle glycogen metabolism changes in rats fed early postnatal a fructose-rich diet after maternal protein malnutrition: effects of acute physical exercise at the maximal lactate steady-state intensity.

BACKGROUND: The objective was to evaluate the muscle glucose metabolism in rats fed a fructose-rich diet after fetal protein malnutrition, at rest and after acute physical exercise at maximal lactate steady-state intensity. METHODS: The male offspring born of mothers fed on a balanced or low-protein diet were split in four groups until 60 days: Balanced (B): balanced diet during the whole period; Balanced/Fructose (BF): balanced diet in utero and fructose-rich diet after birth; Low protein/Balanced (LB): low-protein diet in utero and balanced diet after birth; Low protein/Fructose (LF): low protein diet in utero and fructose-rich diet after birth. RESULTS: Acute physical exercise reduced the muscle glycogen concentrations in all groups, although the LF group showed higher concentrations at rest. There was no difference among the groups in the glucose uptake and oxidation rates in the isolated soleus muscle neither at rest nor after acute exercise. However, glycogen synthesis was higher in the LF muscle than in the others at rest. Acute physical exercise increased glycogen synthesis in all groups, and the LF group showed the highest values. CONCLUSION: The fructose-rich diet administered in rats after fetal protein malnutrition alters muscle glycogen concentrations and glycogen synthesis in the rest and after acute exercise at maximal lactate steady-state intensity.

Muscle protein metabolism in neonatal alloxan-administered rats: effects of continuous and intermittent swimming training.

BACKGROUND: This study aimed to examine the effects of intermittent and continuous swimming training on muscle protein metabolism in neonatal alloxan-administered rats. METHODS: Wistar rats were used and divided into six groups: sedentary alloxan (SA), sedentary control (SC), continuous trained alloxan (CA), intermittent trained alloxan (IA), continuous trained control (CC) and intermittent trained control (IC). Alloxan (250 mg/kg body weight) was injected into newborn rats at 6 days of age. The continuous training protocol consisted of 12 weeks of swimming training in individual cylinder tanks while supporting a load that was 5% of body weight; uninterrupted swimming for 1 h/day, five days a week. The intermittent training protocol consisted of 12 weeks of swimming training in individual cylinder tanks while supporting a load that was 15% of body weight; 30 s of activity interrupted by 30 s of rest for a total of 20 min/day, five days a week. RESULTS: At 28 days, the alloxan animals displayed higher glycemia after glucose overload than the control animals. No differences in insulinemia among the groups were detected. At 120 days, no differences in serum albumin and total protein among the groups were observed. Compared to the other groups, DNA concentrations were higher in the alloxan animals that were subjected to continuous training, whereas the DNA/protein ratio was higher in the alloxan animals that were subjected to intermittent training. CONCLUSION: It was concluded that continuous and intermittent training sessions were effective in altering muscle growth by hyperplasia and hypertrophy, respectively, in alloxan-administered animals.

Different exercise protocols improve metabolic syndrome markers, tissue triglycerides content and antioxidant status in rats.

BACKGROUND: An 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). METHODS: Animals 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. RESULTS: Groups 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. CONCLUSIONS: We concluded that all physical activity protocols improved the antioxidant systems of the animals and decreased the storage of triglycerides in the investigated tissues.

Recovery of rat growth and lipid profiles in adult rats subjected to fetal protein malnutrition with a fructose-rich diet.

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.