SEARCH · PubMed Health

Results for “Refeeding”

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.

At least 415 records · Page 23Linked to original sources

PubMed2003

Dexamethasone blocks the refeeding-induced phosphorylation of cAMP response element-binding protein in the rat hypothalamus.

We previously reported that dexamethasone pretreatment abolishes the refeeding-induced neuronal nitric oxide synthase (nNOS) expression in the rat paraventricular nucleus (PVN). It was reported that nNOS upstream carries cAMP response element (CRE) and nNOS expression is mediated by a CRE-binding protein (CREB)-dependent mechanism. In this study, CREB phosphorylation was co-localized in the nNOS neurons of the rat PVN regardless of feeding conditions. The relative amount of phosphorylated CREB in the hypothalamic tissue lysates increased by 1 h of refeeding following 48 h of food deprivation, and interestingly, this increase was blocked by dexamethasone administration before the food onset. These results suggest that glucocorticoids exert an inhibitory role in CREB phosphorylation directed by nutritional stimuli in the rat hypothalamus, and this inhibition may be related to nNOS gene expression in this brain region.

Animals↗

PubMedDate not supplied

The importance of the refeeding syndrome.

In this review we discuss the refeeding syndrome. This potentially lethal condition can be defined as severe electrolyte and fluid shifts associated with metabolic abnormalities in malnourished patients undergoing refeeding, whether orally, enterally, or parenterally. It can be associated with significant morbidity and mortality. Clinical features are fluid-balance abnormalities, abnormal glucose metabolism, hypophosphatemia, hypomagnesemia, and hypokalemia. In addition, thiamine deficiency can occur. We describe which patient groups are more at risk for this syndrome and the clinical management of the condition.

Body Fluids↗

PubMed1978

Evidence for a role of insulin in the regulation of lipogenesis in lactating rat mammary gland. Measurements of lipogenesis in vivo and plasma hormone concentrations in response to starvation and refeeding.

Fatty acid synthesis in the mammary gland of lactating rats in vivo was 5-fold higher than in the liver. Starvation decreased fatty acid synthesis in the gland 50-fold, whereas refeeding for 2h completely reversed this change. The plasma insulin concentration decreased 2-fold in starvation and was restored to the fed-rat value on refeeding. Glucagon and prolactin concentrations did not always change in parallel with lipogenesis, suggesting that insulin may be a regulator of this process in the gland.

Animals↗

PubMed1988

Acute inhibition by ethanol of intestinal absorption of glucose and hepatic glycogen synthesis on glucose refeeding after starvation in the rat.

1. Intragastric administration of ethanol (75 mmol/kg body wt.) at 1 h before glucose refeeding of 24 h-starved rats inhibited hepatic glycogen deposition (by 69%) and synthesis (by approx. 70%), but was without significant effect on muscle glycogen deposition and synthesis. 2. Treatment of ethanol-administered rats with methylpyrazole (an inhibitor of alcohol dehydrogenase) did not significantly diminish the inhibitory effect of ethanol on hepatic glycogen deposition after glucose refeeding, suggesting that the inhibition was not dependent on ethanol metabolism. 3. Ethanol delayed and diminished intestinal glucose absorption, at least in part by delaying gastric emptying. 4. At a lower dose (10 mmol/kg body wt.), ethanol inhibited hepatic glycogen repletion and synthesis without compromising intestinal glucose absorption. Ethanol inhibited glycogen deposition (by 40%) in hepatocytes from starved rats provided with glucose + lactate + pyruvate as substrates, consistent with it having a direct effect to diminish hepatic glycogen synthesis by inhibition of gluconeogenic flux at a site(s) between phosphoenolpyruvate and triose phosphate in the pathway. 5. It is concluded that ethanol acutely impairs hepatic glycogen repletion by inhibition at at least two distinct sites, namely (a) intestinal glucose absorption and (b) hepatic gluconeogenic flux.

Animals↗

PubMed1989

Comparison of the flux of carbon to hepatic glycogen deposition and fatty acid and cholesterol synthesis on refeeding rats fed ad libitum or meal-fed rats with a chow-diet meal.

Meal-fed rats and rats fed ad libitum had similar rates of hepatic glycogen deposition on refeeding with a chow meal. In contrast, the rate of hepatic lipid synthesis (cholesterol plus fatty acids) was 6-fold higher on refeeding in the meal-fed group compared with the 'ad libitum' group. There were no significant differences in the gastrointestinal or hepatic contents of glucose or lactate between the two groups. It is suggested that in the meal-fed group exogenous glucose may be directly converted into glycogen, whereas the substrate for lipid synthesis is a C3 unit.

Adipose Tissue↗

PubMed1992

Refeeding meal-fed rats increases lipoprotein lipase activity and deposition of dietary [14C]lipid in white adipose tissue and decreases oxidation to 14CO2. The role of undernutrition.

Meal-fed (3 h) rats had a decreased food intake, body weight and carcass fat compared with rats fed ad libitum. On refeeding a chow meal containing [1-14C]triolein, the production of 14CO2 was lower (45%) and the accumulation of carcass [14C]lipid higher (37%) in the meal-fed rats. There was higher lipoprotein lipase activity and greater accumulation of [14C]lipid in the epididymal and subcutaneous adipose-tissue depots of the meal-fed rats. In contrast, heparin-releasable lipoprotein lipase was not increased in perfused hearts of meal-fed rats on refeeding. Return of meal-fed rats to feeding ad libitum reversed these changes before the restoration of body weight or carcass fat. Evidence is presented that decreased dietary intake rather than meal pattern is an important determinant of the alterations in adipose lipid metabolism in the meal-fed rat in response to a meal.

Adipose Tissue↗

PubMed1990

Role of thyroid hormones in the regulation of hepatic glucokinase and phosphoenolpyruvate-carboxykinase gene expression during the starvation-refeeding transition.

Thyroid hormones act at the transcriptional level in the induction of the important hepatic glucoregulatory enzyme PEP-carboxykinase and glucokinase (Fig. 1 and Fig. 2). They have no significant effect on the degradation of both enzymes, nor on the degradation of the specific mRNAs. A T3-receptor interaction is essential for their effect. Suggestions have been made for a thyroid hormone regulatory element in the promotor region of T3-dependent genes (for a review see [18]). Thyroid hormones probably do not determine the direction of the metabolic flux; however, they significantly enhance in a permissive way the transition from one state, e.g. starvation, to another, e.g. refeeding. And by enhancing significantly the activity of important regulatory enzymes, they enhance the flux of metabolites under different metabolic conditions, such as in starvation or after refeeding.

Animals↗

PubMed1998

Immunodeficiency associated with anorexia nervosa is secondary and improves after refeeding.

Several studies have addressed the question of starvation effects on immune function by means of changes in lymphocyte subsets, cytokine induction or lymphocyte activation. Anorexia nervosa (AN) patients are severely malnourished and contradictory results have been obtained regarding the accompanying immunodeficiency, including its assignation as a part of the primary nervous disorder. In the present work, an extensive immunological function examination was carried out on 40 AN patients who were compared with a control group of 14 healthy girls. The AN patients were also classified according to their nutritional status (by the Body Mass Index: BMI), this being critical for a better understanding of these secondary immunodeficiency bases. Moreover, another immune system study was performed on five patients after refeeding. Lymphocyte subsets and function, cytokine induction and peripheral blood concentrations, and innate as well as humoral immunity were evaluated. Deregulation in the cytokine network, owing to the interaction of the central nervous (CNS) and immune systems, seems to be the initial immune alteration in AN immunodeficiency but it has not been disproved that the immunodeficiency is a direct consequence of the original psychiatric perturbation. Spontaneous high levels of circulating interleukin-1beta (IL-1beta) and tumour necrosis factor-alpha (TNF-alpha) have been observed; this is probably one of the causes of the anomalies found in the T-cell subpopulations (mainly the naive CD4+CD45RA+ reduction and the cytotoxic CD8+ increase) and T-cell activation status (mainly the down-regulation of the CD2 and CD69 activation pathways). This finally leads to an impairment, not only in T-cell function but also in T-cell to B-cell co-operation. The AN specificity of these results is confirmed by the fact that these immune alterations improve after refeeding and when nutritional status becomes less critical, which also suggests that AN immunodeficiency is indeed secondary to malnutrition.

Adolescent↗

PubMed1983

Quantitative correlation between proteolysis and macro- and microautophagy in mouse hepatocytes during starvation and refeeding.

Cytoplasmic protein in hepatocytes is sequestered and degraded by two general classes of lysosomes, overt autophagic vacuoles (macroautophagy) and dense bodies (microautophagy). Volumes of the apparent space in each class that contain the internalized protein, together with estimates of cytoplasmic protein concentration, were used as a basis for predicting rates of protein degradation by the lysosomal system in livers of fed, 48-hr starved, and starved-refed mice. Assuming that the turnover of all sequestered protein is equal to that previously determined in overt autophagic vacuoles (0.087 min-1), we obtained close agreement between predicted and observed rates in the three conditions studied. The two autophagic components, though, exhibited different patterns of regulation. Microautophagy followed a downward course through starvation and into refeeding, a trend that explained fully the fall in absolute rates of protein degradation during starvation. By contrast, macroautophagy remained constant throughout starvation but was virtually abolished with refeeding. Whereas regulation of the latter can be explained largely by immediate responses to the supply of amino acids, present evidence together with results of others indicate that microsequestration could be linked to functional and quantitative alterations in the smooth endoplasmic reticulum. Both types of regulation contributed equally to the marked suppression of proteolysis during cytoplasmic regrowth.

Animals↗

PubMed1999

Phosphatidylinositol 3-kinase translocates onto liver endoplasmic reticulum and may account for the inhibition of glucose-6-phosphatase during refeeding.

By using a rapid procedure of isolation of microsomes, we have shown that the liver glucose-6-phosphatase activity was lowered by about 30% (p < 0.001) after refeeding for 360 min rats previously unfed for 48 h, whereas the amount of glucose-6-phosphatase protein was not lowered during the same time. The amount of the regulatory subunit (p85) and the catalytic activity of phosphatidylinositol 3-kinase (PI3K) were higher by a factor of 2.6 and 2.4, respectively (p < 0.01), in microsomes from refed as compared with fasted rats. This resulted from a translocation process because the total amount of p85 was the same in the whole liver homogenates from fasted and refed rats. The amount of insulin receptor substrate 1 (IRS1) was also higher by a factor of 2.6 in microsomes from refed rats (p < 0. 01). Microsome-bound IRS1 was only detected in p85 immunoprecipitates. These results strongly suggest that an insulin-triggered mechanism of translocation of PI3K onto microsomes occurs in the liver of rats during refeeding. This process, via the lipid products of PI3K, which are potent inhibitors of glucose-6-phosphatase (Mithieux, G., Danièle, N., Payrastre, B., and Zitoun, C. (1998) J. Biol. Chem. 273, 17-19), may account for the inhibition of the enzyme and participate to the inhibition of hepatic glucose production occurring in this situation.

Adipocytes↗

PubMed1984

Dietary components and plasma insulin responses to fasting and refeeding in genetically obese hyperglycaemic (ob/ob) mice.

To investigate the role of dietary components in the hyperinsulinaemia of the obese hyperglycaemic (ob/ob) syndrome, plasma insulin responses to fasting and refeeding were examined in Aston ob/ob mice supplied with standard diet, non-digestible-carbohydrate test food, and isoenergetic test foods from which either carbohydrate, protein or fat was omitted. During fasting, plasma insulin concentrations fell more rapidly and to a greater extent than plasma glucose. Refeeding the standard diet raised insulin concentrations above normal, associated with a 25% compensatory increase in food intake over 24 h. Test foods supplied to previously fed or fasted mice produced glucose responses consistent with the available carbohydrate content. Carbohydrate-free food (protein and fat) provided a small insulinotropic stimulus; the effect of protein-free food (carbohydrate and fat) was greater; and the combination of carbohydrate with protein (fat-free food) evoked a marked insulin response. In contrast, insulin concentrations declined in mice given the non-digestible-carbohydrate food. Consumption of the standard diet was increased after 24 h feeding non-digestible-carbohydrate food, but was unaffected by a 30 h fast initiated 54 h previously. These results demonstrate that hyperinsulinaemia in ob/ob mice is not merely triggered by the ingestion of bulk, but depends on the type of nutrient ingested. Dietary carbohydrate appears to be the major stimulus to the hyperinsulinaemia, with an important augmentation in the presence of protein. Since direct glucose stimulation of insulin release is defective in ob/ob mice, the hyperinsulinaemia must be mediated by increased activity of the enteroinsular axis.

Animals↗

PubMed1997

Effect of long-term refeeding on protein metabolism in patients with cirrhosis of the liver.

Patients with cirrhosis of the liver require an increased amount of protein to achieve N balance. However, the utilization of protein with increased protein intake, i.e. the slope from regression analysis of N balance v. intake, is highly efficient (Nielsen et al. 1995). In the present study, protein requirement and protein utilization were investigated further by measuring protein synthesis and degradation. In two separate studies, five or six patients with cirrhosis of the liver were refed on a balanced diet for an average of 2 or 4 weeks. Protein and energy intakes were doubled in both studies. Initial and final whole-body protein metabolism was measured in the fed state by primed continuous [15N]glycine infusion. Refeeding caused a statistically significant increase of about 30% in protein synthesis in both studies while protein degradation was only slightly affected. The increase in protein synthesis was associated with significant increases in plasma concentrations of total amino acids (25%), leucine (58%), isoleucine (82%), valine (72%), proline (48%) and triiodothyronine (27%) while insulin, growth hormone, insulin-like growth factor (IGF)-I and IGF-binding protein-3 were not changed significantly. The results indicate that the efficient protein utilization is due to increased protein synthesis, rather than decreased protein degradation, and suggest that increases in plasma amino acids may be responsible for the increased protein synthesis. A comparison of the patients who had a normal protein requirement with the patients who had an increased protein requirement suggests that the increased protein requirement is due to a primary increase in protein degradation. It is speculated that this is due to low levels of IGF-I secondary to impaired liver function, since initial plasma concentration of IGF-I was about 25% of control values and remained low during refeeding.

Dietary Proteins↗

PubMed2001

Refeeding the patient with anorexia nervosa.

Successful treatment of persons with anorexia nervosa is possible when a multidisciplinary team consisting of a mental health professional, a dietician, and a medical professional with expertise in eating disorders direct treatment. One of the primary goals of treatment is the restoration of weight. Refeeding by oral, enteral, or parenteral routes is a cornerstone of treatment but must be under-taken with care in order to avoid the widespread dysfunction associated with the refeeding syndrome.

Journal Article↗

PubMed1982

Refeeding after fasting in the rat: energy substrate fluxes and replenishment of energy stores.

Rats were fasted and refed and concentrations of plasma glucose, glycerol, triglyceride, insulin, and glucagon as well as glucose kinetics after injection of labeled glucose and glycerol were determined. In addition, concentrations and synthesis in vivo (from tritiated water) and in vitro of glycogen, triglycerides, and protein were followed in liver, muscle, and adipose tissues. The refeeding state after fasting was characterized by a decrease in glucose and triglyceride concentrations in plasma. Glucose turnover rate was increased. Protein losses were repleted, first in the liver then in muscle tissue. Synthesis of glycogen and lipid increased above control in liver and adipose tissue. These results are compatible with an increased outflux during refeeding of different energy substrates from plasma into the depleted protein and energy stores to an extent causing lower concentration of these substrates. Such phenomena might be of importance for energy intake regulation during the phase.

Adipose Tissue↗

PubMed1983

Refeeding after fasting in the rat: effects of dietary-induced obesity on energy balance regulation.

Obesity was induced in male Sprague-Dawley rats by overfeeding a cafeteria-style diet. The obesity was characterized by both adipocyte hypertrophy and hyperplasia. Body weight was then reduced by starvation to match that of control animals that had been fed ordinary Purina Chow. The previously obese rats were then refed to match the same body weight as controls, or given the same amount of Purina Chow as consumed by the controls. This resulted in a remaining moderate obesity, now due only to adipocyte hyperplasia with normal fat cell size. The previously obese rats needed less energy to keep their body weight equal to controls, and they spontaneously ate less than controls. They were, however, less food efficient because they did not accumulate as much energy in fat and protein depots during the period of refeeding as the controls did, and consequently must have transformed more energy into heat. This is in sharp contrast to nonobese animals subjected to a similar experimental procedure. Lipogenic enzymes and lipoprotein lipase activity in adipose tissue as well as plasma insulin concentrations were elevated in overfed rats but normalized during refeeding of Chow after fasting.

Adipose Tissue↗

PubMed1983

A comparison between muscle function and body composition in anorexia nervosa: the effect of refeeding.

Skeletal muscle function, body composition (total body nitrogen and total body potassium) and standard parameters of nutritional assessment were measured in six severely depleted patients with primary anorexia nervosa, both on admission and during oral refeeding. The function of the adductor pollicis muscle was assessed by electrical stimulation of the ulnar nerve. On admission muscle function was markedly abnormal in the patients with anorexia nervosa (n = 6) compared with normal subjects (n = 22), with a significant increase in the force of contraction at 10 Hz, with a mean +/- SEM of 48.0 +/- 3.7% and 28.8 +/- 1.2%, respectively (p less than 0.001). There was slowing of the maximal relaxation rate, 6.6 +/- 0.6% and 9.6 +/- 0.2%, respectively (p less than 0.001) and increased muscle fatigue 18.6 +/- 5.9% and 3.5 +/- 0.8%, respectively (p less than 0.01). Initially, the mean serum albumin was normal (4.0 +/- 0.1 g/dl), although there was evidence of severe depletion of somatic protein stores, with a low total body nitrogen and creatinine-height index. Within 4 wk of oral refeeding, maximal relaxation rate and muscle fatigability were restored to normal, and within 8 wk all parameters of muscle function were normal. During the study total body nitrogen increased by only 13% and was still 19.4% below the predicted normal total body nitrogen, whereas total body potassium increased by 32% and body fat by 46%. Normalization of muscle function may be related to restoration of muscle electrolytes rather than repletion of body nitrogen.

Adult↗

PubMed1990

Aggressive oral refeeding in hospitalized patients.

Malnutrition is an important clinical condition leading to increased morbidity and mortality. This report describes an aggressive oral refeeding program of high-caloric foods, which was instituted in severely anorectic patients because of their refusal to eat meals or supplements. After ascertaining a patient's favorite sweet, hospital personnel and family collaborated in providing the food. Frequently, sweets were the patient's only intake for weeks. We saw a gradual return of appetite, inclusion of other foods in the diet, and overall clinical improvement in comorbid conditions. These cases suggest that aggressive oral refeeding with high-caloric foods is an underutilized therapy for multiply impaired elderly patients.

Aged↗

PubMed1991

Altered maturation of small intestinal function in the absence of intraluminal nutrients: rapid normalization with refeeding.

The absence of intraluminal nutrients during weaning in rats was shown to result in altered intestinal growth and maturation. In this study intestinal length, mucosal weight, DNA, protein, and total disaccharidase activities were significantly lower in animals sustained by intravenous nutrients over the normal weaning age than were normally weaned controls but were greater than preweaning values. Absorptive capacity for sucrose (assessed by hydrogen-gas production) was diminished, directly linking incomplete maturation of sucrase to diminished intestinal function. To determine whether these alterations were permanent, rats previously deprived of intraluminal nutrients over the weaning period were refed. Eight days after refeeding, all variables except total lactase had attained values found in normally weaned age-matched controls, including absorptive capacity for sucrose. Although intestinal growth and maturation is abnormal in the absence of intraluminal nutrients during weaning, the abnormalities are not permanent and are rapidly corrected upon refeeding.

Animals↗