SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Refeeding syndrome can occur when nutrition is reinstituted in a starved patient and, if abnormalities are not corrected, can be lethal. This article describes metabolic adaptations to starvation, risk factors for the development of refeeding syndrome, and causes as well as symptoms of refeeding syndrome. Adverse consequences of hypophosphatemia, hypomagnesemia, and hypokalemia are described. Nursing implications to prevent refeeding syndrome are outlined.
In the rat, small intestine preparation was studied with the aid of our modification of Na(+)-dependent nutrient absorption short-circuit current method. In experiments on rats, it was shown that reaction of the gut to animal state changes (fasting, satiety and refeeding) depended on its medial or distal localization. Active Na+ absorption in medial part of small intestine after refeeding rose 3-6-fold depending on period of previous fasting (2 or 5 days). Two states of satiety were elucidated: when the rats were in cage with meal and after refeeding following a 5-day fasting; at least in distal small intestine, absorption of nutrients in the latter state was much higher. Fast nutrient adaptation (approximately 30 min) of absorption was revealed, second responses of short-circuit current to glyala were 3.4-fold higher than the first one: 33.4 +/- 9.7 (n = 6) and 9.9 +/- 2.9 microA/cm2 (n = 6) (P < 0.05). It is possible that increased nutrients (glucose and aminoacids) entering in mucose after the 5th day refeeding play role as a primary signal for change of animal behavior.
BACKGROUND: Early enteral feeding (EF) may result in fever, elevated white blood cell count, increased serum levels of liver enzymes, and diarrhea. We name the complications "enteral refeeding syndrome", as a subtype of refeeding syndrome, because they are likely to result from long-term lack of lumen nutrition. The aim of this study was to investigate the characteristics of enteral refeeding syndrome after long-term total parenteral nutrition (TPN), and the solution for the disease. METHODS: We collected the clinical data of 100 patients with gastrointestinal fistula, who were cured from Apirl 2001 to July 2002. Their fasting time, daily stool frequency, body temperature, heart rate, respiratory rate, levels of transaminases, alkaline phosphatase (AKP), and gamma-glutamylcyclotransferase (gamma-GT), white blood cell count, and systemic inflammatory reaction syndrome (SIRS) score were recorded before and 1, 3, 5, 10, and 15 days after EF. Student's t test and analysis of variance were used to analyze the data. RESULTS: Of the 100 patients, 56 were cured after selective resection of intestinal fistula, 15 were cured by emergency operation, and 29 recovered spontaneously. The levels of AKP and gamma-GT increased significantly on the 3rd day after EF [On the 3rd day after EF, (243.0 +/- 121.6) U/L and (177.2 +/- 109.9) U/L vs. before EF (181.5 +/- 127.5) U/L and (118.4 +/- 94.2) U/L, P < 0.05], and decreased gradually afterwards. The SIRS scores on the 1st day (1.05 +/- 1.08) and 3rd day (0.96 +/- 1.11) after EF were significantly higher than that before EF (0.72 +/- 0.84), then decreased to 0.83 +/- 0.91, 0.49 +/- 0.73 and 0.32 +/- 0.60 on the 5th, 10th and 15th days after EF. The number of patients with diarrhea at 1, 3, 5, 10 and 15 days post-EF were 31, 26, 12, 13, and 7, respectively. CONCLUSIONS: The longer the TPN lasts, the more severe the enteral refeeding syndrome becomes. Continuous EF is effective for the syndrome. Early enteral nutrition is useful in preventing it.
Chronic caloric restriction (CCR) prevents mammary tumorigenesis in rodents, but a protective effect for intermittent caloric restriction (ICR) is less well documented. We recently reported that ICR reduced mammary tumor (MT) incidence of mouse mammary tumor virus-transforming growth factor (MMTV-TGF)-alpha mice to a greater extent than did CCR. Here, we repeated this protocol and obtained serum and tissue samples. Ad libitum (AL) MMTV-TGF-alpha mice were fed AIN-93M diet. Beginning at 10 weeks of age, ICR mice received isocaloric AIN-93M-mod diet (2-fold increases in protein, fat, vitamins, and minerals) at 50% of ad libitum for 3 weeks followed by 3 weeks refeeding with AIN-93M diet. CCR mice were pair-fed AIN-93M:AIN-93M-mod (2:1) matching intakes for restriction/refeeding cycles. Mice were sacrificed for MT size, at 79 (end of 12th restriction) or at 80 (1 week after 12th refeeding) weeks of age. AL and ICR-80 mice had heavier body weights than ICR-79 and CCR mice (P < 0.0001). Cumulative food intakes of ICR and CCR mice were reduced 12% and 15% versus AL mice (P < 0.0001). However, ICR mice consumed significantly (P < 0.0001) more food than did AL mice during refeeding. MT incidence was 84%, 13%, and 27% for AL, ICR, and CCR mice, respectively. MT weight (P < 0.0011) and number (P < 0.01) were higher for AL mice compared with ICR and CCR mice. AL and ICR-80 mice had similar serum IGF-I levels, but only AL values were higher than those of ICR-79 and CCR mice (P < 0.0017). ICR mice had more MT DNA breaks compared with AL and CCR mice, suggesting enhanced apoptosis (P < 0.02). AL mice had higher mammary fat pad ObR and ObRb leptin receptor mRNA expression than did ICR and CCR mice (P < 0.001), but there was no effect on MTs. These results confirm that ICR prevents development of MTs to a greater extent than does CCR, although "overeating" during refeeding may compromise this protection.
In order to determine whether the metabolism of individual free fatty acids is affected by fasting, plasma levels were measured daily in seven obese females during ten days of fasting and four days of refeeding. There was a gradual rise in free fatty acids throughout the fasting period with some variability during the last three days. Free fatty acids remained high during early refeeding followed by a decrease at the end of refeeding. Changes in concentration were most pronounced for oleic (18:1w9) and palmitic (16:0) acids which had the highest initial levels. Expressed as percent change from baseline, oleic, palmitic, and linoleic (18:2w6) acids had similar patterns, while changes were more dramatic for palmitoleic acid (16:1) and less so for stearic acid (18:0) than the others. When expressed as proportion of total free fatty acids, there was very little change in any individual free fatty acid despite the large fluctuations in actual plasma values. It appears that the five major free fatty acids in plasma undergo similar changes during fasting and refeeding, and the palmitic and oleic acids can serve as suitable tracers for metabolic studies.
Proteolytic activities at pH 5.0 and pH 7.4 in both kidney and liver during refeeding of protein-depleted mice were determined. Under this nutritional condition, the in vivo rate of protein breakdown is inhibited. Protein depletion caused in both kidney and liver a loss of pH 5.0 proteolytic activity. It was restored to normal values after 12 hours of refeeding with a complete diet. The pH 7.4 proteolytic activity also decreased as a consequence of protein depletion, but remained low during refeeding. Both re-fed kidney and liver lysosomes showed an increased stability to osmotic shock and, therefore, a decreased autophagic activity. The results indicate that both kidney and liver exhibit a similar behavior. The decreased activity of the lysosomal-vacuolar system, and the low pH 7.4 proteolytic activity may account for the observed in vivo protein breakdown inhibition during refeeding of protein-depleted mice.
The effects of fasting/refeeding and untreated or insulin-treated diabetes on the bifunctional enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase and its mRNA in rat liver were determined. Both enzymatic activities fell to 20% of control values with fasting or streptozotocin-induced diabetes and were coordinately restored to normal within 48 h of refeeding or 24 h of insulin administration. These alterations in enzymatic activities were always mirrored by corresponding changes in amount of enzyme as determined by phosphoenzyme formation and immunoblotting. In contrast, mRNA for 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase did not decrease during starvation or in diabetes, but there was a 3-6-fold increase upon refeeding a high carbohydrate diet to starved rats or insulin treatment of diabetic rats. The decrease of the enzyme in starved or diabetic rats without associated changes in mRNA levels suggests a decrease in the rate of mRNA translation, an increase in enzyme degradation, or both. The rise in enzyme amount and mRNA for 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase with refeeding and insulin treatment suggests an insulin-dependent stimulation of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase gene expression. Northern blots of RNA from heart, brain, kidney, and skeletal muscle probed with restriction fragments of a full-length cDNA from liver showed that only skeletal muscle contained an RNA species that hybridized to any of the probes. Skeletal muscle mRNA for 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase was 2.0 kilobase pairs but in contrast to the liver message (2.2 kilobase pairs) was not regulated by refeeding.
Thyroid hormones, sympatho-adrenomedullary activity and metabolic responses have been studied in eight healthy obese subjects during modified fasting (0.8 MJ, 200 kcal/d) for 14 d, followed by hypocaloric-carbohydrate refeeding (2.4 MJ, 600 kcal/d) for 3 d. In the week preceding modified fasting, the subjects received a 7.2 MJ (1800 kcal) diet daily containing 20 mmol sodium, in order to distinguish the effects of salt depletion from those of energy restriction. Sodium (20 mmol/d) and potassium (80 mmol/d) were kept constant throughout the study. During modified fasting a low T3-high rT3 state developed; concomitantly a marked decrease in sympatho-adrenomedullary activity (assessed by 24-h urinary excretion of catecholamines) was observed. Upon refeeding plasma T3 increased and plasma rT3 decreased, but not completely to pre-fast values. Upon refeeding urinary catecholamine excretion markedly increased. A strong inverse relationship was found between the marked decrement of both thermogenic hormones and the catabolism of protein. No correlation between these parameters was found during brief refeeding. The observed decline of both thermogenic hormones may represent an adaptation to protect tissues from the catabolic effect of these substances during severe energy deficiency.
The effects of prolonged fasting and refeeding on insulin secretion were examined in seven obese non-diabetic subjects. Plasma insulin and C-peptide concentrations were measured before and after fasting for 7 days, and after refeeding with a low caloric diet. Urine C-peptide excretion during 24 h was determined daily during the study period. Plasma insulin and C-peptide levels fell by about 50 percent during fasting and returned to the prefasting values after refeeding. During fasting the 24-h urine C-peptide excretion was markedly diminished; after 7 days it was less than 10 percent of the prefasting level; on refeeding a low caloric diet, it increased significantly although not to the initial basal values. It is concluded that in human obesity pancreatic insulin secretion is markedly diminished by prolonged fasting.
The hypoglycemic agents, glibenclamide and repaglinide, when administered intragastrically to overnight fasted hereditarily diabetic animals, were found to oppose the rise in the plasma insulin/glucose ratio otherwise evoked by refeeding of the GK rats. Such was not the case after oral administration of glimepiride, despite the fact that this sulfonylurea minimized the rise in glycemia associated with refeeding. The altered restoration of a high insulin/glucose ratio in GK rats that received glibenclamide or repaglinide before refeeding suggests that these long-acting hypoglycemic agents may delay the refeeding-induced relief of the B-cell from the fasting-associated refractoriness to glucose.
OBJECTIVE: To examine metabolic responses of chronically starved horses to refeeding with 3 isoenergetic diets. DESIGN: Uncontrolled clinical trial. ANIMALS: 22 mature mixed-breed horses that were emaciated but otherwise clinically normal. PROCEDURE: Horses were fed 1 of 3 diets: alfalfa hay, oat hay, or a combination diet of half oat hay and half commercially prepared ration. Digestible energy of diets was gradually increased throughout the refeeding period. One pre- and 4 postprandial blood samples were obtained daily, and analyses included RBC count, Hct, and determination of hemoglobin, glucose, insulin, free fatty acid, total bilirubin, 2,3-diphosphoglyceric acid, phosphorus, magnesium, calcium, sodium, and potassium concentrations. Body weight, fecal output, and feed and water consumption were measured and recorded daily. Repeated-measures ANOVA was used to examine dietary and temporal (day) effects of the 3 dietary regimens during 10-day trials. RESULTS: 19 Horses survived. Three horses (2 fed alfalfa diet, 1 fed combination diet) died of metabolic or gastrointestinal problems. Increasing temporal effects in serum concentrations of glucose, insulin, magnesium, calcium, and sodium; decreasing temporal effects in serum concentrations of free fatty acid, 2,3-diphosphoglyceric acid, and phosphorus; and dietary effects in serum concentrations of glucose, insulin, magnesium, and potassium were detected in the 19 surviving horses. Serum phosphorus and free fatty acid concentrations decreased dramatically during the first 5 days of refeeding with all 3 diets. Serum magnesium concentrations increased in horses fed the alfalfa hay diet, whereas improvement was not evident in horses fed oat hay or combination diets. Horses receiving the alfalfa and oat hay diets had lower postprandial glucose and insulin concentrations than horses receiving the combination diet. Horses fed oat hay alone ate 92% of feed offered, compared with 98% feed consumption for horses fed alfalfa hay or combination diets. CLINICAL IMPLICATIONS: Clinically normal emaciated horses can be successfully rehabilitated by gradual refeeding with a high forage diet.
A case of anorexia nervosa (AN) is reported where heart failure occurred secondary to severe hypophosphatemia despite oral phosphate supplementation. We recommend starting patients with AN on oral phosphate when refeeding is begun, monitoring serum phosphate every 1 to 2 days for at least the first week of refeeding, and discontinuation of refeeding during phosphate supplementation should severe hypophosphatemia develop.
OBJECTIVE: To examine changes in plasma leptin levels and resting energy expenditure (REE) during short-term refeeding of patients with anorexia nervosa (AN). METHOD: This was a longitudinal study of 21 women meeting the DSM-IV criteria for AN who were admitted to the hospital for renutrition. Height, weight, percent body fat (assessed by skin fold thickness), REE (measured by indirect calorimetry), and circulating plasma leptin concentration were assessed at the time of admission and 7 days later. RESULTS: Over the course of 1 week of refeeding, body mass index (BMI) increased 0.75 +/- 0.15 kg/m(2) (p <.0001), body fat increased 0.9 +/- 0.2% (p <.0001), and REE increased 107 +/- 33 kcal/24 hr (p =.0037). The change in mean leptin levels was not statistically significant (0.45 +/- 0.44 ng/ml; p =.32). DISCUSSION: Leptin is unlikely responsible for the increase in REE observed with short-term refeeding.
Food deprivation blocks sexual behavior and disrupts estrous cycles in mammals. We asked whether reduced copulatory behavior, produced by limited food intake, could be reversed by brief refeeding intervals in the female musk shrew. In Experiment 1, animals were food restricted to 60% of ad lib (FR), and an additional group of FR females were refed for 90 min prior to testing (RF). Refed and ad lib (AL) fed females were significantly more likely to mate than FR females. To test the hypothesis that food-induced restoration of copulatory behavior is not the result of changes in peripheral steroids, we repeated Experiment 1 using ovariectomized and testosterone-implanted females. The results from Experiment 2 were similar to those found in the first study. Next, a more severe refeeding schedule was employed; females were restricted to 50% of ad lib intake. Females in the RF and FR groups were significantly less likely than the AL animals to mate. In the last experiment, females were food restricted to 50% and longer refeeding intervals were employed. Four and one-half hours of food intake did not reinstate sexual behavior, but females refed for 12 h were as likely to mate as ad lib fed controls. We also did not detect any differences in plasma concentrations of testosterone and cortisol in AL, FR, and RF ovary-intact animals. These results define a nutritional threshold for copulatory behavior in the musk shrew. Since this species is highly sensitive to small alterations in food intake, it is a useful model for studies of interactions between metabolic fuels and behavior.
The zonal distribution of phosphoenolpyruvate carboxykinase (PCK) and tyrosine aminotransferase (TAT) mRNA in liver was studied by in situ hybridization with radiolabelled cRNA probes and the abundance of PCK and TAT mRNA was quantified by Northern blot analysis of total RNA with biotinylated cRNA probes. Livers were taken from rats during a normal 12 h day/night rhythm, when they had access to food only during the dark period from 7 pm to 7 am, or during refeeding, when they had access to food after having been starved for 60 h. 1. Daily feeding rhythm: High levels of PCK mRNA were distributed mainly in the periportal and intermediate zone during the fasting period at noon and 6 pm. Feeding caused a rapid decrease in PCK mRNA level and a restriction of PCK mRNA localization to the periportal area within the first 2 h. No further alterations were observed during the following hours of the feeding period. TAT mRNA was distributed also in the periportal and intermediate zone during the fasting period. Feeding first reduced the mRNA level without changing the distribution pattern. Then towards the end of the feeding period TAT mRNA increased again to half-maximal levels and became restricted mainly to the periportal area. 2. Starvation-refeeding cycle: High amounts of PCK mRNA as well as of TAT mRNA were localized predominantly in the periportal and intermediate zone after 60 h of starvation. PCK and TAT mRNA both decreased markedly during the first 2 h of refeeding and then remained almost constant.(ABSTRACT TRUNCATED AT 250 WORDS)
Colon carcinoma was implanted into the mesenterium of syngeneic BD IX rats, and 10 weeks later the animals were fasted for 48 h and refed. Control animals were kept fasted for an additional 24-h period. DNA synthesis was measured in mucosal scrapings from the normal colon and in the tumor before and after refeeding. Autoradiography was used to determine the epithelial DNA synthesis index (labeling index) in the progenitor cells from normal colon mucosa, in the adenocarcinoma cells from the tumor, and in the tumor lymphocytes. DNA synthesis increased over control values in the normal mucosa in situ (p less than 0.01), and in the implanted tumor (p less than 0.05) at 16 h after refeeding. The labeling index also increased over control values in the progenitor cells from normal mucosa (p less than 0.01), and in the adenocarcinoma cells from the tumor (p less than 0.01) at 16 h after refeeding. No increase in labeling index was observed in the tumor lymphocytes. These data suggest that cell proliferation in normal colon epithelium as well as in colon adenocarcinoma cells may be stimulated by a common physiological factor released after feeding.
The mouse gallbladder epithelium was studied with light microscopic autoradiography and quantitative electron microscopy during fasting, refeeding and experimental gallstone formation. To determine the intracellular pathway of glycoproteins, H3-galactose was injected at different time intervals into the mice. At 10, 25 and 40 min after an intraperitoneal injection the gallbladders were fixed and prepared for light microscopy. As early as 10 min after injection, label was observed in supranuclear cytoplasmic regions and at 25 min, an increased radioactivity was present throughout the apical cytoplasm. At 40 min, silver grains were mainly present at the cell surface. Autoradiographs processed 25 min after an intraperitoneal H3-galactose injection after fasting for 48 h showed decreased supranuclear and apical radioactivity. After refeeding (12 h) there was an enhanced activity in both these regions. Animals fed a lithogenic diet for one month showed a marked increase of radioactive label mainly in cells of crypts and invaginations of the mouse gallbaldder mucosa. Morphometric measurements of the Golgi apparatus revealed that deprivation of food significantly dimished the volume density of the Golgi apparatus. Refeeding the amimals restored the volume density values to normal levels, In the course of gallstone formation there was a further significant increase in the volume density of the Golgi complexes as compared to controls.
Hypocaloric feeding (HCF) depresses heart function causing cardiac atrophy, bradycardia, and decreased cardiac output. We tested the hypothesis that HCF results in decreased myocardial Ca- and ATP cycling. We reduced protein-calorie intake of adult rats by 20% for 7 days and then allowed them to recover for 3 days. Changes in ionized Ca concentration (nM/s) of 2.5% myocardial homogenates that were attributable to the Ca-ATPase pump and Ca-release channel (CRC), respectively, of the sarcoplasmic reticulum (SR) were depressed 41 and 85% by HCF from 61.6 +/- 9.4 and 24.7 +/- 3.3, to 36.1 +/- 2.8 and 3.6 +/- 2.9. Activity of the Ca-pump was restored after 3 days of refeeding, whereas the CRC remained 23% depressed (all p < 0.05). Additionally, the CRC activity was inhibited to a 3-fold greater extent than controls by HCF, but was disinhibited within one day of refeeding. The greater effect on CRC than Ca-pump activity resulted in net Ca-uptake being unaffected by HCF. In addition to depression of Ca-cycling, ATP sythetase and total ATPase activities (IU/g), respectively, were depressed 20 and 15% by HCF from 174 +/- 19 and 51.3 +/- 3.8 to 140 +/- 15 and 43.7 +/- 4.7, but were restored to control values within one day of refeeding. We conclude that HCF produces a compensatory, reversible, and asymmetric downregulation and inhibition of Ca-cycling, with the CRC being preferentially affected.