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PubMed1976

Fluctuations in the affinity and concentration of insulin receptors on circulating monocytes of obese patients: effects of starvation, refeeding, and dieting.

The binding of 125I-insulin to insulin receptors on circulating monocytes of obese patients and normal volunteers has been determined under various dietary states. In the basal, fed state the monocytes of obese patients with clinical insulin resistance (n= 6) bound less insulin than normals (n =10) because of a decrease in insulin receptor concentration (obese = 6,000-13,000 sites per monocyte versus normals 15,000-28,000 sites per monocyte). The single obese patient without evidence of clinical insulin resistance demonstrated normal binding of insulin with 16,000 sites per monocyte. In all patients, the total receptor concentration was inversely related to the circulating levels of insulin measured at rest after an overnight fast. For the obese patients with basally depressed insulin binding, a 48-72-h fast lowered circulating insulin and increased binding to normal levels but only at low hormone concentrations; this limited normalization of 125I-insulin binding was associated with increased receptor affinity for insulin without change in receptor concentration. Refeeding after the acute fasting periods resulted in return to the elevated plasma insulin levels, the basal receptor affinity, and the depressed insulin binding observed in the basal, fed state. Chronic diet restored plasma insulin levels, insulin binding, and receptor concentration to normal without change in affinity. When the data from this study are coupled with previous in vivo and in vitro findings they suggest that the insulin receptor of human monocytes is more sensitive to regulation by ambient insulin than the receptors of obese mice and cultured human lymphocytes. The results further indicate than an insulin receptor undergoes in vivo modulation of its interaction with insulin by changing receptor concentration and by altering the affinity of existing receptors.

Adolescent↗

PubMed1984

Time course and significance of changes in hepatic fructose-2,6-bisphosphate levels during refeeding of fasted rats.

The time course of changes in hepatic fructose-2,6-bisphosphate (F-2,6-P2) and glycogen content was examined in fasted rats infused with glucose intragastrically or allowed to eat a chow diet ad lib. Initial values for the two parameters were approximately 0.4 nmol/g and 2 mg/g of tissue, respectively. Contrary to what might have been expected on the basis of reported studies with hepatocytes exposed to glucose (i.e., a rapid elevation of F-2,6-P2), the rise in F-2,6-P2 levels in vivo was a late event. It began only 4-5 h after glucose administration or refeeding, at which time glycogen content had reached approximately 35 mg/g of tissue. Thereafter, [F-2,6-P2] climbed rapidly, attaining fed values in the region of 10 nmol/g as glycogen stores became maximal (approximately 60 mg/g of tissue). Although the biochemical basis for these changes is still unclear, the delayed increase in [F-2,6-P2] is entirely consistent with the fact that much of the glycogen deposited in liver in the early postprandial phase is gluconeogenic in origin. The later rise in [F-2,6-P2] likely represents a key signal for the attenuation of gluconeogenic carbon flow into glycogen as the latter approaches repletion levels.

Animals↗

PubMedDate not supplied

The refeeding syndrome: a review.

Refeeding syndrome has been used to describe those phenomena, such as severe hypophosphatemia and other metabolic complications, seen in malnourished patients receiving concentrated calories via total parenteral nutrition. The purpose of this review is to clarify and broaden this definition, as well as to make recommendations for its recognition and, more importantly, prevention.

Humans↗

PubMedDate not supplied

Enteral supplementation of phosphate does not prevent hypophosphatemia during refeeding of cachectic patients.

Hypophosphatemia due to parenteral nutrition has been described frequently. It was attributed to the lack of phosphorus content in parenteral nutrition solutions. With modern parenteral nutrition regimens containing phosphorus, this problem has been virtually eliminated. Enteral nutrition solutions contain adequate phosphate for patients with normal phosphate stores. Hypophosphatemia has therefore rarely been reported in enteral nutrition. We describe two patients with protein-energy malnutrition who developed severe hypophosphatemia during tube feeding with phosphorus-containing formula diets. Chronic alcoholism and vitamin D deficiency due to malabsorption because of Crohn's disease were additional risk factors in these two patients. Patients with depleted phosphate stores and high metabolic demand have a higher daily requirement for phosphorus than is available in routine isotonic enteral formulas. This case report emphasizes the importance of monitoring serum phosphate concentration daily during the first week of refeeding.

Adult↗

PubMed2003

Short-term food restriction and refeeding alter expression of genes likely involved in brain glucosensing.

Several genes involved in glucosensing of the endocrine pancreas have been proposed to serve a similar function in the brain. These genes include the glucose transporter-2 (Glut-2) and glucokinase (GK). In addition, the glucagon-like peptide 1 receptor, which serves as a downstream signal modulator in pancreatic glucosensing and centrally alters feeding, is also of interest. We used quantitative real-time RT-PCR to measure changes in hypothalamic and brainstem Glut-2, GK, and Glp-1R expression of these genes induced by food restriction and refeeding. Sprague-Dawley rats were 50% food restricted for 1 day; one-half of the food-restricted rats were refed with chow for 1 hr before sacrifice. In both hypothalamus and brainstem, gene expression of Glut-2, GK, and Glp-1R was significantly lower in refed rats compared with food-restricted rats. The measures of gene expression in two feeding control groups (ad libitum and voluntarily overfed animals) were intermediate between the food-restricted and refed groups, but were not significantly different from each other. The results indicate that putative glucosensing (GK, Glut-2, and Glp-1R) gene expression in the hypothalamus and brainstem is reduced in response to food intake, depending on prior nutritional status.

Animals↗

PubMedDate not supplied

Hypophosphatemia and refeeding: a corrective or a preventive attitude?

Hypophosphatemia is a rare but potentially lethal complication of the refeeding of cachectic patients. Up until now a careful monitoring of the serum phosphor level was recommended and the deficit was corrected as needed. Illustrated by two case reports we propose the use of a preventive schedule in patients with a normal renal function. We show that preventively treated patients do not develop hypophosphatemia and thereby avoid serious complications such as sudden death. In the presence of normal kidney function we propose to administer phosphor at 2 x 10 mmol/day orally or between 10 and 30 mmol IV depending on the initial phosphor levels. Further treatment is then adapted to measured levels. In the presence of kidney malfunction we propose to keep the corrective schedule.

Adult↗

PubMed1984

A comparison of lenient and strict operant conditioning programmes in refeeding patients with anorexia nervosa.

The present paper compares a lenient and a strict operant conditioning programme in refeeding patients with anorexia nervosa. Sixty-five consecutive in-patients participated in the study. We found no significant difference in the rate of weight-gain between the two treatments. There were, however, a number of practical advantages in using the more lenient programme: it was more economical of nursing time, and patients were more accessible to psychotherapy. The programme was also more acceptable to the patients.

Adolescent↗

PubMed2006

Inactivation of signal transducer and activator of transcription 3 in proopiomelanocortin (Pomc) neurons causes decreased pomc expression, mild obesity, and defects in compensatory refeeding.

Leptin is an adipocyte-derived hormone that signals body energy status to the brain by acting on multiple neuronal subgroups in the hypothalamus, including those that express proopiomelanocortin (Pomc) and agouti-related protein (Agrp). Signal transducer and activator of transcription 3 (Stat3) is an important intracellular signaling molecule activated by leptin, and previous studies have shown that mice carrying a mutated leptin receptor that abolished Stat3 binding are grossly obese. To determine the extent to which Stat3 signaling in Pomc neurons was responsible for these effects, we constructed Pomc-specific Stat3 mutants using a Cre recombinase transgene driven by the Pomc promoter. We find that Pomc expression is diminished in the mutant mice, suggesting that Stat3 is required for Pomc transcription. Pomc-specific Stat3 female mutant mice exhibit a 2-fold increase in fat pad mass but only a slight increase in total body weight. Mutant mice remain responsive to leptin-induced hypophagia and are not hypersensitive to a high-fat diet; however, mutant mice fail to mount a normal compensatory refeeding response. These results demonstrate a requirement for Stat3 in transcriptional regulation of Pomc but indicate that this circuit is only one of several components that underlie the neuronal response to leptin and the role of Stat3 in that response.

Animals↗

PubMed1990

1,25-Dihydroxyvitamin D3 enhances the effect of refeeding on steady state preproinsulin messenger ribonucleic acid levels in rats.

To elucidate the regulatory mechanism of vitamin D action on insulin biosynthesis and secretion, we examined preproinsulin (ppI) mRNA levels in the pancreas of normal rats, vitamin D-deficient rats, and rats supplemented with 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] or calcium (Ca) for 3 days. The ppI mRNA levels determined by dot blot analysis in vitamin D-deficient, 1,25-(OH)2D3-replete, and Ca-replete rats were 39.1%, 68.7%, and 66.7%, respectively, of values in normal rats. These results concur with previously reported levels of insulin secretion in the perfused rat pancreas. The reduced level of ppI mRNA should lead to a decrease in insulin biosynthesis and, thus, impair insulin secretion in vitamin D-deficient rats. The observed partial recovery of ppI mRNA levels through supplementation of 1,25-(OH)2D3 or Ca may be one mechanism by which insulin secretion is restored in rats after 1,25-(OH)2D3 or Ca repletion. We examined further the time course of ppI mRNA accumulation in rats after a single administration of 1,25-(OH)2D3. When fasting was continued for an additional 24-h period after an overnight fast, ppI mRNA levels were not changed significantly in either vitamin D-deficient or replete rats. However, in the rats that were pair-fed after overnight fasting, ppI mRNA levels in 1,25-(OH)2D3-replete rats increased at 8 and 24 h, whereas ppI mRNA in vitamin D-deficient rats increased only at 24 h. Moreover, the increment at 24 h was significantly larger in 1,25-(OH)2D3-replete rats than in vitamin D-deficient rats. We conclude that 1,25-(OH)2D3 enhances steady state levels of ppI mRNA only under conditions of refeeding and during feeding.

Animals↗

PubMed2001

Rat PPARs: quantitative analysis in adult rat tissues and regulation in fasting and refeeding.

PPARs are members of the nuclear hormone receptor superfamily and are primarily involved in lipid metabolism. The expression patterns of all 3 PPAR isotypes in 22 adult rat organs were analyzed by a quantitative ribonuclease protection assay. The data obtained allowed comparison of the expression of each isotype to the others and provided new insight into the less studied PPAR beta (NR1C2) expression and function. This isotype shows a ubiquitous expression pattern and is the most abundant of the three PPARs in all analyzed tissues except adipose tissue. Its expression is especially high in the digestive tract, in addition to kidney, heart, diaphragm, and esophagus. After an overnight fast, PPAR beta mRNA levels are dramatically down-regulated in liver and kidney by up to 80% and are rapidly restored to control levels upon refeeding. This tight nutritional regulation is independent of the circulating glucocorticoid levels and the presence of PPAR alpha, whose activity is markedly up-regulated in the liver and small intestine during fasting. Finally, PPAR gamma 2 mRNA levels are decreased by 50% during fasting in both white and brown adipose tissue. In conclusion, fasting can strongly influence PPAR expression, but in only a few selected tissues.

Animals↗

PubMed1997

Effect of fasting, refeeding, and dietary fat restriction on plasma leptin levels.

The factors responsible for the variability in plasma leptin levels observed among individuals with similar body compositions remain unclear. To examine the impact of dietary variables, we compared the changes in leptin levels induced by fasting and dietary fat restriction with the expected decrease following a significant loss in adipose mass. A 21.4 +/- 3.7% weight loss led to a 76.3 +/- 8.1% decrease in mean plasma leptin level (25.2 +/- 9.3 to 6.1 +/- 3.4 ng/mL, P = 0.0001) in a group of 9 obese males. Despite a weight loss of only 2.6 +/- 0.8%, mean plasma leptin levels fell by 61.9 +/- 25.2% (8.5 +/- 4.5 to 2.4 +/- 0.5 ng/mL, P < 0.01) in 7 nonobese females subjected to 3 days of fasting. Leptin levels in fasted subjects returned to baseline within 12 h of refeeding. Individual high- and low-fat meals given to 19 subjects after an overnight fast had no effect on plasma leptin levels. Reduction in dietary fat content from 37-10% of total calories for 7 weeks was also without effect on plasma leptin levels in these subjects. We conclude that plasma leptin levels primarily reflect total adipose mass, rather than meal consumption or dietary energy source, but that the reduction in leptin levels with ongoing fasting is disproportionate to the reduction in adipose mass. The ability of fasting to deactivate this presumed physiological satiety system may have been advantageous in environments characterized by rapid changes in food availability.

Adult↗

PubMed1999

Comparative study on the metabolic responses of subterranean and surface-dwelling amphipods to long-term starvation and subsequent refeeding

The effects of long-term starvation and subsequent refeeding on intermediary and energy metabolism were investigated in two subterranean aquatic crustaceans, Niphargus rhenorhodanensis and Niphargus virei, and in a morphologically similar surface-dwelling species, Gammarus fossarum. The metabolic response to prolonged food deprivation was monophasic in G. fossarum, showing an immediate, linear and large decline in all of the energy reserves. In contrast, both subterranean organisms displayed successive periods of glucidic, proteo-glucidic then lipidic-dominant catabolism during food deprivation. In both subterranean species, lipids (51 % of the energy consumed during a 180-day starvation period) and proteins (44 %) were the most metabolized substrates in terms of total energy, whereas glycogen (5 %) contributed little energy. G. fossarum displayed a different energetic strategy: proteins comprised 56 % of the energy losses during a 28-day starvation period, total lipids some 39 % and glycogen reserves only 5 %. We propose an energy strategy for food-limited subterranean crustaceans involving the possession of (1) higher amounts of stored arginine phosphate, triglycerides and glycogen and (2) lower utilization rates of stored metabolites than G. fossarum and numerous other surface-dwelling crustaceans, making the fueling of food deprivation possible for a longer time. In addition, these species had a faster and more efficient assimilation of available nutrients during recovery from food deprivation, enabling preparation for a new nutritional stress. These specific adaptive responses might be considered, for N. virei and N. rhenorhodanensis, as an efficient energy-saving strategy for an environment where extended starvation periods alternate with sporadic feeding events, therefore improving their competitive advantages.

Journal Article↗

PubMed2001

Behavioural, physiological and metabolic responses to long-term starvation and refeeding in a blind cave-dwelling (Proteus anguinus) and a surface-dwelling (Euproctus asper) salamander.

The effects of long-term starvation and subsequent refeeding on haematological variables, behaviour, rates of oxygen consumption and intermediary and energy metabolism were studied in morphologically similar surface- and cave-dwelling salamanders. To provide a hypothetical general model representing the responses of amphibians to food stress, a sequential energy strategy has been proposed, suggesting that four successive phases (termed stress, transition, adaptation and recovery) can be distinguished. The metabolic response to prolonged food deprivation was monophasic in the epigean Euproctus asper (Salamandridae), showing an immediate, linear and large decrease in all the energy reserves. In contrast, the hypogean Proteus anguinus (Proteidae) displayed successive periods of glucidic, lipidic and finally lipido-proteic-dominant catabolism during the course of food deprivation. The remarkable resistance to long-term fasting and the very quick recovery from nutritional stress of this cave organism may be explained partly by its ability to remain in an extremely prolonged state of protein sparing and temporary torpor. Proteus anguinus had reduced metabolic and activity rates (considerably lower than those of most surface-dwelling amphibians). These results are interpreted as adaptations to a subterranean existence in which poor and discontinuous food supplies and/or intermittent hypoxia may occur for long periods. Therefore, P. anguinus appears to be a good example of a low-energy-system vertebrate.

Adaptation, Physiological↗

PubMedDate not supplied

Refeeding problems in a severe anorexia nervosa case.

Anorexia Nervosa (AN) is an eating disorder of puberty or adolescence. It is characterized by self-induced weight loss; various psychological disturbances including distorted body image, fear of obesity, active pursuit of thinness and loss of recognition of a number of body enteroreceptive sensations; and secondary physiological abnormalities. The treatment of AN includes individual psychotherapy, family therapy, and nutritional rehabilitation. Hospital treatment is required when the patient's medical condition is in danger due to hypovolemia or hypotension. If cardiac arrhythmias occur without electrolyte disturbances or if oral therapy fails, nutrition should be repleted by the safest method available. This can be done by nasogastric tube or intravenous hyperalimentation. The management of AN is challenging, because the treatment process and anticipated outcome is in direct conflict with the sufferer's own wishes. A comprehensive treatment plan including both psychiatric and medical approaches is necessary. We report a severe AN case, who has refeeding problems after a three months' hospitalisation period. She was admitted to the child intensive care unit due to deterioration of her vital signs. We tried to solve her problems as a team, and believe that AN has a number of crucial problems thus requiring a multi-faceted treatment approach.

Adolescent↗

PubMed2004

Effects of carbohydrate refeeding on physiological responses and psychological and physical performance following acute weight reduction in collegiate wrestlers.

The purpose of this study was to determine the effects of carbohydrate refeeding on intermittent sprint exercise, blood lactate response, and mood following a typical weight-reduction program practiced by college wrestlers. Fifteen collegiate wrestlers from the University of Northern Iowa completed 3 trials of intermittent arm cranking and a mood inventory prior to weigh-ins (baseline), after weigh-ins, and 1 hour postconsumption of either 1.5 g carbohydrate (CHO)/kg body mass carbohydrate beverage (25% solution) or placebo taken within 1 hour after weigh-ins. Blood lactate responses were determined with each trial. Repeated measures analysis of variance indicated no significant interaction between group and trial for total work (p = 0.08), blood lactate (p = 0.29), positive mood (p = 0.49), or negative mood (p = 0.78). Simple effects analysis indicated a significant difference in lactate response between trials (p = 0.002); however, no difference for work (p = 0.75), positive mood (p = 0.13), or negative mood (p = 0.08). The results of this study suggest that intermittent sprint exercise, blood lactate response, and mood were not positively affected by ingestion of CHOs following an acute weight-reduction period.

Adolescent↗

PubMed1982

The effect of starvation and refeeding with oral versus intravenous glucose on serum 3,5-,3,3'-and 3'-5'-diiodothyronine and 3'-monoiodothyronine.

The effect of complete fasting on the serum concentrations of the iodothyronines 3,5-diiodothyronine (3,5-T2), 3,3'T2, 3', 5'-T2 and 3'-monoiodothyronine (3'-T1) was evaluated. Fourteen obese women underwent a complete fasting for 4 days. Caloric restriction resulted in the following serum hormone levels (before vs 3. day): T4: 103 vs 109 nmol/l (NS), T3: 1.83 vs 1.24 nmol/l (p less than 0.01), rT3: 0.276 vs 0.407 nmol/l (P less than 0.01), 3.5-T2: 70 pmol/l (NS), 3.3'-T2: 42 vs 39 pmol/l (p less than 0.01), 3',5'-T2: 63 vs 93 pmol/l (P less than 0.01), and 3'-T1 60 vs 116 pmol/l (P less than 0.01). All subjects were refed with 200 g (800 kcal, 3350 kJ) d-glucose per day in divided doses for 2 days. Refeeding tended to normalize the changed iodothyronine concentrations and there was no difference whether the glucose was administered by the oral (n = 7) or the intravenous route. In can be concluded that starvation in man is accompanied by profound changes in peripheral metabolism of the T2's and 3'T1. There seems to be no qualitative difference of the effect on the thyroid hormone metabolism of d-glucose administered by the oral or the intravenous route.

Administration, Oral↗

PubMed2006

Effects of feed restriction and subsequent refeeding on energy utilization in growing pigs.

An experiment was carried out to evaluate the metabolic utilization of energy in crossbred barrows during feed restriction and subsequent refeeding. Ten pigs, initially weighing 52 kg, were used in 5 blocks of 2 littermates each. A 7-d adaptation period (P1) was used in which pigs were offered feed at 2.60 MJ of ME.kg of BW(-0.60).d(-1). This adaptation period was followed by a 7-d period (P2), in which 1 pig of each block continued to receive feed at the same level of feeding, whereas for its littermate a 40% reduction in feed intake was imposed (i.e., 1.55 MJ of ME.kg of BW(-0.60).d(-1)). During the subsequent 7-d period (P3), both pigs were offered feed at 2.60 MJ of ME.kg of BW(-0.60).d(-1). After P3, pigs were fasted for 1 d. Heat production (HP) was measured for all pigs during the last 3 d of P1 and on all days for P2 and P3. Heat production was measured using an open-circuit respiration chamber. Energy and N balances were determined for P1, P2, and P3. The HP was partitioned into HP due to physical activity, the short-term thermic effect of feeding, and resting HP. Feed restriction during P2 decreased (P < 0.01) total HP, resting HP, short-term thermic effect of feeding, and retained energy, whereas HP due to physical activity was not affected by feed restriction (P = 0.50). Likewise, fecal and urinary N loss, protein gain, lipid gain, and ADG were reduced during feed restriction (P < 0.01). There were no differences in components of HP and metabolic utilization of energy between the 2 groups during P1 and P3. Nevertheless, urinary N loss was decreased (P < 0.05) and ADG increased (P < 0.01) during P3 for pigs that were restricted in P2. Compensatory growth after a period of feed restriction does not seem to be related to a change in the metabolic utilization of energy for gain but more likely is due to gain in water and gut contents.

Animal Feed↗

PubMed1988

Comparative effects of insulin and refeeding on DNA synthesis, HMP shunt and cholesterogenesis in diabetic and fasted rats.

DNA synthesis, cholesterogenesis and the enzymes of the hexosemonophosphate (HMP) shunt pathway were investigated in liver of diabetic rats treated with insulin and in fasted/re-fed rats. Both insulin and refeeding were found to induce liver cell proliferation, accompanied by a remarkable increase in cholesterogenesis. An enhancement of glucose-6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate dehydrogenase (G6PD) activities was also found in insulin-treated diabetic rats and in re-fed rats, supporting the concept that these two enzymes are involved in the proliferative process. Since insulin did not exert the same biochemical effects in a non replicating cell population, such as in insulin-treated normal rats, these studies provide new evidence of a close correlation between DNA, cholesterol synthesis and HMP shunt enzymes during cell proliferation.

Animals↗