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.
Introdução: Evidências apontam que a ingestão exacerbada de frutose pode desencadear distúrbios característicos da síndrome metabólica. Objetivos: Analisar os efeitos da ingestão de dieta rica em frutose sobre aspectos metabólicos de ratos da linhagem Wistar. Adicionalmente, verificar a capacidade aeróbia através da identificação da máxima fase estável de lactato (MFEL). Métodos: Dezesseis ratos foram separados em dois grupos de oito animais: a) controle, alimentados com dieta balanceada, e b) frutose, alimentados com dieta rica em frutose. Foram analisadas a tolerância à glicose (área sob a curva de glicose durante teste de tolerância à glicose), sensibilidade à insulina (taxa de remoção da glicose sérica após sobrecarga exógena de insulina), perfil lipídico sérico e concentração de lactato sanguíneo [lac]s durante exercício na intensidade da MFEL. Resultados: Teste t não pareado (p < 0,05) revelou diferença para a tolerância à glicose e triglicérides, porém não houve diferença na sensibilidade à insulina e na [lac]s. Anova one way com post hoc de Newman-Keuls (p < 0,05) revelou diferença para a cinética da glicose durante o teste de tolerância, mas não para a cinética do lactato durante exercício na MSSL. Conclusão: As alterações fisiológicas provocadas pela dieta rica em frutose e inerentes à síndrome metabólica não prejudicam a capacidade aeróbia de ratos.Palavras-chave: máxima fase estável de lactato, síndrome metabólica, exercício. ABSTRACTIntroduction: Evidence points that exacerbated ingestion of fructose may trigger disturbs characteristic of the metabolic syndrome. Objectives: To analyze the effects of a fructose rich diet on metabolic aspects of Wistar lineage rats. Additionally, to verify the aerobic capacity, through the identification of the maximal lactate steady state (MSSL). Procedures: Sixteen rats were separated in two groups of eight animals: a) Control, fed a balanced diet, and b) fructose, fed a fructose-rich diet. The glucose tolerance, (area under serum glucose during a glucose tolerance test), insulin sensibility (glucose disappearance rate after exogenous insulin administration), serum lipid profile and blood lactate concentration [lac]b during exercise at MSSL intensity, have been analyzed. Results: Non-paired t test (p<0.05) revealed difference between groups in the area under the curve of glucose and serum triglycerides, no difference in insulin sensibility or in [lac]b was detected, though. One-way ANOVA with Newman Keuls post hoc revealed difference in the glucose kinetics during tolerance test, but not in the lactate kinetics during the MSSL. Conclusion: The physiological alterations promoted by fructose-rich diet and intrinsic to the metabolic syndrome do not harm the aerobic capacity of rats.
Newborn rats (6 days old) received alloxan intraperitoneally (A= 250 mg/kg b.w). Rats injected with vehicle (citrate buffer) were used as controls (C). After weaning, half of the animals were submitted to 1 hour/day, 5 days/week swimming and with supporting overload of 5% b.w. At 28 days, no signifi cant differences were found among the groups in fasting glycemia and insulinemia. At 60 days, the fasting glycemia (30 min after oral glucose administration) was higher in alloxan than in controls groups and lower in the alloxan group submitted to training than in the correspondent sedentary group. The glucose tolerance of the alloxan rats was reduced in comparison to controls, both at 28 and 60 days, since the area under the blood glucose curve during the OGTT was higher in the alloxan than in the control. No difference was found among the groups both at 28 and 60 days in the HOMA index. However, a slight reduction was observed in the values of the trained groups suggesting slightly increased insulin sensitivity in the animals. These results suggest that this diabetes mellitus animal model presents interesting characteristics for the study of the role of the physical exercise in diabetes outcome.
Background: Animal models appear well‐suited for studies into the role of exercise in the prevention of non‐insulin‐dependent diabetes mellitus (NIDDM). The aim of the present study was to analyze glucose homeostasis and blood lactate during an exercise swimming test in rats treated with alloxan during the neonatal period and/or fed a high calorie diet from weaning onwards. Methods: Rats were injected with alloxan (200 mg/kg, i.p.) or vehicle (citrate buffer) at 6 days of age. After weaning, rats were divided into four groups and fed either a balanced diet or a high‐caloric diet as follows: C, control group (vehicle + normal diet); A, alloxan‐treated rats fed the normal diet; H, vehicle‐treated rats fed the high‐caloric diet; and HA, alloxan‐treated rats fed the high‐caloric diet. Results: Fasting serum glucose levels were higher in groups A and AH compared with the control group. The Homeostatic Model Assessment index varied in the groups as follows: H>A>HA = C. There were no differences in free fatty acids or blood lactate concentrations during the swim test. Conclusions: Alloxan‐treated rats fed a normal or high‐caloric diet have the potential to be used in studies analyzing the role physical exercise plays in the prevention of NIDDM.
Background: Ninety percent of cases of diabetes are of the slowly evolving non-insulin-dependent type, or Type 2 diabetes. Lack of exercise is regarded as one of the main causes of this disorder. In this study we analyzed the effects of physical exercise on glucose homeostasis in adult rats with type 2 diabetes induced by a neonatal injection of alloxan.
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