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PubMed1984

The Golgi apparatus and lysosomes of rat pancreatic acinar cells following refeeding.

The short term effects of refeeding on the Golgi apparatus and lysosomes of the rat exocrine pancreas were evaluated by ultrastructural, morphometric and cytochemical methods. Ten minutes after refeeding, there was a significant enlargement of Golgi cisternae and a significant increase, compared with the controls, in the number of condensing vacuoles and lysosomes. These modifications were accompanied by the appearance of acid phosphatase activity in stacked Golgi cisternae (as well as GERL) of some cells. One hour after refeeding, there were about the same numbers of condensing vacuoles and lysosomes as in the controls; Golgi cisternae were still significantly enlarged, compared with the controls, but they were no longer reactive for acid phosphatase. In both fasting and refed animals, acid phosphatase activity was demonstrable in tubular lysosomes. The data are interpreted in terms both of membrane disposal and recycling, leading to enhanced formation of zymogen granules, during physiologically stimulated secretion.

Acid Phosphatase↗

PubMed1995

Predominant periportal expression of the fructose 1,6-bisphosphatase gene in rat liver: dynamics during the daily feeding rhythm and starvation-refeeding cycle.

Expression of the gene of the key gluconeogenic enzyme fructose 1,6-bisphosphatase (FBPase) was studied in rat liver during the daily feeding cycle and during refeeding after starvation. Total abundance of FBPase mRNA could be quantified by Northern blotting analysis with a digoxigenin-labelled 40-mer oligonucleotide probe. The zonal localization could not be demonstrated by in situ hybridization under several varied conditions with the 32P-end-labelled oligonucleotide probably due to insufficient sensitivity but was demonstrated with a 35S-labelled cRNA probe; the latter was synthesized from a polymerase chain reaction (PCR)-amplified 751 bp cDNA fragment inserted into a pBluescript. During a normal 12:12 h day/night rhythm (darkness with feeding from 1900 to 0700 hours), the total amount of FBPase mRNA stayed almost the same throughout the whole day. After 60 h of starvation the FBPase mRNA level decreased from a maximum at 1800 hours by approximately one-third at the end of refeeding at 0700 hours. Both during the normal feeding rhythm, after 60 h of starvation and during refeeding, i.e. under all conditions, FBPase mRNA was predominantly distributed in the periportal zone. The results clearly show that the preferentially periportal distribution of the FBPase enzyme activity is controlled mainly at a pretranslational level.

Animals↗

PubMed2003

Changes in glucose, glycogen, thyroid activity and hypothalamic catecholamines in tench by starvation and refeeding.

The effects of short-term food deprivation (7 days) and refeeding (2 days) on different biochemical and neuroendocrine parameters were studied in tench. A 7-days fast resulted in a significant reduction of plasma glucose and glycogen hepatic content, supporting the key role of liver glycogen as energy depot for being consumed during fasting. The rapid recovery of normal values of blood glucose and glycogen stores by refeeding indicates a rapid replenishment of liver glycogen stores. The short-term starvation decreased circulating thyroid hormones (both T3 and T4) and T4 release from thyroid, supporting an interaction between nutritional state and thyroid function in tench. All these metabolic and hormonal changes were partial or totally reversed under refeeding conditions. An increase in hypothalamic content of norepinephrine and dopamine was found in fasted fish. This result might be a consequence of stress induced by starvation.

Analysis of Variance↗

PubMed1986

Inability of glucagon to regulate glycogen metabolism in rat hepatocytes isolated after fasting and refeeding high-carbohydrate diets.

Studies are described which demonstrate that the ability of glucagon, epinephrine, and dibutyryl-cAMP to stimulate glycogenolysis is impaired in rat hepatocytes isolated from animals starved for 24 h and then refed a sucrose-rich diet or refed standard rat chow. The impaired regulation of glycogenolysis by glucagon was observed within 24 h after refeeding and persisted for at least 3 days. The inability of glucagon to stimulate glycogen breakdown in the refed condition appeared to be due to a suppressed activation of glycogen phosphorylase and phosphorylase b kinase by the hormone. The capacity of glucagon to regulate pyruvate kinase and glycolysis was not altered by refeeding, suggesting that the defect lies beyond interaction of the hormone at its receptor. Prolonged incubation of hepatocytes from refed rats was accompanied by depletion of glycogen reserves and was accompanied by restoration of hormonal stimulation of glycogenolysis. Addition of glycogen to cell-free extracts was found to inhibit phosphorylase b kinase but not phosphorylase. The findings of this investigation are consistent with the interpretation that high levels of glycogen present of liver after refeeding may lead to a diminished activity of phosphorylase b kinase and its hormonal regulation.

Animals↗

PubMed1992

Prospective evaluation of immediate versus delayed refeeding and prognostic value of endoscopy in patients with upper gastrointestinal hemorrhage.

The effects of immediate vs. delayed refeeding and the prognostic value of endoscopic findings in patients with major upper gastrointestinal hemorrhage were assessed in a prospective randomized study. Entry criteria were clinical evidence of major hemorrhage and endoscopic evidence of a Mallory-Weiss tear or an ulcer with a clean base, flat spot, or clot. Two hundred fifty-eight patients were randomly assigned to groups receiving a regular diet immediately or nothing by mouth for 36 hours, then clear liquids for 12 hours, and a regular diet thereafter. Outcomes in the immediate and delayed refeeding groups were comparable: rebleeding occurred in 4% vs. 5%; urgent intervention, 2% vs. 2%; and deaths, 1% vs. 1%, respectively. Rebleeding occurred in 2 (2%) of 96 patients with cleanbased ulcers, 5 (8%) of 65 with ulcers with spots, 3 (14%) of 21 with ulcers with clots (P = 0.05, 3 x 2 chi2 test), and 1 (2%) of 66 with Mallory-Weiss tears. It is concluded that the time of refeeding does not influence the hospital course of patients with a low risk of recurrent bleeding. Patients with clean-based ulcers or nonbleeding Mallory-Weiss tears may be refed and discharged home immediately after stabilization.

Endoscopy↗

PubMed1988

Effects of starvation, refeeding, and insulin on energy-linked metabolic processes in catfish (Rhamdia hilarii) adapted to a carbohydrate-rich diet.

The effects of starvation and of a short period of refeeding on energy-linked metabolic processes, as well as the effects of insulin administration, were investigated in an omnivorous fish (catfish, Rhamdia hilarii) previously adapted to a carbohydrate-rich diet. Following food deprivation blood sugar levels declined progressively to about 50% of fed values after 30 days. During the same period plasma free fatty acid (FFA) concentration increased twofold. Starvation resulted in reduced concentrations of lipid and glycogen in the liver and of glycogen, lipid, and protein in white muscle. However, taking into account the initial and final concentrations of tissue constituents, the liver weight, and the large fractions of body weight represented by muscle, it could be estimated that most of the energy utilized during starvation derived from the catabolism of muscle lipid and protein. Refeeding starved fishes for 48 hr induced several-fold increases in the rates of in vivo and in vitro incorporation of [14C]glucose into liver and muscle lipid and of [14C]glycine into liver and muscle protein. Incorporation of [14C]glucose into liver glycogen was also increased. However; refeeding did not affect the incorporation of labeled glucose into muscle glycogen, neither in vivo nor in vitro. Administration of pharmacological doses of insulin to normally fed catfishes resulted in marked increases in the in vivo incorporation of 14C from glucose into lipid and protein in both liver and muscle. In contrast, labeled glucose incorporation into muscle glycogen was not affected by insulin and label incorporation into liver glycogen was actually lower than that in noninjected controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

PubMed1985

Refeeding differentially affects tumor and host cell proliferation.

Tumor and host tissue DNA synthesis in C3H female mice with MA16/C tumors were examined for the effects of starvation and refeeding. Animals with subcutaneously implanted tumors were randomized to either regular diet or starvation for 48 hr followed by refeeding for 6, 12, 24, 48, or 72 hr. With starvation, both tumor and host tissues demonstrated a decrease in DNA synthetic activity. After refeeding, resumption in DNA tumor synthesis preceded that of host tissues and was greatest within the first 6-12 hr. Host tissue DNA synthetic activity resumed at different times in the various tissues examined with bone marrow being earlier than spleen or liver. The differential time course between induction of tumor and host DNA synthesis could allow a more precise modeling in studies dealing with the interaction of nutritional repletion and antitumor therapy.

Animals↗

PubMed1991

Hepatic steatosis due to total parenteral nutrition: the influence of short-gut syndrome, refeeding, and small bowel transplantation.

This study was undertaken to determine whether refeeding through the native small intestine or through a small bowel transplant would reverse hepatic steatosis induced by total parenteral nutrition (TPN), and of what influence a coexisting short-gut syndrome is. Three short-gut syndromes of different severity were established in Lewis rats (short-gut I, mild; short-gut II, moderate; short-gut III, severe). TPN was administered for 10 days and the animals were refed for 20 days. A liver biopsy after the TPN period confirmed a mild to moderate fatty infiltration of the liver in all groups. After the refeeding period a second liver biopsy was obtained and no evidence of hepatic steatosis was observed in Groups 1, 2, 3, and 4 (normal Lewis rat, short-gut I, II, and III). The animals in group 5 (short-gut I) received a syngeneic small bowel transplant after discontinuation of TPN. After the refeeding period the liver biopsies showed no evidence of fatty infiltration. The intestinal graft also reversed the nutritional deficiencies which were observed in the animals with short-gut and showed normal body weight gain and nitrogen and fat uptake in comparison to the normal animals (Group 1). These data show that a small bowel graft is capable of reversing the deleterious sequelae of short-gut syndrome as well as the TPN-related hepatic steatosis.

Animals↗

PubMed1992

Unexpected regulation of hypothalamic neuropeptide Y by food deprivation and refeeding in the Zucker rat.

Neuropeptide Y strongly stimulates food intake when it is injected in the hypothalamic paraventricular (PVN) and ventromedian (VMN) nuclei. In Sprague-Dawley (SD) rats, NPY synthesis in the arcuate nucleus (ARC) is increased by food deprivation and is normalized by refeeding. We have previously shown that the obese hyperphagic Zucker rat is characterized by higher NPY concentrations in this nucleus. NPY might therefore play an important role in the development of hyperphagia. The aim of the present study was to determine if the regulation by the feeding state works in the obese Zucker rat. For this purpose, 10 weeks-old male lean (n = 30) and obese (n = 30) Zucker rats were either fed ad libitum, either food-deprived (FD) for 48 hours or food-deprived for 48 h and refed (RF) for 6 hours. NPY was measured in several microdissected brain areas involved in the regulation of feeding behavior. NPY concentrations in the ARC was about 50% greater in obese rats than in lean rats (p less than 0.02) whatever the feeding state. In the VMN, NPY concentrations were higher in the lean FD rats than in the obese FD rat (p less than 0.001). Food deprivation or refeeding did not modify NPY in the ARC, in the VMN or in the dorsomedian nucleus whatever the genotype considered. On the other hand, food deprivation induced a significant decrease in NPY concentrations in the PVN of lean rats. This decrease was localized in the parvocellular part of this nucleus (43.0 +/- 1.9 (FD) vs 54.2 +/- 2.1 (Ad lib) ng/mg protein; p less than 0.005). Ad lib levels were restored by 6 hours of refeeding. These variations were not observed in the obese rat. The regulation of NPY by the feeding state in the Zucker rat was therefore very different from that described in the SD rats. Strain or age of the animals used might explain these differences. High NPY levels and absence of regulation in obese Zucker rats could contribute to the abnormal feeding behavior of these rats.

Animals↗

PubMed1977

The role of vasopressin and prolactin in abnormal salt and water metabolism of obese patients before and after fasting and during refeeding.

Arginine vasopressin (AVP) and prolactin (PRL) concentrations were measured in the plasma of grossly obese subjects to determine if abnormalities in salt and water homeostasis could be related to these hormones. Acute oral water loads and hypertonic saline infusions were administered during baseline obesity, after prolonged fasting, and after hypocaloric refeeding. Only 64.7%, 46.1%, and 70.1% of a water load was excreted during the respective three stages. Pre-water load plasma AVP levels were normal, but after the water load the obese failed to suppress AVP secretion in a normal fashion; this defect was corrected after fasting and with refeeding. Salt loading resulted in appropriate osmolality and AVP responses. Serum prolactin levels, normal at baseline during all phases, rose slightly after water loading during fasting. Hypertonic.saline produced no changes in prolactin levels in the obese or in the normal controls. In the disordered salt and water metabolism of the obese, persistently high AVP values during water loading appeared to be a factor in the delay of water excretion. In the observed water retentionduring dietary restriction and refeeding, secretion of AVP and PRL did not appear to have a major regulatory function.

Adult↗

PubMed1986

Polyribosome concentration in human skeletal muscle after starvation and parenteral or enteral refeeding.

Posttraumatic and septic states cause a loss of body proteins resulting in a negative nitrogen balance. The major part of the excreted nitrogen is derived from the proteins of skeletal muscle. The loss in proteins is due to a decrease in protein synthesis rather than an increase in protein degradation. Nutritional support may increase protein synthesis, and determination of its activity in skeletal muscle will give information on the utilization of nutrients in catabolic patients. The effect of nutritional support on healthy subjects was studied to achieve a background for future clinical studies. Male volunteers between 20 and 40 years old were refed parenterally or enterally after three days of starvation. Muscle biopsies (50 mg) were analyzed for the size distribution of ribosomes in a sucrose density gradient, and the ribosome concentration was determined per mg of DNA. Changes in the percentage content of polyribosomes preceded those of the total ribosome concentration. The total polyribosome concentration per gram wet weight of skeletal muscle decreased significantly during starvation. After one and two days of refeeding, a significant increase was observed, but the original level of the nonstarved subjects was not reached. The total ribosome concentration increased upon refeeding, but was not significantly different from that of the starved condition. The nitrogen balance was negative during starvation but attained equilibrium after two days of refeeding. Nutrition administered by the parenteral or enteral route were equally effective in restoring protein synthesis.

3-Hydroxybutyric Acid↗

PubMed1993

Refeeding after fasting increases apparent oxidation of N-3 and N-6 fatty acids in pregnant rats.

The intake, excretion, and accumulation of long-chain fatty acids was analyzed to test the hypothesis that during pregnancy in the rat whole-body partitioning of n-6 and n-3 fatty acids between net accumulation or disappearance (apparent oxidation) is determined by both maternal energy status and fetal development. From midpregnancy to term in ad libitum-fed rats consuming-rodent chow, 30% more saturates and monounsaturates accumulated in the whole body than were consumed, whereas 28% of dietary n-6 fatty acids and 55% of dietary n-3 fatty acids were apparently oxidized. After 48 hours of fasting during midpregnancy (days 13 to 15) followed by refeeding to term, net accumulation of saturates and monounsaturates was equivalent to intake, but whole-body disappearance of n-6 fatty acids exceeded intake by 6% (NS), whereas n-3 fatty acid disappearance exceeded intake by 43%. Thus during refeeding after fasting, dietary n-6 and n-3 fatty acids were apparently completely oxidized and there was actually a net loss of n-3 fatty acids from whole-body stores. Fasting during midpregnancy did not significantly affect fetal weight gain or maternal gestational hyperlipidemia toward term. We conclude that during pregnancy n-6 and n-3 fatty acids are not only required for maternal and fetal structural and storage lipids, but are also used to meet energy requirements, especially during refeeding after fasting.

Animals↗

PubMed1988

Insulin responses and glucose levels in plasma and cerebrospinal fluid during fasting and refeeding in the rat.

The present experiments were designed to investigate the rate of penetration of insulin from the plasma into the cerebrospinal fluid (CSF) during 24 hr of fasting and refeeding in the light phase. The results show that under these conditions basal CSF-immunoreactive insulin (IRI) levels were positively correlated with plasma IRI levels. Basal plasma IRI fell during a fast but was similar to prefast control after one day of refeeding. Although CSF-IRI levels rose during glucose infusion, CSF-IRI was not elevated by glucose during a fast. During refeeding, CSF-IRI responses returned toward control, prefeeding values. This study suggests a decreased transport of insulin from plasma to CSF during fasting. The lower CSF-IRI levels achieved under these conditions may determine meal size by allowing larger meals after a fast.

Animals↗

PubMed1989

Refeeding after various times of ingestion of a low protein diet: effects on food intake and body weight in rats.

Rats born of protein-deprived mothers were fed on a low protein (LP) diet (5% casein) from weaning. In each time sequence (0, 1, 3, 5, 8 and 16 weeks after weaning), 12 of them were refed on an isocaloric well-balanced diet (18% casein) for 2 weeks. Food intake, body and adipose tissue weights and protein efficiency ratio (PER) were measured in the refed rats as well as in 12 LP rats. At weaning and after one week, refed (RF) rats immediately increased their food intake. This increase was delayed at weeks 3, 5 and 8 occurred during the second week of refeeding only. At week 16, there was a significant decrease during the first week when compared with LP rats. Body weight increased regularly during each refeeding period without any significant augmentation of the proportion of adipose tissue. During all the experiment (except at week 16), PER in the RF group remained high (about 3 g body weight/g protein) during the first week of refeeding, and fell to 2.0-2.5 g/g during the second week. It was particularly significantly greater than that of the LP rats between week 3 and 5 where an important decrease was observed in this group (1.99 +/- 0.36 vs. 3.23 +/- 0.58 g body weight/g protein during the 1-3 weeks period). It appeared therefore that protein restriction during gestation and lactation in dams had no effect on the mechanisms controlling food intake of their offspring at weaning.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

PubMed1985

Influence of fasting and refeeding on the elongation step of protein synthesis in rat liver of young (3M) and aging (18M) animals.

The in vitro binding capacity for AA-tRNA of ribosomes, catalysed by EF1 enzyme, was studied in livers of rats, which had been starved for 5 days and re-fed for 3, 9, and 24 hours. The experiments were carried out with 3 and 18-month-old rats. The results were compared to those obtained with normally fed rats of the same ages. For both age groups, there was a similar change in the binding capacity, including a return to normal values after 24 hours of refeeding. When ribosomes of old control animals were treated with different enzymes, we obtained lower binding activities for all the experimental groups than in homologous cell-free systems (ribosomes and EF1 isolated from the same group). The ribosomes of young animals, tested in the presence of different enzymes, display an increased binding capacity, when the enzymes used were those of old (control and re-fed) animals. The recovery of the catalytic activity of EF1 on the binding process was observed after 9 hours in old animals, whereas it was not seen for young re-fed animals at that time of refeeding. EF1 seems to play an important role in the adaptation of older animals to fasting and refeeding.

Aging↗

PubMed1990

Effects of underfeeding and refeeding on GH and thyroid hormone secretion in young, middle-aged, and old rats.

The effects of a 50% reduction in normal food intake for a period of 10 weeks were measured on secretion of growth hormone (GH), thyroxine (T4), and triiodothyronine (T3) in 5 1/2-6 1/2-month old, 13 1/2-month-old, and 17 1/2-18 1/2-month-old male rats. In full-fed controls, GH, T3, and T4 were lower in the old and middle-aged than in the young rats. By the 10th week of underfeeding, GH, T3, and T4 were reduced in all age groups, but the decrease in T3 and T4 in the middle-aged and old rats was greater than in the young rats. Pulses of GH ceased in all the underfed groups. Upon refeeding for 5 days, pulses of GH and levels of GH returned to full-fed control values in the young and middle-aged but not in the old rats. T3 values in the young and middle-aged rats returned to full-fed control levels, but remained below control levels in the old rats. T4 values reached control levels in all age groups upon refeeding. The differences in the response to underfeeding and refeeding by the middle-aged and old rats as compared to the young rats may be due to their initially lower secretion of GH and thyroid hormones and to the age-related decrease in neuroendocrine function.

Aging↗

PubMedDate not supplied

Age-related changes in polyamine biosynthesis after fasting and refeeding.

The effect of aging on ornithine decarboxylase (ODC) activity and polyamine biosynthesis in the proximal small intestine was studied in two groups of male Fisher 344 rats (young [4-month old] and aged [26- to 27-month old]) using a fasting and refeeding model. In control (nonfasted) rats, levels of polyamines (putrescine, spermidine and spermine) and ODC activity were significantly higher in aged compared with young rats. In aged rats, fasting significantly reduced the levels of putrescine by 41%, spermidine by 23%, and spermine by 11%; however, fasting had no effect on polyamine levels in young rats. ODC activity was decreased 75% in young and 50% in aged rats after fasting compared with the respective age-matched controls. Conversely, 2 h after reinstituting a chow diet increased ODC activity by 17-fold in young rats but only 8-fold in aged rats. Putrescine levels were also increased in both age groups after refeeding; however, similar to ODC activity, these increases were much less in aged rats. In addition, spermidine and spermine levels remained significantly depressed in the aged groups even after 24 h of refeeding. These findings suggest that the normal rigid control of gut polyamine biosynthesis and proliferation noted in young rats is markedly altered with aging.

Aging↗

PubMed2003

A case study utilizing an enteral refeeding technique in a premature infant with short bowel syndrome.

Premature and full-term infants may be born with congenital abnormalities or develop acquired lesions of the gastrointestinal tract that require the placement of an enterostomy. Enterostomies can result in significant segments of excluded small bowel, creating a functional short bowel syndrome. Infants with enterostomies can develop dehydration, electrolyte imbalance, and failure to thrive. An illustrative case report of a premature infant with short bowel syndrome treated with enteral refeedings via a mucous fistula is presented. This report highlights the lessons learned from the interdisciplinary team's collective 10-year experience with enteral refeeding in infants with enterostomies. The physiologic basis for this approach is reviewed and literature reports are outlined. The specific nursing care and step-by-step techniques to deliver enteral refeeding through the mucous fistula are provided along with implications for clinical practice, education, and research.

Adaptation, Physiological↗