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PubMed1985

Effect on the interaction of dietary carbohydrate and fat on the responses of rats to starvation-refeeding.

The interacting effects of sucrose or starch with corn or coconut oil on the lipogenic responses of rats to starvation-refeeding was studied. Rats were either ad libitum-fed or starved for 48 h and refed for 48 h. Four different diets were used: 65% starch-5% corn oil, 65% starch-5% coconut oil, 65% sucrose-5% corn oil, 65% sucrose-5% coconut oil. Lipogenesis was assessed in two ways: glucose-6-phosphate dehydrogenase (G6PD) activity, malic enzyme (ME) activity and percent liver lipid (expt 1) and tritium (3HOH) incorporation into fatty acids (expt 2). Starved-refed rats had more liver lipid, greater enzyme activity and greater 3H incorporation into fatty acids than ad libitum-fed rats. Sucrose-fed rats had more lipogenic activity than starch-fed rats. Rats fed coconut oil were more lipogenic than rats fed corn oil. There were highly significant correlation coefficients between the enzyme activities (G6PD and ME) and the percent liver lipid and between the enzyme activities and 3H incorporation into fatty acid. Analysis of variance of these data revealed significant dietary effects on these lipogenic responses to starvation-refeeding. We conclude that both dietary carbohydrate and lipid play a significant role in the determination of the magnitude of the lipogenic response to starvation-refeeding.

Animals↗

PubMed1987

Messenger RNA levels of plasma proteins in rat liver during protein depletion and refeeding.

The levels of mRNA for albumin, transferrin, transthyretin, the beta-chain of fibrinogen and apolipoprotein E in livers from rats during protein depletion and refeeding were measured by hybridization to specific cDNA probes. A period of protein depletion of 3 d resulted in a 30-40% decrease in mRNA levels for all five proteins. These levels were further decreased by only 15-20% after additional protein depletion for 6 d. There was no noticeable change in mRNA levels within 4 h of refeeding by gavage with a casein hydrolysate suspension supplemented with L-tryptophan and L-arginine. Upon refeeding a 30% protein diet, mRNA levels returned to normal after 3 d. The work presented here suggests that changes observed in the protein synthetic rate following protein depletion and repletion are due to changes in mRNA levels altered as a consequence of the availability of dietary protein.

Animals↗

PubMed1991

Refeeding of rats fasted 36 hours with five different carbohydrates and with malt extract: differential effects on glycogen deposition in liver and muscle, on plasma insulin and on plasma triglyceride levels.

Rats fasted for 36 h were refed for 1, 2, 4 or 6 h with a diet containing 12 g/100 g casein, 2 g/100 g NaCl and 86 g/100 g glucose, fructose, maltose, sucrose, starch or malt extract. Blood glucose reached constant levels after 1 to 2 h of refeeding. The increase in plasma insulin paralleled food intake rather than the increase in blood glucose. Plasma triglycerides decreased upon refeeding starch, maltose and malt extract and increased with sucrose and fructose. Recovery of absorbed carbohydrates was highest in rats refed malt extract. Glycogen deposition in muscle was highest in rats fed malt extract and lowest in those fed fructose; sucrose yielded intermediate values. Glucose, maltose and starch resulted in muscle glycogen depositions slightly lower than those obtained with malt extract. In liver, sucrose and fructose were better precursors for glycogen than glucose and starch. With carbohydrates containing only glucose units, much more glycogen was found to be deposited in total muscle than in liver. This asymmetry was less notable or even was reversed with sucrose and fructose. Glycogen deposition in muscle and in liver is influenced by the carbohydrate used for refeeding, and muscle, rather than liver, is the main glycogen storing tissue.

Animals↗

PubMed1995

Rat plasma VLDL composition and concentration and hepatic lipase and lipoprotein lipase activities are impaired during two types of protein malnutrition and unaffected by balanced refeeding.

The relationships between VLDL concentrations and composition and changes in hepatic lipase and lipoprotein lipase activities were determined in rats, during the consumption of two low protein diets (2% casein or 5% gluten) (protein malnutrition) for 28 d, followed by the refeeding of a balanced diet for 14 d (15% casein) (refeeding). A control group was fed 15% casein for 42 d. In the control group, total lipolytic activity increased with age (r = 0.83, P < 0.001), whereas in both depleted groups, this activity remained low and stable throughout the period of protein malnutrition. At d 28 of protein malnutrition, plasma total lipolytic activities were significantly reduced in both depleted groups, (P < 0.05); hepatic lipase values represented 23% of the control value and lipoprotein lipase activity was about 11% of the control value. Moreover, lipid supply was even more dramatically diminished by the strong reduction in plasma VLDL concentration in both depleted groups. At d 14 of refeeding, lipoprotein lipase activities remained low in both depleted groups. Hepatic lipase activity was similar in the control and casein groups, but significantly higher in the gluten group. The VLDL composition varied significantly with each type of protein malnutrition and could be attributable to the different low levels of plasma VLDL-apolipoprotein C of rats fed both depleted protein diets, which involve an inhibiting or activating effect on lipoprotein lipase activity. Therefore, our results indicated that both protein-deficient diets investigated may diminish fatty acid supply in the various tissues involved.

Animals↗

PubMed1996

Protein and lipid refeeding changes protein metabolism and colonic but not small intestinal morphology in protein-depleted rats.

In this study, we fed rats a 2% casein AIN 76 diet for 2 wk to produce protein malnutrition. We determined in these animals the effects of different concentrations of dietary protein refeeding (2% and 20% casein) on recovery and gut mucosal repletion and the potential role of type of dietary fat in the regulation of protein metabolism and mucosal growth by providing conventional long-chain triglyceride (LCT), a structured lipid composed of long-, medium- and short-chain fatty acids (SC/SL), or a physical mixture of the same components present in the structured lipid given as individual pure triglycerides (SC/PM) along with adequate amounts of protein and energy. The results confirmed that protein malnutrition can be reversed rapidly by protein refeeding, as indicated by an increase in body weight, positive nitrogen balance, liver growth and elevations in plasma concentrations of insulin-like growth factor-1, leucine and albumin. In the colon, crypt cell number, crypt depth and number of crypt cells in the rapidly proliferating fraction of the colon were greater in rats fed the higher protein diet. However, the general architecture of small intestinal mucosa, including duodenum, jejunum and ileum, was not affected by protein malnutrition. Although the number of colonic cells was similar with fat refeeding, there were significantly fewer displaying the proliferating cell nuclear antigen in the colonic epithelium when rats were fed SC/PM compared with SC/SL. Therefore, changes in colonic mucosal proliferation were only seen with repletion by adequate protein and by SC/SL feeding.

Absorption↗

PubMedDate not supplied

Management of the patient with refeeding syndrome.

Refeeding syndrome is a metabolic complication that can occur when nutrition is reintroduced for patients who are severely malnourished. This syndrome can occur with any form of nutrition (oral, enteral, or parenteral), and it is fatal if not recognized and treated properly. This article discusses the body's adaptation to starvation, the pathophysiology and risk factors of refeeding syndrome, and the pharmacologic treatment of complications that threaten the lives of patients who experience this disorder. Additionally, this article discusses standards of care to ensure the early recognition of patients at risk for refeeding syndrome and the nursing considerations that can be implemented to prevent it.

Acclimatization↗

PubMed2004

Refeeding syndrome: implications for the inpatient rehabilitation unit.

Patients admitted to inpatient rehabilitation units commonly have underlying medical disorders and are at risk for poor oral intake and malnutrition, which may be compounded by dysphagia and anorexia. The refeeding syndrome is an underappreciated but clinically important entity characterized by acute electrolyte abnormalities, fluid retention, and dysfunction of various organ systems, which can result in significant morbidity and, occasionally, death. Reinstitution of nutrition by any route in a undernourished patient may lead to acute electrolyte shifts and fluid retention, which are hallmarks of the refeeding syndrome. As such, this article briefly summarizes the clinical manifestations and treatment of refeeding syndrome as it relates to patients admitted to the inpatient rehabilitation unit.

Aged↗

PubMed2005

Contribution of the vagus nerve and lamina terminalis to brain activation induced by refeeding.

Following refeeding, c-fos expression is induced in a particular set of brain regions that include the nucleus of the solitary tract (NTS), parabrachial nucleus (PB), central amygdala (CeA), paraventricular hypothalamic nucleus (PVH), supraoptic nucleus (SON) and the circumventricular organs. Within the PVH, the expression is particularly intense in the magnocellular division of the nucleus and it is as yet not clear how this activation occurs. The respective contribution of the vagus afferents and lamina terminalis, which conveys signals entering the brain through the forebrain circumventricular organs, has been investigated in rats subjected to a unilateral cervical vagotomy (UCV) or a unilateral lesion of the fibres running within the lamina terminalis (ULT) and projecting to the neuroendocrine hypothalamus. UCV significantly decreased postprandial c-fos expression in the NTS, PB, CeA and parvocellular division of the PVH. In contrast, ULT impaired postprandial activation of the magnocellular neurons in the PVH and SON. The present study also characterized the types of neurons activated in the PVH and SON during refeeding. In the magnocellular regions, arginine-vasopressin (AVP) neurons were activated upon refeeding whereas there was no apparent induction of Fos expression in oxytocin cells. In the parvocellular PVH, postprandial Fos was induced only in 30% of the corticotrophin-releasing factor (CRF) and AVP neurons. The results of the present study suggest that the postprandial activation of the brain requires the integrity of both the vagal- and lamina terminalis-associated pathways.

Animals↗

PubMed1997

The metabolic responses to starvation and refeeding in adolescents with anorexia nervosa.

Adaptive changes in metabolism result in decreased energy requirements in AN. A retrospective study of 21 hospitalized female AN patients demonstrated that indirect calorimetry (IC) measurement of resting energy expenditure (REE) was significantly lower than REE calculated by the Harris-Benedict equation (HBE). The HBE was adjusted by multiple-regression analysis to reflect the hypometabolic state of AN, and the adjusted equation was prospectively validated in 37 hospitalized female AN patients. Refeeding requires an understanding of both baseline requirements and metabolic changes that occur during nutritional rehabilitation. In our present study, we prospectively evaluated changes in fasting and postprandial REE in 50 hospitalized female patients meeting DSM-IV criteria for AN. Baseline IC measurements of fasting and postprandial REE were obtained within three days of admission, and every two weeks thereafter. Mean fasting REE increased significantly from 72 (+/-11.7) to 83.2 (+/-12.6) percent of predicted (p < 0.001) during the first two weeks of hospitalization. Likewise, postprandial REE also increased significantly from 17.5 (+/-18.2) to 27.9 (+/-15.9) percent above fasting REE during the same time period (p < 0.01). Significant increases in both REE and postprandial REE persisted in patients requiring longer hospitalizations. Despite the fact that prescribed energy intake and triiodothyronine (T3-RIA) levels increased during refeeding, there was no significant relationship between postprandial REE and energy intake or T3 levels after baseline. We conclude that energy metabolism in AN adapts to semistarvation by a reduction in fasting REE. With refeeding there is a reversal of this adaptive function, demonstrated by an increase in both fasting and postprandial energy expenditure. The increase in postprandial REE is not related to energy intake or thyroid function.

Adolescent↗

PubMed2003

Ubiquitin-proteasome-dependent muscle proteolysis responds slowly to insulin release and refeeding in starved rats.

The central role of the ubiquitin-proteasome system in the loss of skeletal muscle protein in many wasting conditions has been well established. However, it is unclear what factors are responsible for the suppression of this system during periods of protein gain. Thus, the aim of these studies was to examine the short-term effects of insulin release and nutrients on skeletal muscle protein turnover in young rats starved for 48 h, and then infused intravenously with amino acids (AA), or fed an oral diet. Forty-eight hours of starvation (i.e. prolonged starvation in young rats) decreased muscle protein synthesis and increased proteasome-dependent proteolysis. Four-hour AA infusion and 4 h of refeeding increased plasma insulin release and AA concentrations, and stimulated muscle protein synthesis, but had no effect on either total or proteasome-dependent proteolysis, despite decreased plasma corticosterone concentrations. Both muscle proteasome-dependent proteolysis and the rate of ubiquitination of muscle proteins were not suppressed until 10 h of refeeding. The temporal response of these two measurements correlated with the normalised expression of the 14-kDa E2 (a critical enzyme in substrate ubiquitination in muscle) and the expression of the MSS1 subunit of the 19S regulatory complex of the 26S proteasome. In contrast, the starvation-induced increase in mRNA levels for 20S proteasome subunits was normalised by refeeding within 24 h in muscle, and 6 h in jejunum, respectively. In conclusion, unlike protein synthesis, skeletal muscle proteasome-dependent proteolysis is not acutely responsive in vivo to insulin, AA, and/or nutrient intake in refed starved rats. This suggests that distinct and perhaps independent mechanisms are responsible for the nutrient-dependent regulation of protein synthesis and ubiquitin-proteasome-dependent proteolysis following a prolonged period of catabolism. Furthermore, factors other than the expression of ubiquitin-proteasome pathway components appear to be responsible for the suppression of skeletal muscle proteasome-dependent proteolysis by nutrition.

Amino Acids↗

PubMed2006

Computational model of in vivo human energy metabolism during semistarvation and refeeding.

Changes in body weight and composition are the result of complex interactions among metabolic fluxes contributing to macronutrient balances. To better understand these interactions, a mathematical model was constructed that used the measured dietary macronutrient intake during semistarvation and refeeding as model inputs and computed whole body energy expenditure, de novo lipogenesis, and gluconeogenesis as well as turnover and oxidation of carbohydrate, fat, and protein. Published in vivo human data provided the basis for the model components that were integrated by fitting a few unknown parameters to the classic Minnesota human starvation experiment. The model simulated the measured body weight and fat mass changes during semistarvation and refeeding and predicted the unmeasured metabolic fluxes underlying the body composition changes. The resting metabolic rate matched the experimental measurements and required a model of adaptive thermogenesis. Refeeding caused an elevation of de novo lipogenesis that, along with increased fat intake, resulted in a rapid repletion and overshoot of body fat. By continuing the computer simulation with the prestarvation diet and physical activity, the original body weight and composition were eventually restored, but body fat mass was predicted to take more than one additional year to return to within 5% of its original value. The model was validated by simulating a recently published short-term caloric restriction experiment without changing the model parameters. The predicted changes in body weight, fat mass, resting metabolic rate, and nitrogen balance matched the experimental measurements, thereby providing support for the validity of the model.

Adipose Tissue↗

PubMed1983

Effects of severe long-term food deprivation and refeeding on adipose tissue cells in the rat.

To determine whether it is possible to use diet to cause a loss of adipocytes, adipose tissue cellularity was examined in adult male rats subjected to unusually prolonged semistarvation. After 1 wk of total fast, rats were given a nutritionally inadequate glucose-electrolyte diet for up to 7 wk. This caused a 49% reduction of body weight, up to a 99% reduction in the weight of adipose tissue, and significant losses of total adipose tissue DNA content. Nevertheless, there was no evidence that fat cells had been lost. The number of fat cells in the right epididymal depots of the food-deprived rats equaled both the number seen in left depots after refeeding and the number seen in corresponding depots of nonfasted controls. Adipose tissue DNA synthesis, which declined 88% below control values during fasting, did increase as much as 2,000% above control values during refeeding. However, autoradiographs showed that the increase reflects only the replacement of lost endothelial and nonadipocyte mesenchymal cells; no labeled fat cell nuclei were found. Thus, severe, long-term food deprivation followed by refeeding causes loss and recovery of stromal-vascular cells in adipose tissue but no loss of fat cells.

Adipose Tissue↗

PubMed1983

Role of insulin in thermogenic responses to refeeding in 3-day-fasted rats.

Refeeding 3-day-fasted rats with 40 kJ carbohydrate (CHO; corn flour) or protein (gelatin) caused a rise in plasma insulin levels 3 h later, but refeeding fat or injection of norepinephrine (400 micrograms/kg) had no effect. Injection of insulin (0.25 U) caused a 15% rise in metabolic rate 24 h later in fasted rats that could be inhibited by treatment with propranolol. Refeeding rats with a single CHO meal produced an increase in oxygen consumption (15%) 24 h later that was inhibited by injection of diazoxide or 2-deoxy-D-glucose given at the time of the meal. The thermogenic response to insulin injection was unaffected by treatment with diazoxide or 2-deoxy-D-glucose. Genetically obese Zucker rats failed to increase metabolic rate after insulin or CHO. In normally fed lean rats, maintained on a stock diet or a palatable cafeteria diet, insulin (4 U) enhanced the thermogenic response to norepinephrine and stimulated resting metabolic rate (16%) in the cafeteria-fed rats. These data suggest that insulin is involved in the thermogenic responses to food and catecholamines.

Animals↗

PubMed1985

Insulin action during fasting and refeeding in rat determined by euglycemic clamp.

To further characterize the role of insulin in glucose metabolism during fasting and refeeding, euglycemic-hyperinsulinemic clamps were performed in control, 3 day-fasted, and 3 day-fasted then 3 day-refed rats. Glucose production and utilization were measured by using [3-3H]glucose. In control and refed rats, hepatic glucose production was totally suppressed at insulin concentration higher than 500 microU/ml; by contrast, during fasting, hepatic glucose production was not suppressed even at insulin concentration tenfold higher. Maximal increment of glucose utilization was lower in fasted than in control rats. Three days of refeeding restored almost entirely normal responses to insulin for glucose utilization. Blood glucose concentration was clamped at a different level in fasted and in control and refed rats; however, increment in glucose clearance in response to insulin was lower in fasted rats than in the two other groups. Thus fasting produces a state of insulin unresponsiveness both at the hepatic and peripheral levels, normal responsiveness being restored after 3 days of refeeding.

Animals↗

PubMed1988

Regulation of glycogen synthase in muscle and adipose tissue during fasting and refeeding.

Using immunoblot analysis, we examined the electrophoretic mobility of glycogen synthase from rat skeletal muscle and adipose tissue. Extracts from muscle freeze clamped in situ contained at least three forms of synthase with different electrophoretic mobilities. Extracts from adipose tissue also contained multiple forms but lacked the form with greatest mobility found in the muscle extracts. Phosphorylation at multiple sites of glycogen synthase is known to deactivate the enzyme and retard its electrophoretic mobility in sodium dodecyl sulfate gels. These results suggest that there is very little or no dephosphorylated glycogen synthase in adipose tissue and that phosphorylated forms of glycogen synthase synthesize adipose tissue glycogen. Relative to control, it is known that fasting decreases and refeeding increases glucose incorporation into glycogen in rat epididymal adipose tissue but not skeletal muscle incubated in vitro in the presence of insulin. Fasting did not change the electrophoretic pattern of muscle synthase but decreased the relative amount of adipose tissue forms with greater mobility. Refeeding increased above control the relative amount of adipose tissue synthase with greater mobility. These results indicate that changes in the phosphorylations that retard mobility contribute to the effects of fasting and refeeding on adipose tissue glycogen metabolism.

Adipose Tissue↗

PubMed1988

Effects of repeated cycles of fasting-refeeding on brown adipose tissue composition in mice.

Mice fasted for 24 h showed reductions in carcass fat and gonadal fat depots and atrophy of brown adipose tissue (BAT) that was characterized by loss of protein and succinate dehydrogenase. These changes were reversed on 24 h of refeeding. Cycling mice experienced 14 cycles of 1 day of fast followed by 2 days of refeeding, whereas control mice were fed ad libitum. Weight loss during each fast remained constant, and the animals lost and regained in excess of twice their initial weights within 6 wk. However, final weight and carcass and gonadal fat weights were similar to those of animals fed ad libitum. Total food intake was similar between cycling mice and those fed ad libitum suggesting an increase in feeding efficiency. There was no development of resistance to food deprivation since the preceding fasting experience of the animal had no effect on weight and carcass fat loss during a 24- or 48-h fast. Norepinephrine-stimulated oxygen consumption that was reduced in cycling mice was probably the result of a reduction of BAT thermogenic capacity. BAT succinate dehydrogenase content and the concentration of uncoupling protein in isolated mitochondria were significantly reduced. These changes in BAT composition were not observed when the refeeding period of each cycle was increased to 6 days. These results suggest that reduced energy expenditure in BAT may play a role in the conservation of energy during intermittent and frequent bouts of food deprivation.

Adipose Tissue, Brown↗

PubMed1988

Refeeding hypertension in dietary obesity.

A novel model of nutritionally induced hypertension in the rat is described. Dietary obesity was produced by providing sweet milk in addition to regular chow, which elicited a 52% increase in caloric intake. Despite 54% greater body weight gain and 139% heavier retroperitoneal fat pads, 120 days of overfeeding failed to increase systolic pressure in the conscious state (125 +/- 8 vs. 121 +/- 4 mmHg in chow-fed controls) or mean arterial pressure under urethan anesthesia (71 +/- 4 vs. 63 +/- 3 mmHg). In contrast, mild hypertension developed in intermittantly fasted obese animals (a 21-mmHg increase in systolic blood pressure measured in the conscious state and a 16-mmHg increase in mean arterial pressure under anesthesia relative to chow-fed controls). The first 4-day supplemented fast was initiated 4 wk after the introduction of sweet milk, when the animals were 47 g overweight relative to chow-fed controls. Thereafter, 4 days of starvation were alternated with 2 wk of refeeding for a total of 4 cycles. A rapid fall in systolic blood pressure (12 +/- 2 mmHg at 2 days) accompanied the onset of supplemented fasting and was maintained thereafter (2.7 +/- 2.6 mmHg further decrease during the latter half of the fast). With refeeding, blood pressure rose precipitously (13 +/- 3 mmHg in the 1st 2 days), despite poststarvation anorexia. Blood pressure tended to rise slightly over the remainder of the realimentation period (5.2 +/- 2.8 mmHg). After the 4th supplemented fast, hypertension was sustained during 30 days of refeeding. Cumulative caloric intake in starved-refed rats fell within 2% of that in chow-fed controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1998

Slow restoration of LH pulsatility by refeeding in energetically disrupted women.

In other energy-restricted mammals, a single large meal restores luteinizing hormone (LH) pulsatility within a few hours. To determine whether this is so in women, we measured LH pulsatility during the 5th day of low energy availability [dietary energy intake - exercise energy expenditure = 10 kcal . kg lean body mass (LBM)-1 . day-1] and during a 6th day of aggressive refeeding (90 kcal . kg LBM-1 . day-1) in 15 meals providing 4,100 kcal for an energy availability of 75 kcal . kg LBM-1 . day-1. Low energy availability raised beta-hydroxybutyrate 1,000% (P < 0.001) and reduced plasma glucose 15% (P < 0.01), insulin 63% (P < 0.001), and triiodothyronine 22% (P < 0.005). In five of eight subjects, low energy availability also unambiguously suppressed LH pulse frequency 57% to 8.2 +/- 1.5 pulses/24 h (P < 10(-4)) and raised LH pulse amplitude 94% to 3.1 +/- 0.3 IU/l (P < 10(-4)), levels below the 5th and above the 95th percentile, respectively, in energy-balanced women. Aggressive refeeding restored beta-hydroxybutyrate, glucose, and insulin, but not triiodothyronine. In the five women with unambiguously disrupted LH pulsatility, aggressive refeeding had no effect on LH pulse amplitude (P > 0.9) and raised LH pulse frequency only slightly (2.4 +/- 0.6 pulses/24 h, P = 0.04) and not above the fifth percentile. This striking contrast between women and other mammals may be another clue to the unidentified mechanism mediating the effect of energy availability on LH pulsatility.

3-Hydroxybutyric Acid↗