The risks of chronic diseases associated with the increasing consumption of fructose-laden foods are amplified by the lack of regular physical activity and have become a serious public health issue worldwide. Moreover, childhood eating habits are strongly related to metabolic syndrome in adults. Thus, we aimed to investigate the preventive role of exercise training undertaken concurrently with a high fructose diet on cardiac function, hemodynamics, cardiovascular autonomic modulation and oxidative stress in male rats after weaning. Male Wistar rats were divided into 4 groups (n = 8/group): Sedentary control (SC), Trained control (TC), Sedentary Fructose (SF) and Trained Fructose (TF). Training was performed on a treadmill (8 weeks, 40–60% of maximum exercise test). Evaluations of cardiac function, hemodynamics, cardiovascular autonomic modulation and oxidative stress in plasma and in left ventricle (LV) were performed. Chronic fructose overload induced glucose intolerance and an increase in white adipose tissue (WAT) weight, in myocardial performance index (MPI) (SF:0.42±0.04 vs. SC:0.24±0.05) and in arterial pressure (SF:122±3 vs. SC:113±1 mmHg) associated with increased cardiac and vascular sympathetic modulation. Fructose also induced unfavorable changes in oxidative stress profile (plasmatic protein oxidation- SF:3.30±0.09 vs. SC:1.45±0.08 nmol/mg prot; and LV total antioxidant capacity (TRAP)- SF: 2.5±0.5 vs. SC:12.7±1.7 uM trolox). The TF group showed reduced WAT, glucose intolerance, MPI (0.35±0.04), arterial pressure (118±2mmHg), sympathetic modulation, plasmatic protein oxidation and increased TRAP when compared to SF group. Therefore, our findings indicate that cardiometabolic dysfunctions induced by fructose overload early in life may be prevented by moderate aerobic exercise training.
The term refeeding syndrome has been used to describe the adverse consequences that can occur in all malnourished patients in the early stages of nutrition repletion whether the method of refeeding is oral, enteral or parenteral. Those consequences include acute thiamine deficiency resulting in Wernicke's encephalopathy and Korsakoff syndrome, with the potential for permanent cognitive impairment; hypophosphatemia, hypokalemia, hypomagnesemia and fluid overload resulting in cardiac failure. Adaptive changes in metabolism occur during a period of starvation or fasting: levels of glucose fall within 24 to 72 hours, as response, glucagon levels rise and insulin concentrations decrease. Glucose levels are maintained by glycogenolysis at first and gluconeogenesis latter. The reintroduction of nutrition leads to a switch from fat to carbohydrate metabolism and an increase of insulin concentration. Insulin stimulates the movement of potassium, phosphate, and magnesium into the cell leading to its depletion in extracellular compartment. Reactivation of carbohydrate metabolism increases degradation of thiamine, a cofactor required for cellular enzymatic reactions in Kreb's cycle. Deficiency in all these nutrients can then occur. Patients with anorexia nervosa are at risk of suffering from refeeding syndrome. This psychiatric disorder causes potentially life-threatening, physical complications and has the highest mortality rate among psychiatric disorders. The purpose of this review is to clarify recommendations for prevention and treatment of refeeding syndrome in anorexia nervosa.Disclosure of interestThe authors have not supplied their declaration of competing interest.
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