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PubMed1998

Refeeding reverses cardiac myosin shifts induced by undernutrition in aged rats: modulation by growth hormone.

Growth hormone (GH) was administered (1 mg/day, i.p., 7.5 months) to male Fischer 344 rats, in conjunction with refeeding (RF) after chronic undernutrition (UN), from middle age (17 months old) to senescence (24.5 months old), during which cardiac myosin heavy chain (MHC) profiles were determined by gel-electrophoresis. At 17 months of age, respective MHC-alpha and -beta composition was 74 and 26% in the right ventricle (RV), and 58 and 42% in the left ventricle (LV), of ad libitum-fed controls. At 24.5 months of age, MHC profiles of controls were shifted toward the MHC-beta isoform in both RV (alpha=53%, beta=47%) and LV (alpha=40%, beta=60%), indicating a significant effect of aging on MHC composition in both ventricles. At 17 months of age, 7.5 months of UN likewise resulted in a shift toward the MHC-beta isoform in both RV (alpha=31%, beta=69%) and LV (alpha=22%, beta=78%) as compared to controls, indicating a significant effect of UN in both ventricles. Continued UN into senescence maintained these altered profiles in both ventricles, at 24.5 months of age (RV: alpha=35%, beta=65%; LV: alpha=24%, beta=76%). RF+GH administered from middle age into senescence restored the MHC composition in both ventricles (RV: alpha=57%, beta=43%; LV: alpha=43%, beta=57%), to that of the controls. RF, alone, likewise reversed ventricular MHC composition toward that of MHC-alpha, but appeared to overcompensate (RV: alpha=67%, beta=33%; LV: alpha=46%, beta=54%), surpassing the control and RF+GH profiles, significantly in the RV. These data suggest that GH is a modulator of restoration of cardiac MHC composition, when RF is administered to counter the effects of chronic UN, in the aging rat heart.

Aging↗

PubMed1988

Influence of a 36 h fast followed by refeeding with glucose, glycerol or placebo on metabolism and performance during prolonged exercise in man.

Five men were studied during exercise to exhaustion on an electrically braked cycle ergometer at 70% of VO2max. The four experimental treatments were as follows: fasted for 36 h (A); fasted (36 h) and refed with glucose (B) or glycerol (C); postabsorptive (overnight fast, D). In B and C the subjects were given a drink containing glucose or glycerol (1g per kg body weight) 45 min before starting exercise. A placebo drink was given 45 min before exercise on treatments A and D. Despite an increased availability of circulating free fatty acids, beta-hydroxybutyrate and glycerol exercise time to exhaustion was significantly lower after fasting (treatment A 77.7 +/- 6.8 min) compared with treatment D (119.5 +/- 5.8 min). Refeeding with glucose or glycerol did not significantly improve performance (92.4 +/- 11.8 min and 80.8 +/- 3.6 min respectively) compared with treatment A and lowered circulating levels of FFA and beta-HB during exercise compared with A. Despite the probability of low liver glycogen levels after fasting, none of the subjects became hypoglycaemic (blood glucose less than 4 mmol.l-1) during exercise and their blood lactate concentrations were not high at exhaustion. Plasma levels of branched chain amino acids (BCAA) decreased progressively during exercise on treatments A, B and C and were considerably lower at exhaustion compared with treatment D. Falling plasma concentrations of BCAA during prolonged exercise may be implicated in the generation of central fatigue.

3-Hydroxybutyric Acid↗

PubMed1987

The effects of starving and refeeding on the intra-acinar distribution pattern of alcohol-dehydrogenase activity in rat liver.

Microquantitative determinations of ADH activity were carried out on the livers of male and female rats. The animals were either starved for 84 h, or starved and then refed with a carbohydrate-rich diet for 6 nights. When the enzyme activity is expressed in mumoles/min/g dry weight, fasting does not appear to alter liver ADH activity, while in starved and subsequently refed rats it is diminished by 20%. Microquantitative measurements of ADH activity in 50-150 ng lyophilized tissue samples, microdissected the whole way along the sinusoidal length, made the computer-aided plotting of intra-acinar distribution patterns possible. The results showed that, under the feeding conditions selected, only minor changes in the ADH activity profiles occur in the liver acinus. These are within the range of the standard deviations of the normal mean values. From these results it can be deduced that fasting and refeeding do not lead to specific inhibition or induction of liver ADH activity. - The decrease of ADH activity of total liver (mumol/min) per total body weight in starved rats is obviously the result of a loss of protein which affects the liver cells of all acinar zones almost equally.

Alcohol Dehydrogenase↗

PubMed1984

Alterations in mammary-gland blood flow and glucose metabolism in the lactating rat induced by short-term starvation and refeeding.

Six-hour starvation of lactating rats caused a 75% decrease in mammary-gland lipogenesis. The inhibition of lipogenesis was accompanied by a 45% decrease of blood flow to the mammary gland and a 60% decrease in glucose uptake. Within 2 h of refeeding, lipogenesis and glucose uptake by the gland increased to fed values though blood flow to the gland remained at only 63% of that in the fed state. It is concluded that blood flow, and hence substrate supply, is not a rate-limiting factor for lipogenesis by the lactating mammary gland in the rat.

Animals↗

PubMed1978

Effect of parathyroidectomy on the fasting-refeeding response in the rat colon.

Following fasting and refeeding, the colonic epithelium of the rat exhibits a marked hyperplasia. This response is of a similar magnitude but of a longer duration to that observed in mice. This response is not affected by reducing serum calcium levels to those reported to alter normal tissue proliferation in vivo.

Animals↗

PubMed1988

Relationship between DNA and cholesterol synthesis in kidney after refeeding.

DNA and cholesterol synthesis were investigated in the kidneys of fasted-refed rats. Refeeding resulted in an increase in kidney DNA synthesis, as measured by 3H-thymidine incorporation, starting at 72 h. The increase in DNA synthesis was accompanied by a stimulation of cholesterol synthesis, as measured by 14C-acetate incorporation into cholesterol.

Animals↗

PubMed2000

Effect of fasting and refeeding on in vitro muscle cell proliferation in rainbow trout (Oncorhynchus mykiss).

The effects of short-term fasting and refeeding were studied on satellite cells extracted from white epaxial muscle of juvenile rainbow trout (1-3 g body weight). In vitro changes in the proliferation of satellite cells were analyzed using bromodeoxyuridine (BrdU) incorporation over a 24-h period. Proliferation in fed control fish was characterized by an initial basal proliferation rate of 5-10% BrdU-labeled nuclei x day(-1), followed by an exponential increase at a rate of +18-20% x day(-1), up to a maximum of 60-70% BrdU-labeled nuclei x day(-1). Characteristics of satellite cells extracted from starved fish, namely extraction yield, morphology, and proliferation, were different from those of fed fish. Fasting (8-10 days) completely suppressed initial proliferation of satellite cells in vitro over a period of 4 days. After this delay, proliferation resumed and changes in proliferation rates over time were similar to those of the control group. In fish fed for 4 days after an 8-day fast, the initial proliferation rate and the changes in proliferation rates over time were completely restored. These findings demonstrate that satellite cells express different behavior depending on feeding status, which could be due to the presence of different satellite cell populations.

Age Factors↗

PubMed2004

Time course of total and distrectual weight gain after refeeding in anorexia nervosa.

Anorectic patients who achieve complete recovery from the eating disorder can obtain a favorable psychosocial outcome but the long-term nutritional outcome is ill-defined. We investigated the time course of total and distrectual body composition during and after refeeding in 32 female patients with anorexia nervosa. Patients were enrolled at their lowest weight (T0) and re-examinated after a 15% weight gain (at a mean of 3 months, T1; n=17) and after 3 years of stable weight recovery (T2; n=8). At T2 patients were compared to a control group of 8 healthy females matched for age and body mass index. All subjects underwent dual X-ray absorptiometry and anthropometry at each visit. At T0, the 32 subjects were at 61%+/-8% of ideal body weight (IBW) with severe reductions in fat mass (FM; 7.1%+/-4.5%), fat free mass (FFM) and bone mineral content (BMC). At T2, the 8 subjects had gained 40% of initial weight, but remained at 85.1%+/-7.7% of IBW ( p<0.01 vs. controls), with a percent FM comparable to that of controls and an absolute FFM still deficient. BMC did not improve at T2 and remained 79% of that in controls. FM depletion was more severe in the limbs than in the trunk and at T2 the trunk/limb FM ratio remained greater than that in controls. These data strongly suggest that continued nutritional surveillance and support is necessary throughout these patients' lives, even after correction of the psychiatric illness and of severe underweight.

Anorexia Nervosa↗

PubMed1989

Levels of mRNAs coding for lipogenic enzymes in rat lung upon fasting and refeeding and during perinatal development.

The relative amounts of mRNAs coding for fatty-acid synthase (EC 2.3.1.85), acetyl-CoA carboxylase (EC 6.4.1.2), ATP citrate lyase (EC 4.1.3.8) and malic enzyme (EC 1.1.1.40) were determined in lungs and livers of adult rats that were normally fed, starved for 48 h or starved for 48 h and subsequently refed for 72 h with a carbohydrate-rich, fat-free diet. In the liver, starvation caused a small decrease in the relative abundance of the mRNAs which was not statistically significant. Subsequent refeeding caused a statistically significant increase in mRNAs for all of the enzymes studied. In the lung, no significant changes were found, indicating that the regulation of the abundance of mRNAs encoding the lipogenic enzymes in the lung differs from that in the liver. In the developing rat lung, mRNA for fatty-acid synthase increased 3-fold in abundance between fetal days 18 and 20 and decreased directly after birth (at day 22 of gestation). A similar pattern was observed for ATP citrate lyase mRNA. The level of acetyl-CoA carboxylase mRNA decreased significantly after birth. These observations indicate that in perinatal rat lungs, pretranslational regulation is involved in the control of the synthesis of these enzymes. The abundance of acetyl-CoA carboxylase mRNA did not change in the prenatal period, a time during which the specific activity of this enzyme increases. This lack of correlation between the specific activity of acetyl-CoA carboxylase and the abundance of its mRNA may indicate that translational regulation of the synthesis of the enzyme or post-synthetic regulatory effects on enzyme molecules are involved in the control of this enzyme in the prenatal period. No changes in the abundance of lung malic enzyme mRNAs were observed throughout the perinatal period.

ATP Citrate (pro-S)-Lyase↗

PubMed1992

In vitro apolipoprotein B mRNA editing activity can be modulated by fasting and refeeding rats with a high carbohydrate diet.

Apolipoprotein B mRNA editing in vivo is subject to tissue specific, developmental and metabolic regulation. We demonstrate for the first time that the metabolic modulation of apo B mRNA editing activity can be assayed in vitro using rat liver extracts. The editing activity in extracts from 48h-fasted rats was suppressed relative to that of normal chow-fed rats. Refeeding with a high-sucrose fat-free chow for 48h stimulated liver in vitro editing activity to approximately three times that of control liver extracts. The physical properties of editosomes assembled in extracts from fasted/refed rats differed from those assembled in control or fasted rat liver extracts. Polypeptide analysis revealed quantitative alterations of several proteins in each treatment group suggesting a complex regulatory process. The data corroborate those from in vivo studies and suggest the potential of the in vitro system in studying factors responsible for metabolic regulation of apo B mRNA editing.

Animals↗

PubMed1991

Pineal and adrenal function before and after refeeding in anorexia nervosa.

Nine female subjects with anorexia nervosa (AN) were studied when emaciated (mean 72% of average body weight), and after refeeding (mean 85% of average body weight). They were compared to 9 individually age-matched female control subjects. On each occasion blood was sampled for serum melatonin and plasma cortisol through the night, and urine was collected over 24 hr to measure sulfatoxy melatonin levels. The AN group did not differ in their level of depression before and after weight gain. There were no significant differences in serum melatonin values among the patient group before or after weight gain and the control group. Levels of urinary sulfatoxy melatonin were also significantly higher in nighttime compared to daytime samples both before and after weight gain. Plasma cortisol values were significantly elevated in the emaciated state and this was accounted for by higher cortisol levels at 9, 10, 11, and 12 PM and at 6 AM compared with the weight restored state and to controls. This study suggests that pineal activity in patients with AN is not altered by chronic changes in weight, and is not closely associated with changes in cortisol.

Adrenal Glands↗

PubMed1986

Glucostatic regulation of hypothalamic and brainstem [3H](+)-amphetamine binding during food deprivation and refeeding.

Saturable and stereospecific binding sites for [3H](+)-amphetamine have been identified in rat hypothalamus and structure-activity studies suggest that these sites may mediate the anorectic actions of amphetamine and related phenylethylamines. In order to determine whether these binding sites may be involved in the physiological control of appetite, [3H](+)-amphetamine binding was measured in crude synaptosomal membranes prepared from various brain regions following food deprivation and refeeding. Rats deprived of food for 24 to 72 h exhibited time-dependent reductions in body weight, blood glucose concentration, and specific [3H](+)-amphetamine binding in hypothalamus and brainstem. No change in specific [3H](+)-amphetamine binding was found in the frontal cortex, striatum, cerebellum, or liver prepared from these same animals. The decrease in specific [3H](+)-amphetamine binding in both the hypothalamus and brain stem following food deprivation was rapidly and completely reversed by allowing animals brief access to food or a 10% glucose solution. The changes in [3H](+)-amphetamine binding in hypothalami and brainstem of food-deprived and refed rats were also highly correlated with blood glucose concentration. Further, parenteral administration of D-glucose, but not L-glucose, to either fed or food-deprived rats significantly increased the number of [3H](+)-amphetamine binding sites in hypothalamus. These data suggest that the [3H](+)-amphetamine binding site in the hypothalamus and (or) brainstem may function in the 'glucostatic' regulation of appetite.

Animals↗

PubMed1995

Effects of fasting and refeeding on ob gene expression in white adipose tissue of lean and obese (oblob) mice.

A 33-mer antisense oligonucleotide has been utilized as a probe for the rapid chemiluminescence-based detection of ob (obese) mRNA. Expression of the ob gene was evident in several white adipose tissue depots of mice (epididymal, highest; subcutaneous and omental, lowest), but not in other organs. Fasting (24 h) induced a substantial fall in ob mRNA in the epididymal fat of lean mice, which was rapidly reversed on refeeding, responses consistent with the putative role of ob in energy balance. Fasting had no effect, however, on ob mRNA levels in obese (oblob) mice.

Adipose Tissue↗

PubMed1991

Time course changes in glycogen accretion, 6-phosphogluconate, fructose-2,6-bisphosphate, and lipogenesis upon refeeding a high sucrose diet to starved rats.

1. Starved rats refed 60% sucrose diets were used to determine in vivo lipogenesis and levels of hepatic metabolites. 2. Fatty acid synthesis increased 11-fold 4 hr after refeeding. 3. Glycogen rose from 3 to 100 mg/g liver after 8 hr. 4. Fructose-2,6-bisphosphate rose to 6 nmol/g at 1 hr and remained constant. 5. 6-Phosphogluconate increased from 10 to 45 nmol/g liver after 2 hr and remained constant.

Animals↗

PubMed1990

Protein synthesis in skeletal muscle during starvation and refeeding: comparison of data from intact muscle and muscle biopsy material.

The intact extensor digitorum longus (EDL) preparation in rat is a well-documented model for assessing protein synthesis in skeletal muscle. Human muscle biopsy material has also been used, but the extent to which biopsy material is representative for evaluation of muscle protein synthesis has not been established. Therefore, the aim of this study was to compare protein synthesis in intact muscle and in muscle biopsy material simultaneously in rats. The animals (70 g) were divided into three groups: fed (n = 22), starved for 36 hours (n = 22), and refed for 24 hours (n = 19). Protein synthesis and RNA content were measured in each group. Protein synthesis was determined as the incorporation of 14-C-phenylalanine into muscle protein in the intact EDL muscle from one leg and in a muscle biopsy from the contralateral EDL muscle. The incorporation of 14-C-phenylalanine was linear over time in both preparations, but was consistently lower in the muscle biopsy compared with the intact muscle. The relative change in incorporation, in % of that obtained in the fed state, showed a decrease in incorporation after 36 hours of starvation, in both intact muscle and in muscle biopsy material, 33% +/- 10% and 42% +/- 6%, respectively. After 24 hours of refeeding, an overshoot in protein synthesis was seen, to 136% +/- 6% in the intact muscle and to 133% +/- 6% in the muscle biopsy, as compared with the fed state. The RNA content decreased during the starvation period from 21.6 +/- 0.7 to 14.5 +/- 0.4 mg RNA/g protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Effects of feeding, fasting and refeeding on growth hormone and insulin in obese pigs.

This study has indicated that temporal patterns of plasma GH changes were similar in lean and obese pigs with one to two secretory spikes occurring during a 6-hour period. Fasting caused increased GH in both pig strains; however, obese pigs, compared to lean, had lower GH during feeding and fasting. This depressed plasma GH of obese pigs may not be due entirely to impaired pituitary function since refeeding caused increased GH to levels similar to lean pigs. Insulin response per unit of feed intake was greater in obese pigs compared to lean. Together with higher insulin to glucose ratios, these results indicate hyperinsulinemia in the obese pigs. Overall, hormone and glucose responses were influenced by the nutritive status--fed, fasted or refed. Therefore consideration of feeding schedule was important in assessment of hormonal differences between the lean and obese pigs.

Animals↗

PubMed1986

Intravenous self-administration of phentermine in food-deprived rats: effects of abrupt refeeding and saline substitution.

The objectives in these experiments were to determine the effects on intravenous phentermine self-administration of abrupt refeeding and of saline substitution in food-deprived rats. In Experiment 1, 32 naive rats, reduced to 80% free-feeding weight (FFW), were assigned randomly to four equal-sized groups. Two groups self-administered phentermine, the other two saline over two consecutive six-day phases. In phase 1, all animals were maintained at 80% FFW, while in phase 2, one phentermine- and one saline-reinforced group was abruptly food satiated. Results showed that phentermine self-administration was suppressed. In Experiment 2, another 32 naive rats were assigned to four equal-sized groups and tested over two consecutive six-day phases. Two groups were FF, the other two were reduced to 80% FFW. In phase 1, a group of FF and 80% FFW animals self-administered phentermine, the other two saline, while in phase 2, treatments were reversed: previously phentermine-reinforced animals self-administered saline and vice versa. Findings showed that 80% FFW rats rapidly discriminate the introduction or removal of phentermine and alter responding accordingly, while FF animals respond at low rates throughout.

Animals↗

PubMedDate not supplied

Growth hormone receptors in rat liver membranes: effects of fasting and refeeding, and correlation with plasma somatomedin activity.

The effects of fasting and refeeding on hepatic growth hormone receptors, on insulin receptors and on plasma somatomedin activity were studied. Female rats were either subjected to fasting for 4 days, refed for 3 days after a 4-day fasting, or allowed free access to food (controls). The specific binding of 125I-labelled bovine growth hormone was low in liver microsomal membranes (45% that of controls) and in plasma membranes (52% that of controls) of fasted rats. The number of somatotropic sites rather than the affinity of the binding was decreased. Lactogenic sites as judged by the binding of 125I-labelled human growth hormone were not significantly reduced in liver membranes of fasted rats. 125I-labelled insulin specific binding was enhanced in microsomal (184% that of controls) and plasma membranes (136% that of controls) of fasted rats; these modifications were associated with a decreased insulinemia. But immunoreactive rat growth hormone levels were not different in plasma of fasted, refed and control animals. Decreased plasma bioassayable somatomedin was associated with the low number of somatotropic binding sites in liver membranes of fasted rats. Somatomedin activity of refed animals was comparable to controls. A significant correlation between the plasma bioassayable somatomedin and the hepatic level of somatotropic binding sites was found. It is proposed that, in fasting, the loss of somatotropic binding sites in the liver is one of the possible causes of the decreased plasma somatomedin bioactivity.

Animals↗