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PubMed1981

Adaptation of glycolytic enzymes: glucose use and insulin release in rat pancreatic islets during fasting and refeeding.

Starvation refeeding experiments were conducted in rats to test the hypothesis that adaptation of glucokinase (the high Km component of glucose phosphorylation) could be the major determinant of glucose metabolism of pancreatic islet cells and of glucose-stimulated insulin release. It was found that glucokinase of islet homogenates, glucose use by intact isolated islets, and glucose-induced insulin release as studied in a perifusion system were decreased after 24 h of fasting, whereas P-fructokinase and 3-P-glyceraldehyde DH were unaltered. After extended fasting (e.g., 120 h) all three enzymes were decreased but glucose use did not change any further. Refeeding normalized all parameters. These and previous results support the concept that glucokinase serves as the adaptive beta-cell glucoreceptor relating blood glucose to insulin release.

Animals↗

PubMed1981

Effect of diabetes, insulin, starvation, and refeeding on the level of rat hepatic fructose 2,6-bisphosphate.

The influence of alloxan diabetes and starvation for 72 h on the level of rat hepatic fructose 2,6-biphosphate was investigated. Both diabetes and starvation decreased the level to 10% of the value found in livers of normal, fed rats (10 nmol/g liver). The activity of the enzyme responsible for the synthesis of fructose 2,6-bisphosphate, 6-phosphofructo 2-kinase, was also decreased in livers of diabetic rats. Insulin administration for 24 h to diabetic rats restored the level of fructose 2,6-bisphosphate to normal. Refeeding a high carbohydrate diet for 24 h to starved rats resulted in fructose, 2,6-biphosphate levels that were 2.5-fold higher than that in livers of fed rats. The level of fructose 2,6-bisphosphate in diabetes and starvation, and after refeeding correlates as well with the rate of glycolysis and gluconeogenesis in these states and thereby provides further support for its role in regulating hepatic carbohydrate metabolism.

Animals↗

PubMed2003

Fetal programming of perivenous glucose uptake reveals a regulatory mechanism governing hepatic glucose output during refeeding.

Increased hepatic gluconeogenesis maintains glycemia during fasting and has been considered responsible for elevated hepatic glucose output in type 2 diabetes. Glucose derived periportally via gluconeogenesis is partially taken up perivenously in perfused liver but not in adult rats whose mothers were protein-restricted during gestation (MLP rats)-an environmental model of fetal programming of adult glucose intolerance exhibiting diminished perivenous glucokinase (GK) activity. We now show that perivenous glucose uptake rises with increasing glucose concentration (0-8 mmol/l) in control but not MLP liver, indicating that GK is flux-generating. The data demonstrate that acute control of hepatic glucose output is principally achieved by increasing perivenous glucose uptake, with rising glucose concentration during refeeding, rather than by downregulation of gluconeogenesis, which occurs in different hepatocytes. Consistent with these observations, glycogen synthesis in vivo commenced in the perivenous cells during refeeding, MLP livers accumulating less glycogen than controls. GK gene transcription was unchanged in MLP liver, the data supporting a recently proposed posttranscriptional model of GK regulation involving nuclear-cytoplasmic transport. The results are pertinent to impaired regulation of hepatic glucose output in type 2 diabetes, which could arise from diminished GK-mediated glucose uptake rather than increased gluconeogenesis.

Animals↗

PubMed1989

Early effects of refeeding a complete diet on the translational initiation activity in rat liver slices.

A complete diet containing 23% protein was fed to two-day-fasted rats. The effects of this diet on protein biosynthesis, through the examination of liver slices, was investigated. (1) Refeeding enhanced the protein-synthesizing activity with better preservation of heavy polysomes in the liver slices. Protein in the diet was necessary to induce, through refeeding, the activation of protein synthesis in the liver. (2) The incorporation of [3H]methionine into 40S subunits and 80S subunits, where "run-off" 40S and 60S subunits had been accumulated by preincubation with 2 x 10(-6) M pactamycin, was much higher in the liver slices of refed rats than in the liver slices of fasted rats. By using chain initiation inhibitors, it was shown that labeled 40S and 80S subunits were 40S and 80S initiation complexes, respectively.

Animals↗

PubMed1979

Effect of fasting and fasting and refeeding on hepatic and renal gluconeogenic enzymes in the chicken.

The effect of fasting and fasting and refeeding on hepatic and renal gluconeogenic enzyme activities were studied in six-week-old chickens (Gallus domesticus: New Hampshire male x Columbian female). Hepatic pyruvate carboxylase appeared not to be affected by fasting, but the renal enzyme activity increased in four-day fasted chickens. The hepatic mitochondrial and cytosolic phosphoenolpyruvate carboxykinases were essentially not affected by fasting. The renal mitochondrial phosphoenolpyruvate carboxykinase showed a slight increase in activity only after a four-day fast, but the cytosolic enzyme activity increased markedly already after a two-day fast. Also the activities of the hepatic and renal fructose-1,6-diphosphatase and glucose-6-phosphatase increased markedly on fasting. Refeeding for four days after a four-day fast returned these enzyme activities to near control values.

Animals↗

PubMed1999

Serum leptin levels in patients with anorexia nervosa before and after partial refeeding, relationships to serum lipids and biochemical nutritional parameters.

Leptin is a protein hormone produced by adipocytes that provide information about the body fat content. It was previously reported that serum leptin levels were decreased in patients with anorexia nervosa in comparison with healthy control subjects. The aim of our study was to compare serum leptin levels in patients with anorexia nervosa (n=11, initial mean BMI=15.4 kg/m2) before and after partial recovery with control age-matched subjects (n=11, mean BMI= 20.3 kg/m2) and to study the relationships of leptin levels, serum lipids and biochemical nutritional parameters. We found that serum leptin concentrations in patients with anorexia nervosa were significantly reduced in comparison with control subjects (3.61 vs 9.37 ng.ml(-1), p<0.01). Serum cholesterol, triglycerides, total protein and albumin in patients with anorexia nervosa either before or after partial recovery did not differ from the control group. After partial recovery, a significant increase in serum leptin was observed (4.83 vs 3.61 ng.ml(-1), p<0.05), but the values still remained significantly lower than in the control group (p<0.01) Leptin levels correlated positively with the body mass index in the control group and anorexia nervosa group before recovery. The correlation with BMI in the anorexia nervosa group after refeeding was not significant. No significant correlation was found between leptin concentrations and serum lipids, total protein, albumin and prealbumin, respectively. Serum leptin thus represents a sensitive parameter that reflects the nutritional status in patients with anorexia nervosa suitable for long-term follow up during refeeding therapy.

Adult↗

PubMed1999

[The effect of partial refeeding on serum levels of leptin and resting energy expenditure in female patients with anorexia nervosa].

BACKGROUND: Serum leptin levels and resting energy expenditure are significantly decreased in patients with anorexia nervosa compared to healthy subjects. Partial realimentation of patients with anorexia nervosa increases both these parameters. However, there so far are no data concerning the relationship of serum leptin levels and resting energy expenditure in patients with anorexia nervosa. The aim of our study was to follow the relationship of serum leptin levels and resting energy expenditure in patients with anorexia nervosa before and after refeeding. METHODS AND RESULTS: It was found that serum leptin levels in patients with anorexia nervosa both before and after partial realimentation were significantly lower compared to healthy subjects (0.86 +/- 0.9 ng.ml-1 and 1.77 +/- 1.9 ng.ml-1 vs 6.85 +/- 3.0 ng.ml-1, p < 0.05). The total resting energy expenditure in patients with anorexia nervosa both before and after realimentation were significantly lower than in the control group (4973 +/- 979 and 5263 +/- 899 vs 6401 +/- 827 kJ/day, p < 0.05). When expressed per body weight the resting energy expenditure in patients with anorexia nervosa was significantly higher in comparison with the control group (122.3 +/- 20.6 and 121.5 +/- 14.2 vs 104.2 +/- 14.6 kJ/day, p < 0.05). The differences in resting energy expenditure in patients with anorexia nervosa before and after refeeding did not reach statistical significance. The body mass and the body fat content increased significantly after realimentation index (14.5 +/- 1.4 vs 15.6 +/- 1.5 kg.(m2)-1 and 14.9 +/- 3.4 vs 16.6 +/- 3.7, p < 0.05) but remained still below of those of control group (BMI 22.3 +/- 2.7, body fat content 26.9 +/- 4.2). CONCLUSIONS: Our study confirmed the reduced serum leptin levels and the total resting energy expenditure in patients with anorexia nervosa compared to healthy age-matched subjects. No statistically significant relationships were found between serum leptin levels and resting energy expenditure either in healthy subjects or in patients with anorexia nervosa before or after partial realimentation respectively.

Adolescent↗

PubMed1975

[Studies on the number of fat cells and connective tissue cells in white adipose tissue in chronic starvation and after refeeding. I. Investigations on aurothioglucose-obese NMRI-albino-mice(author's transl)].

UNLABELLED: Former investigations (Rakow et al., 1970, 1971 b) on epididymal fat pads of lean NMRI-Albino-mice during starvation and refeeding have shown that the number of fat cells (adipocytes) remained unchanged while the number of cells o connective tissue decreased during starvation and increased during the refeeding period. In the present paper the problem has been investigated whether these variations could be demonstrated also in NMRI-albino-mice obesified by administration of aurothioglucose. MATERIAL AND METHODS: The investigations were performed with male NMRI-Albino-mice rendered obese by administration of aurothioglucose (800 mg per kg body weight). These animals were fed 2.5 g Altromin 1115 R daily for six weeks. After this they were fed Altromin 1115 R and additional oat flakes ad libitum for three (exp. groups HW3) and seven (exp. groups HW 7) days respectively. After this time the animals were sacrificed. The epididymal fat pads were removed and weighed. One of both pads of each animal was used for chemical investigations. After PCA-treatment (0.5 n, 90 degrees C. 15 min.) the DNA (Burton, 1956) and RNA (Ceriotti, 1955) was determined in the supernatant. After NaOH-treatment (0.5 n, 37 degrees C, 24 Hrs) the noncollagen protein content (Lowry et al., 1951) of the sediment was estimated. After HCl-treatment (25%, 110 degrees C, 20 hrs.) the collagen content (Stegemenn, 1958; modified by Rauskolb, 1967) was determined. The remaining fat pad was used for calculations of cell numbers in the fat cell and connective tissue cell compartment. For this reason fat cells were isolated according to Rodbell (1964). The fat cell diameters were determined microscopically and the average masses of the fat cells were estimated. From the wet weight of the fat pads and the average fat cell mass the number of fat cells was calculated. The remaining suspension of fat cells and cells of connective tissue was utilized for cell smears. These smears were stained with Schiff's reagent (Feulgen et al., 1924; Graumann, 1952). With an integrating microdensitometer (Deeley, 1955) the average relative DNA-content of single cell nuclei were measured and the ploidy patterns were estimated. From the whole DNA-content of the fat pads and the DNA-content of the fat cell population the number of cells of the connective tissue was calculated...

Adipose Tissue↗

PubMed2000

Effect of aproteic diet and fasting on insulin, pancreatic noradrenaline and luteinizing hormone. Changes after 24-hour refeeding.

OBJECTIVE AND DESIGN: the objective of this study performed in adult male rats was to determine the alteration in glycemic, insulin and gonadotrophin luteinizing hormone secretion, and noradrenaline pancreatic concentration caused by fasting (F) and aproteic diet (Ap) during 7 and 21 days respectively, as well as the recovery after 24-hour refeeding with control diet (Co). RESULTS: a significant decrease in glycemic levels was only achieved through fasting (F: 86 +/- 5.1 mg %), when compared with controls (Co: 107 +/- 5 mg %). In spite of the high levels of carbohydrates (89%) present in the aproteic diet, the animals fed with this diet showed no differences in glycemic levels (Ap: 120.3 +/- 12.2 mg %), compared with controls. As a result of fasting and aproteic diet, there was a significant decrease in insulin (F: 8.67 +/- 1.36; Ap: 5.7 +/- 0.67; Co: 31 +/- 3.4 uU/ml) and LH levels (F: 10.175 +/- 1.74; Ap: 13.7 +/- 4; Co: 29.83 +/- 4.91 ng/ml). The refed recovered insulin (FR: 50.57 +/- 6.63; ApR: 43.5 +/- 6.85 uU/ml), but not LH levels (FR: 14.25 +/- 3.54; ApR: 13.03 +/- 4.25 ng/ml). A significant increase was observed in the pancreatic noradrenaline concentration (P<0.001) of rats receiving aproteic diet (889.9 +/- 34.65 ng/mg tissue) and fasting during 7 days (827.5 +/- 55.7 ng/mg tissue), compared with controls (531.1 +/- 48.6 ng/mg tissue). CONCLUSIONS: fasting and aproteic diets altered gonadal and metabolic control. When returning to a normal nutritional condition, only the metabolic control, not the reproductive function, could be recovered in the first 24 hours of refeeding. Malnutrition-induced hypoinsulinemia would be caused by an increase in a specific noradrenergic tone.

Journal Article↗

PubMed1975

[Studies on the number of fat cells and connective tissue cells in white adipose tissue in chronic starvation and after refeeding. II. Investigations on obese and lean C 57 BL/6 J-mice (author's transl)].

UNLABELLED: Former investigations (Rakow et al., 1970, 1971a, b 1974) have demonstrated a constancy of the adipocyte number in white adipose tissue (parepididymal fat pads) of lean NMRI-albino-mice and aurothioglucose-obese NMRI-albino-mice during starvation and subsequent refeeding. In contrast the number of cells of connective tissue showed great variations under the experimental conditions mentioned above. The present paper describes which changes of the different cell populations within the adipose tissue could be demonstrated in lean and obese C57BL/6 J-mice. MATERIAL AND METHODS: The investigations were performed with obese and lean male C57BL/6 J-mice. The control animal groups were fed for six weeks 2.5 g (lean mice) and 2 g (obese mice), respectively, Altromin 1115R daily (starvation phase). After this time some of these animalwere killed (exp. groups H). The remaining animals now were fed Altromin 1115R and additional oat falkes ad libitum. Three (exp. groups HW3) and seven (exp. groups HW 7) days, respectively, after the beginning of the refeeding phase the animals were killed. After sacrifice the epididymal fat pads were weighed and treated with either (fat extraction). The dry mass was hydrolized with PCA (0.5 m, 90 degrees C, 40 min). In the supernatant the DNA (Burton, 1956), RNA (Ceriotti, 1955) and polysaccharide content (Seifter et al., 1950) were measured. The sediment was hydrolized with NaOH (0.5 n, 37 degrees C, 24 hrs). In this solution the protein content (Lowry et al., 1951) was determined. In addition fat cells were isolated according to Rodbell (1964). The fat cell diameters were determined microscopically and the average masses of the fat cells were estimated. From the wet weight of the fat pads and the average fat cell mass and number of fat cells were calculated. The remaining suspension of fat cells and cells of connective tissue were utilized for cell smears. These cell smears were stained with Schiff's reagent (Feulgen et al., 1924; Graumann, 1953). With an integrating microdensitometer (Deeley, 1955) the average relative DNA-content of single cell nuclei was measured and the ploidy patterns were estimated. The DNA-content was measured chemically according to Burton (1956). From the whole DNA-content of the fat pads and the DNA-content of the fat cell population the number of cells of the connective tissue was calculated...

Adipose Tissue↗

PubMed1992

The effect of fasting and refeeding on oxygen consumption by rats.

Oxygen consumption is usually measured on fasted animals to avoid the thermal effect of feeding. However, fasting itself may decrease oxygen consumption as a way of conserving energy. The present study was undertaken to determine how long the fasting period should be to avoid the thermal effect of feeding without promoting a further decrease in oxygen consumption by the activation of energy-conservation mechanisms. Oxygen consumption was also measured to evaluate the effect of refeeding after different fasting periods. There was a 16% decrease in oxygen consumption from 0 to 12 h fasting related to the thermal effect of feeding, followed by a less intense (12%) decrease from 12 to 48 h fasting resulting from the energy conservation mechanism. During refeeding, oxygen consumption was higher during the first 30-min period than during the last 30-min period of the 1-h measurement, indicating the probable presence of a cephalic phase of postprandial thermogenesis. We conclude that 12-h fasting is the most appropriate period to avoid the thermal effect of feeding without significantly stimulating the energy conservation mechanism.

Animals↗

PubMed2004

Tissue-specific effect of refeeding after short- and long-term caloric restriction on malic enzyme gene expression in rat tissues.

Restricting food intake to a level below that consumed voluntarily (85%, 70% and 50% of the ad libitum energy intake for 3 or 30 days) and re-feeding ad libitum for 48 h results in an increase of malic enzyme (ME) gene expression in rat white adipose tissue. The increase of ME gene expression was much more pronounced in rats maintained on restricted diet for 30 days than for 3 days. The changes in ME gene expression resembled the changes in the content of SREBP-1 in white adipose tissue. A similar increase of serum insulin concentration was observed in all groups at different degrees of caloric restriction and refed ad libitum for 48 h. Caloric restriction and refeeding caused on increase of ME activity also in brown adipose tissue (BAT) and liver. However, in liver a significant increase of ME activity was found only in rats maintained on the restricted diet for 30 days. No significant changes after caloric restriction and refeeding were found in heart, skeletal muscle, kidney cortex, and brain. These data indicate that the increase of ME gene expression after caloric restriction/refeeding occurs only in lipogenic tissues. Thus, one can conclude that caloric restriction/refeeding increases the enzymatic capacity for fatty acid biosynthesis.

Adipose Tissue↗

PubMed2004

[A case report of severe hypophosphatemia in the course of refeeding syndrome].

This is a case report of 53 year old male who underwent pancreatoduodenectomy for chronic pancreatitis. Two months after the operation the symptoms of severe malnutrition caused by nutrition digestive disorders developed. The patient was admitted to the hospital with the symptoms of severe malnutrition and general poor medical condition. The patient was put on total parenteral nutrition (TPN) after the preliminary treatment of water-electrolytes imbalance. After 3 days of TPN a severe hypophosphatemia occurred (serum level < or = 0.25 mmol/l). The refeeding syndrome developed despite the use of phosphate supplementation in the hypocaloric TPN regimen. The hypophosphatemia caused the life threatening neurological and cardiovascular symptoms. The patient was put on intensive infusion fluid therapy with phosphate supplementation and transient withdrawal of TPN, which resulted in the patient's recovery. This case confirms the risk of development of refeeding syndrome in the malnourished patients. It indicates the need of close monitoring of phosphate serum level and the need of phosphate supplementation especially during the first days of nutritional treatment in such patients.

Chronic Disease↗

PubMed2005

Refeeding oedema in anorexia nervosa.

Refeeding oedema in patients with anorexia nervosa is a known but yet under-reported and poorly-understood condition. We illustrate this condition in a 19-year-old girl with anorexia nervosa who developed bipedal oedema after she was started on nutritional therapy. It is important to be aware of the differential diagnoses of oedema in such cases, which includes heart failure and previous diuretic abuse. Refeeding oedema generally resolves spontaneously but some individuals may require treatment.

Adult↗

PubMed2005

Refeeding syndrome in early pregnancy. Case report.

Refeeding syndrome is a very serious disorder that is not often observed today, as it is more common during times of mass starvation or war. Nowadays, it is sometimes found in patients suffering from anorexia nervosa or neoplastic diseases. A case recently treated in our Intensive Care Unit is described. The patient was pregnant and suffering from Crohn's disease. It is emphasized that although refeeding syndrome is often fatal if not treated early, it is easily prevented or treated with adequate nutritional support.

Acid-Base Imbalance↗

PubMedDate not supplied

Hepatic steatosis and serum very low density lipoproteins during two types of protein malnutrition followed by balanced refeeding.

The relation of serum very low density lipoproteins (VLDL) to hepatic steatosis was studied during protein malnutrition followed by refeeding of a balanced diet in growing rats. A control group was fed a balanced diet containing 15% casein for 42 days. Two depleted groups were fed low protein diets containing 2% casein (group C) or 5% gluten (group GI) (protein malnutrition phase) for 28 days and then were fed the balanced diet for 14 days (refeeding phase). The concentrations of phospholipids and proteins in both liver and serum VLDL were decreased during protein malnutrition, whereas triacylglycerols, unesterified cholesterol, and cholesteryl esters were higher in the liver and lower in the serum VLDL in the C and GI groups compared with the control group. There was a significant inverse relation between serum VLDL apolipoproteins and liver triacylglycerols on the one hand and between serum VLDL triacylglycerols and liver triacylglycerols on the other hand, in both depleted groups, although this relation was less important in the GI group. The major fatty acid levels of liver triacylglycerols were negatively correlated with those of serum VLDL during protein malnutrition. Our results show that in spite of a similar fatty acid intake, protein malnutrition involved an important decrease in essential fatty acids in VLDL triacylglycerols and phospholipids. Moreover, triacylglycerol accumulation was accompanied by increases in unesterfied cholesterol and cholesteryl esters in the liver of rats fed low protein diets, especially with 5% gluten. Hence, the hepatic steatosis was not entirely attributable to impaired transport of triacylglycerols by VLDL.

Animals↗

PubMed1986

Effects of refeeding on respiration and skeletal muscle function.

This article discusses refeeding in relation to respiratory skeletal muscle function and the subsequent function of the respiratory system as a whole. The characteristic alterations in malnourished skeletal muscle and the response to refeeding are outlined. Following this, a simple energetic model is used to explore future areas of therapeutic research and practical recommendations.

Animals↗

PubMed1985

Lysosomal enzyme activities in muscle following starvation and refeeding in the saithe Pollachius virens L.

Saithe (Pollachius virens L.) were starved for 66 days at 10 degrees C and activities of aryl sulfatase, acid proteinase, beta-glucuronidase, RNAase and acid phosphatase measured in homogenates prepared from fast and slow myotomal muscles. In fed fish, hydrolase activities were generally higher in slow than fast muscles. With the exception of acid proteinase activity in slow muscle, the activities of all the lysosomal enzymes increased by 70 to 100% during starvation. In general, there was a proportionally larger increase in the hydrolase activities in fast than in slow muscle. In a second experiment, fish were starved for 74 days, and refed for up to 52 days. The increases in aryl sulfatase and acid proteinase activity produced in fast muscle with starvation were found to be rapidly reversed by refeeding. Lysosomal enzyme activities in fish sampled after 10 days refeeding were not significantly different from fed controls. Membrane fractions enriched in aryl sulfatase activity were prepared from the fast muscle of 66-day starved fish. These were capable of degrading both myosin heavy chains and actin to lower molecular weight peptides at acid (pH 5.0), but not at neutral pH. The results suggest a role for lysosomal enzymes in the breakdown of myofibrillar proteins during starvation.

Animals↗