Starvation and refeeding in rats: effect on some parameters of energy metabolism and electrolytes and changes of hepatic tissue

Namazi, Fatemeh; Omidi, Arash; Abbasi, Sajjad; Afsar, Mina; Honarmand, Masumeh; Nazifi, Saeed

doi:10.1590/s0100-736x2016001300015

Cited by 5 publications

(5 citation statements)

References 18 publications

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“…Although this amount of energy might be insufficient for RFS development, it is conceivable that our glucose dosage was sufficient to promote refeeding hypophosphatemia in light of previous reports of the effects of reintroduction of carbohydrates in this syndrome (22). Some reports have demonstrated RFS in animals ; however, symptoms appeared after several days (23,24). Because of the direct infusion of glucose solution via intravenous administration, we were able to observe hypophosphatemia within one day.…”

Section: Discussionmentioning

confidence: 54%

“…Since insulin activates ATPase (25), increasing insulin concentrations might stimulate Pi consumption for ATP generation, which is essential for energy production. Namazi et al reported that refeeding after starvation decreased serum K and Pi concentrations, increased insulin levels and altered the hepatic histopathology in rats (24). The effect of changes in glucose or lipid metabolism on liver tissues may be associated with insulin-stimulated Pi consumption.…”

Section: Discussionmentioning

confidence: 99%

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Hypophosphatemia occurs with insulin administration during refeeding by total parenteral nutrition in rats

et al. 2018

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Refeeding syndrome (RFS) refers to the metabolic and clinical changes that occur with rapid or excessive administration of feeding, whether orally, enterally or parenterally, following a period of relative or absolute starvation (1). RFS is characterized by fatal complications such as heart failure, arrhythmia, respiratory failure and cardiac arrest (2) ; thus, the prevention of RFS is vital. In general, individuals with marasmus or kwashiorkor are at risk for RFS, particularly in cases of greater than 10% weight loss over a couple of months. Furthermore, patients are at risk after prolonged fasting, massive weight loss in chronic alcoholism, prolonged intravenous fluid repletion and anorexia nervosa (3, 4). Currently, this syndrome is common among elderly people with poor nutritional intake due to alcoholism or dementia in the clinical practice.Hypophosphatemia is the hallmark of RFS and is key to its prevention and treatment (5). Further, it is reported to be associated with increased mortality in critically ill patients (6, 7). The mechanism of refeeding hypophosphatemia can be described by the following hypothesis. With the reintroduction of carbohydrates to malnutrition patients, anabolism begins immediately and the body shifts to carbohydrate metabolism from fat catabolism. The increased glucose load, with a corresponding increase in the release of insulin, leads to cellular uptake of glucose, potassium (K), magnesium (Mg), and phosphate (Pi). This shift of electrolytes into the cell causes hypokalemia, hypomagnesemia, and hypophosphatemia (8,9). Patients consistently present with hypophosphatemia, although the other symptoms are not always detected. However, the molecular mechanisms of hypophosphatemia and RFS require elucidation.RFS is more likely to occur after parenteral or enteral feeding (10). In a study of patients that received total parenteral nutrition (TPN), the incidence of hypophosphatemia ranged from 30 -38% when Pi was provided in the solution, to 100% when TPN without Pi was administered (11). The RFS guideline of the National Institute for Health and Clinical Excellence (NICE) in England and Wales recommends that nutritional repletion of energy should be started slowly, and Pi supplementation should be given unlessblood levels are high before refeeding (12). Pi supplementation was reported to reduce the incidence of hypophosphatemia in hospitalized patients receiving TPN (13). Thus, Pi has an important role in RFS.Guidelines on the prevention and treatment of this syndrome are available ; however, cases continue to be seen clinically. One reason why the mechanism of RFS is unknown is the lack of an appropriate animal model. To our knowledge, there are no reports of animal models with hypophosphatemia, making investigation of RFS challenging. Thus, the development of an animal model is vital for the detailed evaluation of RFS as well as clarification of its molecular mechanism. In this study, as a first step toward revealing the mechanism of RFS, we attempted to develop an RFS animal model ...

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Section: Discussionmentioning

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Hypophosphatemia occurs with insulin administration during refeeding by total parenteral nutrition in rats

et al. 2018

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“…Therefore, increase in the serum SGPT observed in refeeding animals is a consequence of a number of liver disorders including hydropic changes as well as fatty liver already described. A longer-term study found only vacuoles after starvation and refeeding in the tissues of animals, and the severity of lesions gradually decreased during refeeding [ 34 ].…”

Section: Discussionmentioning

confidence: 99%

Hepatic ballooning degeneration: a new feature of the refeeding syndrome in rats

Jordão¹,

Canale²,

Brunaldi³

et al. 2020

ceh

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Aim of the study: Hepatic changes have been described during the refeeding syndrome due to increase in enzymes and hepatomegaly; however, they have not been properly described. Thus, the objective of this study was to investigate the hepatic histological characteristics and biochemical markers of hepatic steatosis in Wistar rats with refeeding syndrome. Material and methods: Thirty male Wistar rats were allocated to one of three groups: C, F or R. The animals from group C received an AIN-93 diet for 96 hours, and were then sacrificed. Animals allocated to group F were fasted for 48 hours and sacrificed. Animals from group R were also fasted for 48 hours, but were refed for another 48 hours, with AIN-93. The liver, blood and epididymal and retroperitoneal fats were collected. Results: Data obtained in groups F and R show the changes observed in refeeding syndrome, during starvation and refeeding. The serum glucose, magnesium, potassium and phosphorus, in group F, decreased. There was no evidence of hepatic steatosis. Hypophosphatemia, hypomagnesemia and hypokalemia were also observed in group R, confirming refeeding syndrome. The main histological characteristic, in this group, was the extensive presence of ballooning degeneration. This is the first article that has detected such change in liver structure, due to refeeding syndrome. The possible causes are: retention of sodium, causing whole body edema; and/or dysfunction of the sodium/potassium pump of the hepatocytes, as a result of hypophosphatemia. Conclusions: This is the first description of an animal model of hepatic severe ballooning degeneration induced due to refeeding syndrome.

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“…For 2 weeks, rat chow was withheld from a group of rats to test the effect of starving (Namazi et al, 2016 ). During the protracted hunger, none of the rats died.…”

Section: Methodsmentioning

confidence: 99%

Intermittent fasting and exercise therapy abates STZ‐induced diabetotoxicity in rats through modulation of adipocytokines hormone, oxidative glucose metabolic, and glycolytic pathway

Chijiokwu

Nwangwa

Oyovwi

et al. 2022

Physiological Reports

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Diabetes is a global, costly, and growing public health issue. Intermittent fasting (IF) and exercise therapy have been shown to improve insulin sensitivity (IS) in large studies, although the underlying processes are still unknown. The goal of this study, which included both nondiabetic and diabetic rats, was to look at the mechanisms of intermittent fasting and exercise in the management of diabetotoxicity. The effects of starvation and honey on the oral glucose tolerance test, insulin tolerance test, adipocytokines, oxidative glucose metabolic enzymes, glycolytic enzymes, food intake, and body weight in rats with streptozotocin‐induced diabetes were also investigated. In the nondiabetic phase, rats were administered an oral regimen of distilled water (0.5 ml/rat), honey (1 g/kg body weight), and interventions with IF, and starvation for 4 weeks while in the diabetic phase, after STZ or citrate buffer injections, interventions with IF, exercise, starvation, and honey treatment began for 4 weeks. At all OGTT and ITT points, there was a substantial rise in glucose in the STZ group. Adipocytokines hormone, oxidative glucose metabolic enzymes, glycolytic enzymes, and body weight were all affected by STZ when compared to starvation and honey, however, IF and exercise significantly reduced these alterations. In diabetic rats, intermittent fasting and exercise enhanced serum adipocytokines levels. These findings imply that adipokines modulate glycolytic/nonmitochondrial enzymes and glucose metabolic/mitochondrial dehydrogenase to mediate the antidiabetic effects of intermittent fasting and exercise.

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Starvation and refeeding in rats: effect on some parameters of energy metabolism and electrolytes and changes of hepatic tissue

Cited by 5 publications

References 18 publications

Hypophosphatemia occurs with insulin administration during refeeding by total parenteral nutrition in rats

Hypophosphatemia occurs with insulin administration during refeeding by total parenteral nutrition in rats

Hepatic ballooning degeneration: a new feature of the refeeding syndrome in rats

Intermittent fasting and exercise therapy abates STZ‐induced diabetotoxicity in rats through modulation of adipocytokines hormone, oxidative glucose metabolic, and glycolytic pathway

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