Abstract

Objective: This study aimed to investigate the effect of starvation and re-feeding on oxidative stress markers, lipid profile, thyroid hormones, and changes in thyroid tissue and in male Wistar rats. Method: Fifty-six male Wistar rats were divided into 6 groups. After 3 months of feeding animals with specific diet, the first group was used without fasting (day zero). Other rats were exposed to fasting for 14 days. The second group was considered as a group after fasting (day 14). In groups 3 to 6, replenishment was done and then these groups were euthanized on days 16 to 22, and blood and tissue samples were taken. Results: Significant increase was observed in MDA, triglycerides, and VLDL cholesterol. The concentrations of SOD, GPx and T3 were decreased significantly. By re-feeding, SOD, GPx, triglycerides, total cholesterol, and VLDL cholesterol increased. T3 concentration was significantly increased in all groups after re-feeding. In thyroid tissue, the diameter of follicles and the amount of colloid decreased and the number of parafollicular cells increased during starvation. By days 2 and 4 post-refeeding there were follicles with different sizes and the numbers of parafollicular cells were increased. Conclusion: Starvation may act on the depletion of antioxidants, predisposing subjects to oxidative injury highlights with enhanced level of MDA. Oxidative stress, may play a critical role in the pathophysiology of starvation- refeeding syndrome. Starvation results in a decrease in the serum T3 concentration due to decreased peripheral generation of T3 from T4, because carbohydrates are major regulators of T4 deiodination. The increased free fatty acid availability to the circulation and eventually to the liver contribute to increased VLDL synthesis and elevated plasma triglyceride levels after starvation. The negative effects of oxidative stress in considerable time after re-feeding should be considered in future studies.

Highlights

  • Starvation-refeeding syndrome as an unusual multisystem disorder may occur as a consequence of refeeding after a prolonged starvation period [1]

  • Starvation results in a decrease in the serum T3 concentration due to decreased peripheral generation of T3 from T4, because carbohydrates are major regulators of T4 deiodination

  • This study aimed to investigate the effect of starvation and re-feeding on oxidative stress markers, lipid profile, thyroid hormones, and changes in thyroid tissue and in male Wistar rats

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Summary

Introduction

Starvation-refeeding syndrome as an unusual multisystem disorder may occur as a consequence of refeeding after a prolonged starvation period [1]. In the starvation-refeeding syndrome, the body encounters two distinct conditions. The body shifts from carbohydrate to fat and protein utilization to produce glucose and energy. The body shifts back instantaneously to carbohydrate metabolism [2,3,4]. Studies on anorexia nervosa patients and fish species showed that the starvation period has prooxidant effects due to both increased lipid peroxidation levels and the reduced level of antioxidant defenses [5,6,7,8]. Capability of refeeding in anorexia nervosa patients for reducing the oxidative stress or increasing the levels of antioxidant markers is unknown. Thyroid hormones play a significant role in oxidative stress due to their capacity to accelerate the basal metabolism, cellular reactions and changing respiratory rate in mitochondria [9]. Thyroid hormones affect the cell antioxidant mechanisms in different ways

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