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PubMed1977

Metabolic responses to prolonged fasting and subsequent refeeding in the pig.

Metabolic responses associated with prolonged fasting and subsequent refeeding of pigs were investigated. Fasting for 14 or 28 days produced significant increases in serum levels of alanine, aspartic and glutamic acid in the three branched-chain amino acids. Glycine, serine and lysine levels were elevated after 28 days of fasting while the levels of histidine, methionine, threonine and phenylalanine were reduced. Fasting markedly stimulated hepatic and renal gluconeogenesis and the activity of the urea cycle enzymes. Fatty acid synthesis and glucose oxidation were virtually abolished in hepatic and adipose tissue in pigs subjected to a 14- or 28-day fast. After the first day of refeeding, the levels of amino acids returned to the control values. The activity of the hepatic urea cycle enzymes, fructose-1,6-diphosphatase and phosphoenolpyruvate carboxykinase remained elevated after the first day of refeeding but returned to the control levels thereafter. The activity of hepatic glucose-6-phosphate dehydrogenase, malic dehydrogenase and acetyl CoA carboxylase were slightly enhanced in pigs refed for 4 and 8 days. The activity of these enzymes in adipose tissue was enhanced 8 days after refeeding. Hepatic synthesis of fatty acids from glucose was slightly stimulated in refed pigs on days 4 and 8 but returned to control values on day 16. Refeeding did not enhance glucose incorporation into fatty acids in adipose tissue above the values observed in fed controls.

Amino Acids↗

PubMed2000

Acute starvation and subsequent refeeding affect lymphocyte subsets and proliferation in cats.

Although the early identification of patients with suboptimal nutritional status can allow the implementation of nutritional intervention to enhance the ability of the body to fight infection and disease, currently no definitive test of nutritional status exists. Therefore, this study was conducted to identify possible functional indicators of acute nutritional deprivation. The effects of total nutritional deprivation and subsequent refeeding on lymphocyte functions and subpopulations were examined in 23 healthy cats. Peripheral blood samples were analyzed at various times during food deprivation and refeeding periods. During the food deprivation period, decreases were observed in leukocyte number (P: < 0.05), lymphocyte number (P: < 0.05), percentage of CD4(+) cells [before stimulation with concanavalin-A (Con-A); P: < 0.05] and the CD4/CD8 ratio (before stimulation with Con-A; P: < 0.01) compared with d 0. Increases were observed in the percentage of CD8(+) cells [before (P: < 0.05) and after (P: < 0.01) stimulation with Con-A] and in intracellular calcium (P: < 0.01) during acute starvation. During the refeeding period, increases were observed in the percentage of CD4(+) cells (before and after stimulation with Con-A; P: < 0.01), the percentage of CD8(+) cells (before stimulation with Con-A; P: < 0.05) and lymphocyte number (P: < 0.05) compared with d 7. Lymphocyte proliferative capacity tended to decrease (P: = 0.07) during starvation and increased (P: < 0.01) during the refeeding period. These findings suggest that a 7-d starvation period had immunosuppressive effects on cats and that these effects were not completely normalized during 7 d of refeeding. CD4(+)/CD8(+) subset alterations and CD4/CD8 ratio in conjunction with lymphocyte proliferation may be useful as indices of nutritional status.

Animals↗

PubMed2003

Refeeding and insulin regulate S6K1 activity in chicken skeletal muscles.

Broiler chickens are characterized by fast muscle growth and high protein deposition, most likely subsequent to a high protein synthesis. However, the regulation of protein synthesis in chicken muscle is still unknown. In contrast, it has been clearly demonstrated in mammals that S6K1 is a key regulator of protein synthesis. In the present study, S6K1 was characterized in both pectoralis and gastrocnemius muscles in chickens. A 133-bp fragment of chicken S6K1 cDNA had 84% identity to mammalian S6K1. We investigated in vivo the effects of refeeding and insulin treatment after 16 h starvation. S6K1 enzyme activity was significantly increased in both pectoralis and gastrocnemius muscles by refeeding (two- to threefold greater than in food-deprived chickens, P < 0.05). Optimal activation occurred 30 min after refeeding following 16 h starvation. S6K1 activation was associated with its phosphorylation on serine and Thr 389 residues, which occurred within the first 5 min of refeeding. S6K1 was also significantly stimulated in both pectoralis and gastrocnemius muscles after a single insulin injection (nine- to 12-fold greater than in control chickens, P < 0.001). Our results indicate that S6K1 is expressed in chickens muscles and activated by refeeding and insulin treatment.

Animals↗

PubMed2004

Nocturnal nasogastric refeeding for hospitalized adolescent boys with anorexia nervosa.

Boys with anorexia nervosa have nutritional needs exceeding those of their female counterparts. For many males with anorexia nervosa, oral refeeding alone may result in low discharge weight, a critical risk factor in relapse. This study compared the short-term outcomes of oral refeeding (OR) and a combination of OR with supplemental nocturnal nasogastric refeeding (NNGR) in a sample of hospitalized boys. This was a retrospective chart review with a cohort design. Subjects were partitioned into: The OR group (n = 8, mean age = 14.9, SD = 1.7) and the OR + NNGR group (n = 6, mean age = 13.8, SD = 2.0). The NNGR group had greater increase in weight and Body Mass Index. Their average length of hospitalization was also shorter. Nocturnal nasogastric refeeding, complementing oral refeeding, should be considered as an alternative initial therapy for weight restoration in males with anorexia nervosa.

Adolescent↗

PubMedDate not supplied

Effect of zinc level in the refeeding diet in previously starved rats on plasma somatomedin C levels.

White male growing rats were fed rat chow diet for 4 days after which they were fasted for 72 h. At the end of fasting, rats were allotted into four dietary treatments that varied only in the level of zinc (Zn): Zn-deficient group (ZnD), 30, 90, and 140 ppm of Zn. A group of eight rats were not fasted and were fed the rat chow diet throughout the experimental period. Blood was obtained at intervals from all groups for the measurements of Zn and somatomedin C (SMC) in the plasma. Eight rats were randomly selected at zero time (t0) and at the end of fasting period were killed for the measurement of tibia Zn. At the end of refeeding, all rats were killed for tibia Zn determination as well. Results showed that plasma SMC decreased to the hypopituitary level at the 3rd day of fasting. At 48 and 72 h of refeeding, the levels of plasma SMC increased significantly in all experimental groups and the differences among groups were not significant. The levels of SMC in groups fed 140 and 90 ppm of Zn continued to increase significantly with progressive refeeding. However, in groups fed 30 ppm and ZnD diets the levels of SMC started to decline after 72 h of refeeding. The levels of plasma Zn followed similar trend as SMC levels. In addition, the levels of Zn in the tibia were comparable in all groups with SMC and plasma Zn levels at the end of fasting or refeeding period. Previous reports showed that plasma SMC level is a more reliable index used to monitor nutritional responses; thus, it could be concluded that the level of Zn in the diet should be considered carefully when planning nutritional intervention for severe malnutrition or starvation.

Animal Feed↗

PubMed2004

Mucous fistula refeeding in premature neonates with enterostomies.

BACKGROUND: Premature neonates with short bowel syndrome often have diverting enterostomies and distal mucous fistulae. The authors reviewed their experience in 12 premature neonates in whom proximal bowel contents were re-fed into the mucous fistula. METHODS: We reviewed the records of 12 premature neonates who presented with acute abdomen and who underwent intestinal resection with formation of diverting enterostomy and mucous fistula between July 1999 and December 2002. All received parenteral nutrition. Refeeding of enterostomy contents into the distal mucous fistula was commenced after patency of the distal intestine was confirmed by radiologic examination. Demographic data, body weight and clinical outcomes were recorded. RESULTS: Median gestational age was 31 weeks and mean birth weight was 1.59 kg. Diagnoses included necrotizing enterocolitis (n = 6), meconium ileus-like conditions (n = 2), ileal atresia (n = 2), malrotation with volvulus (n = 1) and focal intestinal perforation (n = 1). Refeeding was successfully established in all patients with no complications. The mean duration of refeeding was 63.5 days. All patients achieved good weight gain after refeeding (18.9 +/- 2.9 g/d) with a reduction of parenteral nutrition requirements. All enterostomies were subsequently closed. Four patients died of unrelated causes after reanastomosis and the remaining eight were discharged. CONCLUSIONS: Mucous fistula refeeding is safe in premature neonates with enterostomies. It can prevent disuse atrophy in the distal loop and facilitate subsequent reanastomosis. Furthermore, the increased absorptive function provided by the small bowel incorporated in the mucous fistula can reduce the requirement for total parenteral nutrition.

Enterostomy↗

PubMed2006

The effects of undernutrition and refeeding on metabolism and digestive function.

PURPOSE OF REVIEW: An intimate interrelationship exists between nutritional status and gut function. This review focuses on the consequences of a poor nutritional state on metabolism and digestive function, and evaluates the effects of refeeding. RECENT FINDINGS: Severe undernutrition has been associated with increased fat and protein catabolism, reflected by a decreased respiratory quotient. Resting energy expenditure assessed in relationship to body weight was increased, probably as a consequence of changes in body composition. Protein synthesis, expressed per kg body weight, was decreased in undernourished patients with coexistent disease, but not in anorexia nervosa patients, indicating the detrimental effects of disease states. Severe undernutrition is associated with malabsorption, which improves following refeeding. Despite a high prevalence of villous atrophy in the duodenal mucosa in undernourished patients, mucosal protein fractional synthesis rates appeared normal. Refeeding resulted in a potent trophic response, and normalization of the mucosal morphology. Gastric and pancreatic secretion was significantly impaired by the undernourished state, with significant improvement following refeeding. SUMMARY: Undernutrition is associated with impairment of digestive function, which is likely to further aggravate the nutritional state. Refeeding corrects this dysfunction, and results in disruption of this vicious circle.

Basal Metabolism↗

PubMed2002

Acute alcohol administration inhibits the refeeding response after starvation in rat skeletal muscle.

This study determined whether an acute alcohol dose could inhibit the refeeding response in starved muscle. Rats starved for 24 h were pretreated with alcohol or saline before refeeding by intragastric or intravenous infusion of enteral diet (ENT), total parenteral nutrition (TPN), or saline. Refeeding by TPN or ENT stimulated increases in the fractional rate of protein synthesis (k(s)) in skeletal muscle. Alcohol prevented the increase in k(s) when refeeding occurred intragastrically (TPN or ENT) (P < 0.001) but not intravenously (TPN). Upon intragastric refeeding, alcohol inhibited the increase in both eukaryotic initiation factor 4E-binding protein-1 (4E-BP1) and p70 S6 kinase (p70(S6K)) phosphorylation in plantaris but caused only partial inhibition in soleus muscle (ENT only). When rats were refed intravenously, alcohol had no effect on the increased 4E-BP1 or p70(S6K) phosphorylation in either muscle. Plasma insulin levels were augmented by alcohol. Alcohol-related changes in plasma amino acid concentrations were similar irrespective of the route of feeding, whereas IGF-I levels showed differential changes. This is the first study to demonstrate that acute alcohol ingestion impedes the starved-to-fed response in skeletal muscle.

Amino Acids↗

PubMed1990

Role of corticosterone in adaptive changes in energy expenditure during refeeding after low calorie intake.

We examined the importance of corticosterone in elevated efficiency of energy utilization during refeeding after low food consumption. Energy balance studies during refeeding (over periods of 14 or 16 days) were conducted in rats previously food restricted for 16 days at 50% of normal food intake. Comparisons made with nonrestricted weight-matched controls after validation studies indicated that 2-wk-younger weight-matched controls had similar maintenance energy requirements and similar efficiency of energy utilization above maintenance (i.e., net efficiency) to nonrestricted age-matched controls. Results indicate that relative to controls refeeding after low food consumption was associated with enhanced energy conservation underlain by a 16-18% reduction (P less than 0.001) in total energy expenditure over a 14-day period. This metabolic adaptation for energy conservation resulted in a threefold increase (P less than 0.001) in body fat accretion but no difference in body protein deposition. Bilateral adrenalectomy (ADX) 2 days before refeeding reduced differences in energy expenditure between refed group and controls from 18 to 8% (P less than 0.01) and attenuated body fat gain from a three- to twofold increase (P less than 0.001) above control group. Effects of ADX were prevented by daily corticosterone replacement. Data suggest that after a period of low calorie intake an adaptive neurohormonal switching mechanism facilitates replenishment of fat stores during refeeding. This metabolic reorientation (characterized by an adaptive fall in energy expenditure) has both an adrenal as well as a nonadrenal component, because it is partially reversed by prior bilateral ADX, an effect attributed to removal of corticosterone-induced inhibition of thermogenesis.

Adrenalectomy↗

PubMed2002

Hypothalamic NPY, AGRP, and POMC mRNA responses to leptin and refeeding in mice.

Food deprivation (FD) increases hypothalamic neuropeptide Y (NPY) and agouti-related protein (AGRP) mRNA levels and decreases proopiomelanocortin (POMC) mRNA levels; refeeding restores these levels. We determined the time course of changes in hypothalamic NPY, AGRP, and POMC mRNA levels on refeeding after 24 h FD in C57BL mice by in situ hybridization. After 24 h deprivation, mice were refed with either chow or a palatable mash containing no calories or were injected with murine leptin (100 microg) without food. Mice were perfused 2 or 6 h after treatment. Food deprivation increased hypothalamic NPY mRNA (108 +/- 6%) and AGRP mRNA (78 +/- 7%) and decreased hypothalamic POMC mRNA (-15 +/- 1%). Refeeding for 6 h, but not 2 h, was sufficient to reduce (but not restore) NPY mRNA, did not affect AGRP mRNA, and restored POMC mRNA levels to ad libitum control levels. Intake of the noncaloric mash had no effect on mRNA levels, and leptin administration after deprivation (at a dose sufficient to reduce refeeding in FD mice) was not sufficient to affect mRNA levels. These results suggest that gradual postabsorptive events subsequent to refeeding are required for the restoration of peptide mRNA to baseline levels after food deprivation in mice.

Agouti-Related Protein↗

PubMed2005

Long-Evans and Sprague-Dawley rats exhibit divergent responses to refeeding after caloric restriction.

Mature male Sprague-Dawley (SD) and Long-Evans (LE) rats were instrumented with telemetry transmitters for measurement of heart rate (HR) and housed in room calorimeters for assessment of food intake and oxygen consumption (Vo(2)) at standard laboratory temperatures (23 degrees C) to examine physiological responses to caloric restriction (CR; 60% of baseline ad libitum calories for 2 wk) and refeeding. Ad libitum controls had stable food intake (84-88 kcal/day) and gained weight at rates of 3-4 g/day. Groups from both strains assigned to CR exhibited similar patterns of weight loss and reductions in Vo(2) and HR. Upon refeeding, SD rats exhibited a mild, transient hyperphagic response (1 day) accompanied by sustained suppression of Vo(2) and HR that remained evident 8 days after refeeding. In contrast, LE rats exhibited sustained daily hyperphagia that persisted 8 days after refeeding and was accompanied by a complete restoration of HR and Vo(2). The lower HR and Vo(2) observed during refeeding in SD rats were not due to reduced locomotor activity. The results reveal a strain-dependent divergent response to recovery from CR. We conclude that during recovery from CR, homeostatic stimulation of appetite or suppression of energy expenditure may occur selectively to restore body weight.

Animals↗

PubMed1983

Metabolic responses to fasting and refeeding in lean and genetically obese rats.

Injection of norepinephrine (NE) (25 micrograms/100 g body wt) caused a similar rise in metabolic rate in lean and obese (fa/fa) Zucker rats, but 3-day fasting suppressed the response in lean rats and enhanced the rise in obese mutants. Triiodothyronine (T3) injection (10 micrograms/100 g body wt) caused a significantly greater rise in oxygen consumption (Vo2) in obese than lean rats, but the response was attenuated by fasting in all animals. The thermic response to a single meal of either mixed composition, carbohydrate, or protein (40 kJ) was much smaller in obese rats than lean, but the response to the mixed nutrient meal was similar for all rats after a 3-day fast. Refeeding 3-day fasted lean rats with a single carbohydrate meal (40 kJ) caused a rise in plasma T3 levels after 3 h and a delayed increase in metabolic rate 24 h later. Injection of NE instead of refeeding caused a similar delayed rise in metabolic rate. Carbohydrate refeeding had no effect on plasma T3 levels or oxygen consumption in 3-day fasted obese Zuckers, but injection of NE did produce a significant increase in metabolic rate after 24 h. Refeeding 3-day fasted rats with protein (40 kJ) caused a rise in oxygen consumption 24 h later in lean animals but had no effect in obese animals. The data from lean Zucker rats confirm previous findings in Sprague-Dawley rats and suggest that the thermic response to refeeding involves a complex interaction between the sympathetic nervous system and thyroid hormones. Obese Zuckers responded normally to NE and T3, indicating that their reduced thermogenesis after food may be due to insensitivity to nutrient availability or an inability to activate the sympathetic nervous system.

Animals↗

PubMed1994

Changes in brown adipose tissue composition during fasting and refeeding of diet-induced obese mice.

The objective of this work was to evaluate how obesity would influence the changes in brown fat (BAT) thermogenic capacity during fasting-refeeding. Mice fed either chow or chow + high-fat supplement for 6 wk had body weights of 34 +/- 1 and 43 +/- 1 g, respectively. They were fasted for 48 h followed by ad libitum refeeding for up to 5 days. Loss of carcass fat was similar between food-deprived mice previously fed chow or chow + high-fat supplement. However, even after a 48-h fast, obese mice still had a carcass fat content much greater than that of chow-fed mice. Brown fat atrophy caused by food deprivation was characterized by reductions in tissue weight, fat, mitochondrial proteins and uncoupling protein (UCP), without change in tissue DNA. Obesity did not alter the rate or extent of brown fat atrophy. Upon refeeding 48-h-fasted lean and obese mice, there was recovery of BAT thermogenic capacity that was similar between the two groups. In chow-fed mice, an intact neural input was essential for recovery of BAT thermogenic capacity during refeeding. These results indicate that food deprivation triggers an immediate adaptive response in mice previously fed chow or chow + a high-fat supplement and that reduction in brown fat thermogenic capacity during fasting and its recovery during refeeding appear little affected by the size of the animal energy reserves.

Adipose Tissue, Brown↗

PubMed2004

Efficacy of lanreotide 30 mg on prevention of pain relapse after oral refeeding in patients with necrotizing acute pancreatitis. A phase II prospective multicentre study.

BACKGROUND: Pain relapse after oral refeeding occurs in 21% of the patients with acute pancreatitis, and in 35% of those with CT Balthazar's score > or =D [Gut 1997;40:262]. Somatostatin analogues may decrease the pain relapse rate by inhibiting exocrine pancreatic secretion. AIMS, PATIENTS AND METHODS: To assess the frequency of pain relapse in patients with acute necrotizing pancreatitis after treatment with one intramuscular injection of lanreotide 30 mg on the day before refeeding. The refeeding procedure was standardized and progressive. RESULTS: 23 patients were included in 4 centres. Acute pancreatitis was alcoholic (n = 11), biliary (n = 7), other (n = 5). Twelve patients had > or =3 Ranson's criteria. Balthazar's score (1985) was D or E in 7 and 16 patients, respectively. Median duration of pain and of interruption of oral feeding were 11 (3-23) and 16 (5-34) days, respectively. Median hospital stay was 22 (9-41) days. Only 1 patient (4.3 %) had pain occurring 3 days after refeeding. CONCLUSION: Pain relapse occurred in 4.3% of patients pretreated with the somatostatin analogue lanreotide, and this figure is lower than the expected 35% rate which was previously reported without preventive treatment. This suggests that one intramuscular injection of lanreotide 30 mg on the day before refeeding could decrease pain relapse in patients with acute necrotizing pancreatitis, but has to be confirmed in a phase III study.

Acute Disease↗

PubMed1994

Refeeding hypertension in obese spontaneously hypertensive rats.

Very-low-calorie diets lower blood pressure acutely in obese humans and rats. However, refeeding after dietary restriction produces mild hypertension in rats. Refeeding hypertension was characterized in genetically obese spontaneously hypertensive rats (obese SHR, Koletsky rat), a model of genetic obesity and hypertension. Obese SHR were fed a restricted diet (Optifast) for 12 days, refed ad libitum for 28 days, dieted again for 12 days, and then refed 4 days and killed. Control obese SHR and lean SHR littermates were fed ad libitum continuously. Dietary restriction led to rapid weight loss followed by prompt regain to baseline weight after return to unrestricted food intake. Heart rate fell with institution of the low-calorie diet and returned to baseline on refeeding. Blood pressure became elevated during refeeding in dieted obese SHR relative to ad libitum fed obese SHR controls. The fall in blood pressure after ganglionic blockade with chlorisondamine was exaggerated in refed obese SHR, and cardiac beta-adrenergic receptors were downregulated. Both of these findings imply increased sympathetic tone. The left ventricular wall was thicker in the refed obese SHR than in the ad libitum fed obese SHR. Shorter cycles of weight loss and regain in lean SHR led to transient increases in blood pressure and heart rate. Cycles of dietary restriction and refeeding in obese SHR elicit sustained blood pressure elevation via sympathetic activation and exacerbate cardiac hypertrophy. Drastic fluctuations in nutrient intake may not be advantageous in hypertension.

Animals↗

PubMed2003

Refeeding syndrome in hospitalized pediatric patients.

Refeeding syndrome has been well documented over the years, primarily through case reports and literature reviews. Awareness of refeeding syndrome is crucial in preventing the occurrence of, and the metabolic and physiologic complications associated with, aggressive nutrition support in malnourished populations. Once compromised patients have been identified to be at risk of refeeding syndrome, nutrition rehabilitation should be cautiously initiated. We have found a lack of clinical validation for instituting nutrition support in high-risk pediatric patients who may develop refeeding syndrome. The purposes of our investigation were to determine the incidence of refeeding syndrome in pediatric hospitalized patients beginning on parenteral nutrition and to determine how consistently the Department of Clinical Nutrition standards of care for screening and prevention were followed at our institution.

Journal Article↗

PubMedDate not supplied

Brief refeeding rapidly reverses dietary restriction-induced nuclear factor-kappaB downregulation in peritoneal resident cells.

BACKGROUND: Malnutrition impairs host immunity, resulting in high mortality and morbidity, secondary to infections. Nuclear factor kappaB (NFkappaB) plays a critical role in host defense, but how quickly refeeding normalizes the impaired NFkappaB activity in peritoneal resident cells (PRCs) is unknown. Our aim was to investigate the effects of 1-day ad libitum refeeding on severe diet restriction-induced NFkappaB activity in PRCs. METHODS: Mice received chow, 146 g/kg per day (ad libitum) or 36.5 g/kg per day (severe diet restriction), for 7 days. One-half the mice in the diet-restricted group were then fed ad libitum for 1 day (refeeding). PRCs were harvested by peritoneal lavage. After incubation with tumor necrosis factor-alpha (TNF-alpha), nuclear translocation of NFkappaB in PRCs was investigated using laser scanning cytometry. RESULTS: The main subpopulation of PRCs was macrophages in all groups. Mean fluorescence intensity over the nuclear area at 0 or 100 ng/mL of TNF-alpha was 16 +/- 2 or 31 +/- 8* in the ad libitum, 20 +/- 4 or 19 +/- 3 in the severe diet-restricted, and 20 +/- 4 or 30 +/- 5* in the refeeding group, respectively (*p < .05 versus 0 ng/mL of TNF-alpha in each group versus 100 ng/mL of TNF-alpha in diet-restricted group). Cytoplasmic accumulation of NFkappaB was significantly increased after TNF-alpha stimulation in the refed group but not in the ad libitum group. CONCLUSIONS: The blunted NFkappaB activity in PRCs, after exposure to inflammatory stimuli, was restored after 1 day of refeeding, with increased accumulation of NFkappaB in the cytoplasm. Even brief nutritional replenishment in malnutrition may improve host defense by restoring NFkappaB activity and thereby improving macrophage functions.

Animals↗

PubMedDate not supplied

Cardiac function during protein malnutrition and refeeding in the isolated rat heart.

In an attempt to elucidate the effect of protein restriction and subsequent refeeding on cardiac muscle function, 133 rat hearts were studied on a Langendorff perfusion apparatus: 19 normal controls, 55 rats during 6 weeks of protein restriction, and 59 rats during 6 weeks of refeeding following starvation. During starvation animals lost 14.3% of body weight and 12.8% in heart weight, both to be gained upon refeeding. Both developed force and force velocity tended to decrease in starving rats compared to control or refeeding rats. This trend was present at time 0, but more so after 60 min of perfusion. Furthermore, these differences became even more obvious and significantly different at the higher heart rates of 300 and 400 beats/min, and less so at 100 or 200 beats/min. These protein malnutrition-associated cardiac function derangements reversed almost completely to normal upon refeeding.

Animals↗