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PubMedDate not supplied

Alterations of sensory perceptions in healthy elderly subjects during fasting and refeeding. A pilot study.

BACKGROUND: Sensory perception losses may contribute to age-related malnutrition by affecting food selection and consumption. OBJECTIVE: To determine the effects of a 36-hour fast followed by a 6-hour refeeding period on sensory perceptions in 7 healthy elderly subjects (65-80 years of age) and 6 healthy young subjects (18-35 years of age). METHODS: Self-perceived hunger and olfactory ratings were recorded on visual analogue scales in response to three different classes of odorant stimuli (salt, sweet and sour). Odorant stimuli were administered three times during the study, twice during the fasting period (12 and 24 h fasted) and once at the end of the re-nutrition period. RESULTS: A significant difference was found between the two groups for the self-perceived hunger ratings in response to the sour stimuli. A significant difference was observed between the two groups for olfactory ratings as regards the salt and sour odorant stimuli. Among the metabolic changes associated with fasting and refeeding, blood glucose was significantly related (r(2) = 0.97, p = 0.001) to the perception of hunger in the control group subjects, but no such relationship was found for the elderly subjects (r(2) = 0.16, p = NS). CONCLUSION: (1) Self-perceived hunger and olfactory ratings are specifically affected in healthy elderly. (2) Nutritional status can modulate sensory perceptions in elderly and young during the transition from fasting to refeeding.

Adolescent↗

PubMed1975

Long-term effects of starvation-refeeding in the rat.

The effects of one vs. two episodes of starvation-refeeding were studied in young male rats as a function of elapsed time between the two episodes of starvation-refeeding. Starved-refed rats ate more and gained weight faster than ad libitum-fed rats. The difference in weight gains could be attributed to the greater amount of body fat in the starved-refed rats. The responses of four NADP-linked liver dehydrogenases:isocitrate dehydrogenase (ICD)/LS-isocitrate:NADP oxidoreductase (decarboxylating) (EC 1.1.1.42), glucose-6-phosphate dehydrogenase (G6PD)/D-glucose-6-phosphate:NADP oxidoreductase (EC 1.1.1.49); 6-phosphogluconate dehydrogenase (6PGD/6-phospho-D-gluconate:NADP oxidoreductase (decarboxylating) (EC 1.1.1.44); and malic enzyme (ME)/L-malate:NADP oxidoreductase (decarboxylating) (EC 1.1.1.40) were studied. Starvation-refeeding caused an overshoot of G6PD, 6PGD, and ME, but not of ICD. A second episode of starvation caused an even greater enzyme overshoot; this difference persisted for 3 weeks with G6PD and for 2 weeks with 6PGD and ME. No significant differences in blood cholesterol were detected.

Adipose Tissue↗

PubMed1983

Restoration effects of glucose refeeding on reduced synthesis of albumin and total protein and on disaggregated polyribosomes in liver of starved rats: evidence of a post-transcriptional control mechanism.

Previous studies demonstrated that fasting is accompanied with a reduction of liver protein and albumin synthesis. A protein-deficient diet also leads to a marked change in liver RNA and protein metabolism. Although the reduction of protein synthesis and the disaggregated polyribosomes during fasting can be corrected by a single feeding of protein or a complete amino acid mixture, no or little changes of amino acid concentrations were found in portal blood and liver cytosol of fasted animals as compared to those of the fed group. To determine the effect of glucose on the reduced rate of protein and albumin synthesis of fasted rats, free and membrane-bound polyribosomes were isolated quantitatively from liver of starved rats (42-66 h) at different intervals after a single feeding of glucose and after giving glucose ad libitum for 24 h. (1) The yield of polyribosomal RNA decreased dramatically after a 42- to 66-hour starvation. A glucose refeeding did not change the RNA content. However, the restoration of polyribosome size could be observed rapidly. (2) At various levels of RNA, there was a decreased protein synthesis in fasted animals. However, the synthesis was enhanced after glucose refeeding. The albumin synthesis was also proportionately increased (10-12% of total protein synthesis of membrane-bound polyribosomes). (3) Glucose refeeding had no influence on the content of albumin mRNA sequence and liver RNA. These findings suggest that the effect of glucose on the restoration of protein and albumin synthesis is a sole post-transcriptional event.

Albumins↗

PubMed1991

Effect of fasting and refeeding on basolateral polyamine uptake and metabolism by the rat small bowel.

Fasting reduced the weight, protein, DNA, RNA and polyamine contents of the small intestine of rats, but its effects on the in vivo uptake of intraperitoneally injected 14C-spermidine through the basolateral membrane of the small intestine were small. The uptake of putrescine was nearly doubled by fasting for 48 h. Fasting for 48 h had reduced villus length but was without effects on the crypts. Refeeding for 6 h of rats fasted for 48 h led to hypertrophic growth: the length of both crypts and villi increased by about 50% without changes in cell number. The uptake of spermidine by the small intestine increased above not only that in fasted rats but also that in the controls fed ad libitum. The high putrescine uptake of rats fasted for 48 h was unchanged after refeeding for 6 h, but returned to control values after 12 h. Spermidine in the gut was well conserved, while most of the putrescine was transformed into non-polyamine metabolites. It is concluded that refeeding stimulates basolateral spermidine uptake, and this may be a general mechanism for polyamine accretion in adaptive growth of the small intestine.

Animals↗

PubMed1996

Modulation of putrescine transport in rat intestinal brush-border membrane vesicles by fasting and refeeding.

Fasting and refeeding dramatically alter small intestinal mucosal growth which is greatly dependent on polyamine biosynthesis and transport. The aim of this study was therefore to examine the uptake of the diamine putrescine by brush-border membrane vesicles from the small intestine of rats fasted for 3 days or refed a standard diet after a PERIOD OF FASTING. WHILE THE MICHAELIS-MENTEN CONSTANT KM WAS essentially unaltered, the maximum velocity (Vmax) for putrescine uptake was 1.85-fold higher in fasted animals than in ad libitum-fed controls. Refeeding fasted rats for 24 h caused a 31% decrease in the Vmax value that, however, remained 1.27-fold higher than in control RATS, WHILE THE KM VALUE WAS STILL UNCHANGED. FASTING RATS OR refeeding rats after a period of fasting caused only a 13 or 17% increase, respectively, in the value of the constant for the nonsaturable component (P) of putrescine transport relative to the corresponding control condition. Our study also confirms that both the mucosal polyamine biosynthesis and intestinal content are altered by fasting. We suggest that an increased uptake activity may have a conservative role by preventing a substantial loss of tissue polyamines during fasting.

Animals↗

PubMed1982

Substrate changes during fasting and refeeding contrasted in old and young rats.

Carbohydrate and lipid substrate changes associated with fasting were similar in aged (over 24 months), 1-year-old and young (about 4 months old) rats. In all three age-groups fasting reduced liver and skeletal muscle glycogen, elevated myocardial glycogen and plasm free fatty acid (FFA) levels, but did not significantly affect blood glucose. With refeeding, the myocardium from aged and 1-year-old rats lacked the glycogenesis observed in young rats. Less glycogenesis was also observed in aged soleus muscles during refeeding than in soleus muscles from young or 1-year-old rats. This depressed glycogenesis in the old rats could not be attributed to any change in the tissue triglyceride or plasma FFA response to refeeding, but was accompanied by a slightly greater elevation of glucagon in the aged rats. Though its etiology is unclear, the depressed glycogenesis indicates that aging affects aspects of carbohydrate metabolism in addition to the known decrease in glucose tolerance.

Aging↗

PubMed1982

Effects of starvation and refeeding on lung biochemistry in rats.

Adult rats received one fifth of their measured daily food consumption until they lost 40% body weight. Some of these rats were then refed until they reached their initial body weight. We measured the following in fed, starved, and refed animals: (1) disaturated phosphatidylcholine (DSPC) content of lung tissue and of lavage fluid, (2) protein content of lung tissue and of lavage return, and (3) DNA and RNA content of lung tissue. In starved lungs, tissue and lavage DSPC content, total protein and RNA contents, and RNA/DNA ratios were significantly lower than in fed rats. After refeeding, DSPC values returned completely to normal, whereas protein, DNA, and RNA contents were significantly higher than in fed rats. The RNA/DNA ratio was similar in the fed and refed groups. Changes in lavage DSPC are consistent with the increased surface elastic forces in starvation and their return to normal with refeeding reported by us previously. It appears that starvation leads to a reduction in cell size without changes in cell number and that refeeding is associated with a more significant increase in cell number than in cell size.

Animals↗

PubMed1978

Insulin binding to monocytes and insulin action in human obesity, starvation, and refeeding.

Insulin binding to monocytes and insulin action in vivo was examined in 14 obese subjects during the postabsorptive state and after starvation and refeeding. Tissue sensitivity to insulin was evaluated with the euglycemic insulin clamp technique. The plasma insulin concentration is acutely raised and maintained 100 muU/ml above the fasting level, and plasma glucose is held constant by a variable glucose infusion. The amount of glucose infused is a measure of tissue sensitivity to insulin and averaged 285+/-15 mg/m(2) per min in controls compared to 136+/-13 mg/m(2) per min in obese subjects (P <0.001). (125)I-Insulin binding to monocytes averaged 8.3+/-0.4% in controls vs. 4.6+/-0.5% in obese subjects (P < 0.001). Insulin binding and insulin action were highly correlated in both control (r = 0.86, P < 0.001) and obese (r = 0.94, P < 0.001) groups. Studies employing tritiated glucose to measure glucose production indicated hepatic as well as extrahepatic resistance to insulin in obesity. After 3 and 14 days of starvation, insulin sensitivity in obese subjects decreased to 69+/-4 and 71+/-7 mg/m(2) per min, respectively, whereas (125)I-insulin binding increased to 8.8+/-0.7 and 9.0+/-0.4%. In contrast to the basal state, there was no correlation between insulin binding and insulin action. After refeeding, tissue sensitivity increased to 168+/-14 mg/m(2) per min (P < 0.001) whereas insulin binding fell to 5.0+/-0.3%. We conclude that (a) in the postabsorptive state insulin binding to monocytes provides an index of in vivo insulin action in nonobese and obese subjects and, (b) during starvation and refeeding, insulin binding and insulin action changes in opposite directions suggesting that postreceptor events determine in vivo insulin sensitivity.

Adolescent↗

PubMed1989

Regulation of glucose transporter-specific mRNA levels in rat adipose cells with fasting and refeeding. Implications for in vivo control of glucose transporter number.

Fasting in the rat is associated with a rapid and progressive decrease in insulin-stimulated glucose transport activity in adipose cells, which is not only restored to normal, but increased transiently to supranormal levels by refeeding. The mechanisms for these changes in glucose transport activity appear to involve alterations in both glucose transporter number and intrinsic activity (glucose turnover number). In this study, we use the human hepatoma Hep G2 glucose transporter complementary DNA clone to examine the molecular basis for these alterations. Extractable RNA per adipose cell is decreased 35% with 3 d of fasting and increased to 182% of control with 6 d of refeeding after 2 d of fasting. This parallels changes in adipose cell intracellular water, so that total RNA/water space remains relatively constant. When the changes in total RNA/cell are taken into account, Northern and slot blot analyses with quantitative densitometry reveal a 36% decrease in specific glucose transporter mRNA level in cells from the fasted rats. The mRNA level in cells from the fasted/refed rats is restored to normal. These observations correlate closely with previous measurements of glucose transporter number in adipose cell membrane fractions using cytochalasin B binding and Western blotting. The levels of specific mRNAs for tubulin and actin on a per cell basis show similar but more dramatic changes and mRNAs encoding several differentiation-dependent adipose cell proteins are also significantly affected. Thus, the levels of mRNA for multiple adipose cell genes are affected by fasting and refeeding. In particular, this demonstrates that in vivo metabolic alterations can influence the level of a glucose transporter mRNA in adipose cells. This may have implications for the regulation of glucose transporter number and glucose transport activity.

Adipose Tissue↗

PubMedDate not supplied

The effect of severe undernutrition and subsequent refeeding on whole-body metabolism and protein synthesis in human subjects.

BACKGROUND: To determine the consequences of severe undernutrition and refeeding on whole-body metabolism and protein synthesis. METHODS: Respiratory quotient (RQ), resting energy expenditure (REE), and whole-body protein synthesis (WBPS) were assessed in undernourished patients, with anorexia nervosa (n = 8) or with coexistent disease (n = 17). Results were compared with 17 healthy controls. Six anorexic patients and 13 disease patients consented to study after nutrition support. RESULTS: Mean body mass index was 12.46 +/- 0.53 kg/m2 in the anorexia patients and 13.81 +/- 0.40 kg/m2 in the disease patients (controls 23.71 +/- 0.72 kg/m2; p < .001). Compared with controls, RQ was similar in anorexia patients (0.85 +/- 0.05 vs 0.90 +/- 0.05) but lower in the disease patients (0.76 +/- 0.03 vs 0.90 +/- 0.05; p = .02). REE was lower in the patients (anorexia 1058 +/- 134.0 kcal/d, disease 1189 +/- 101.4 kcal/d vs 1828 +/- 89.76 kcal/d; p < .001); however, expressed as kcal/kg/d, it was higher (anorexia 32.17 +/- 4.25, disease 31.30 +/- 2.14 vs 25.07 +/- 1.00; p < .05). WBPS was lower in the patients (anorexia 140.9 +/- 10.54 g/d, disease 119.8 +/- 8.57 g/d vs 305.0 +/- 21.64 g/d; p < .001); however, when expressed as g/kg/d, the anorexia patients were similar to controls, whereas the disease patients were lower (3.11 +/- 0.24 vs 4.27 +/- 0.32; p < .05). Refeeding increased RQ in the disease patients (0.84 +/- 0.03 vs 0.76 +/- 0.03; p < .05), and normalized REE (anorexia 27.65 +/- 3.05 kcal/kg/d, disease 28.90 +/- 1.85 kcal/kg/d). WBPS increased in the disease patients (173.6 +/- 16.38 g/d vs 116.5 +/- 10.15 g/d; p < .01). CONCLUSIONS: Undernutrition is associated with increased REE (kcal/kg/d). Reduction in RQ and protein synthesis (g/kg/d) was evident in those patients with coexistent disease. Refeeding resulted in normalization of RQ, REE (kcal/kg/d), and protein synthesis (g/kg/d).

Analysis of Variance↗

PubMedDate not supplied

Relationship of jejunostomy and urine polyamine content to refeeding and intestinal structure and function.

The polyamine content of the intestinal mucosa is increased with mucosal proliferation. Our purpose was to determine if urine and jejunostomy polyamine content increases after refeeding and correlates with intestinal length and carbohydrate absorption after intestinal resection. Five patients with intestinal remnant lengths ranging from 1.5 to 8 feet after intestinal resection and jejunostomy formation were studied after refeeding of an elemental diet. Mean putrescine and spermidine levels in the jejunostomy effluent but not in the urine increased significantly after refeeding (p less than 0.05). These changes correlated with intestinal remnant length and carbohydrate absorption. Carbohydrate absorption correlated with polyamine levels in a single patient studied longitudinally. The polyamine content of intestinal fluid may serve as a marker of the status of the intestinal mucosa and may prove useful in the dietary management of individuals with the short bowel syndrome.

Adult↗

PubMedDate not supplied

Morphologic and cytoproliferative patterns of duodenal mucosa in two patients after long-term total parenteral nutrition: changes with oral refeeding and relation to intestinal resection.

The morphologic and cytoproliferative patterns of the duodenal mucosa of two adult patients, one of whom had a short bowel, were evaluated after more than 2 months of postoperative total parenteral nutrition and 2 and 12 months after the resumption of oral alimentation. Morphometric analysis was performed on routinely processed duodenal biopsies. Cell proliferation was evaluated by means of in vitro bromodeoxyuridine uptake. The results were compared with those obtained in five healthy controls. After parenteral nutrition, patients showed significantly lower villus height and crypt depth than those of controls and a normal bromodeoxyuridine labeling index. After 2 months of refeeding, villus and crypt returned to normal, and the labeling index was increased. After 12 months of oral refeeding, labeling index, villus height, and crypt depth were similar to those of controls. The patient with the short bowel showed a number of cells per unit length of villus and crypt significantly greater than those of the controls and of the patient who underwent shorter intestinal resection. In human duodenal mucosa, (1) hypoplasia develops after long-term total parenteral nutrition; (2) mucosal recovery occurs through an increased cell proliferation after oral refeeding; and (3) extensive small bowel resection determines the development of relative hyperplasia.

Adult↗

PubMedDate not supplied

Ventricular muscle and lung protein synthesis in vivo in response to fasting, refeeding, and nutrient supply by oral and parenteral routes.

BACKGROUND: Fasting and other catabolic states are characterized by reductions in the rate of protein synthesis. Most studies have investigated tissues such as skeletal muscle or liver, but impairments in the biochemistry of cardiovascular tissues also contribute to enhanced morbidity. The objectives of the present study were (1) to determine the response of protein synthesis in the heart and lung of young rats to overnight fasting; and (2) to determine whether protein synthesis could be ameliorated or modulated by refeeding or provision of enteral or parenteral nutrition. METHODS: Fractional rates of protein synthesis (ie, the percentage of tissue protein renewed each day, ks) were measured in vivo in the ventricular muscle and lungs of young male Wistar rats (body weight, 100 to 130 g) with a "flooding" dose of L-[4(3)H]phenylalanine. Rats were fed ad libitum or fasted overnight. Fasted rats were subjected to various treatments. RESULTS: When nutrient supply in fasted rats recommenced by refeeding for 1 hour, there were small but significant increases in the rates of ventricular protein synthesis, although the infusion of amino acids and glucose for 1 hour had no significant effect. Increases in ventricular ks were also obtained when amino acids were infused for 6 hours. Infusion of glucose alone for 6 hours did not cause a significant increase in ventricular ks. The effect of infusing a mixture of glucose plus amino acids for 6 hours was similar to the effects of amino acids alone. In all instances, ventricular ks in rats infused with amino acid for 6 hours did not attain rates observed in fed rats. ks was reduced in the lung after overnight fasting but was unresponsive to refeeding or to acute or chronic provision of amino acids and glucose by either IV or oral routes. Measurements also suggested that changes in neither insulin nor glucagon per se were responsible for the amino acid-induced increases in heart protein synthesis. However, acute treatment of rats with anti-insulin serum reduced rates of ventricular ks below values observed in fed rats. Anti-insulin serum also increased lung ks. CONCLUSIONS: It was concluded that rates of heart protein synthesis could be increased by the chronic provision (ie, 6 hours) of nutrients by oral or IV routes. In contrast, the lung was insensitive to these treatments. The observations have important implications for clinical situations, which are characterized by diminished cardiopulmonary protein synthesis.

Administration, Oral↗

PubMedDate not supplied

Refeeding syndrome and hypophosphatemia.

Hypophosphatemia is a potentially life-threatening complication of reinstating nutrition in a malnourished patient. Refeeding syndrome is a term that refers to various metabolic abnormalities that may complicate carbohydrate administration in subnourished patient populations. Hypophosphatemia is the most well-known, and perhaps most significant, element of the refeeding syndrome and may result in sudden death, rhabdomyolysis, red cell dysfunction, and respiratory insufficiency. This review briefly examines refeeding-induced hypophosphatemia in the hospitalized patient in hopes of making clinicians more aware of this common, but often overlooked, potentially dangerous problem.

Dietary Carbohydrates↗

PubMedDate not supplied

Severe hypophosphatemia in a patient with anorexia nervosa during enteral refeeding.

Hypophosphatemia is a seldom but potentially fatal complication of the nutritional recovery or refeeding syndrome in patients with protein-calorie malnutrition or starvation. We report here the case of a 35-year-old anorexic patient who presented a severe but uncomplicated hypophosphatemia during enteral refeeding, despite phosphorus supplementation. Serum phosphorus monitoring is recommended in severely malnourished anorexic patients, particularly during the first week of refeeding, be it parenteral or enteral.

Adult↗

PubMed1991

Refeeding enhances intestinal repair during an acute enteritis in infant rabbits subjected to protein-energy malnutrition.

We examined the effects of refeeding during an acute bacterial enteritis on small intestinal repair in infant rabbits subjected to protein-energy malnutrition and in noninfected and infected dietary controls. Malnutrition was induced by litter expansion at 7 d of age. Randomly selected litters from both dietary groups were infected on d 17 with Yersinia enterocolotica. Inflammation and intestinal damage were observed in the jejunum and ileum at the "acute stage" of infection in 23-d-old animals from both dietary groups, as evidenced by an inflammatory infiltrate, blunted villi, and reduced disaccharidase activities. In addition, ileal glucose-stimulated Na+ absorption was depressed. On d 24, a 7-d period of ad libitum refeeding of breast milk and rabbit feed was initiated in randomly selected litters of infected-malnourished animals and all dietary controls. Mucosal repair was nearly complete at 31 d of age in infected dietary controls and in the infected-malnourished animals that were refed, as demonstrated by the recovery of segmental mucosal mass and ileal glucose-stimulated Na+ transport in association with the resolution of inflammation and diarrhea. Only mucosal disaccharidase activities remain depressed. In contrast, in 31-d-old infected-malnourished animals subjected to ongoing nutrient deprivation, severe intestinal damage persisted as evidenced by increased mortality, ongoing intestinal inflammation, mucosal hypoplasia, depressed disaccharidase activities, and reduced glucose-stimulated Na+ transport. We conclude that a refeeding regimen introduced during an acute bacterial enteritis is well tolerated and promotes recovery of intestinal mass, structure, and function in malnourished infant rabbits and dietary controls.

Animals↗

PubMed1976

Nutrition and somatomedin. I. Effect of fasting and refeeding on serum somatomedin activity and cartilage growth activity in rats.

The relationship between nutrition, somatomedin, and growth was studied in young male rats which were fasted for 72 h, and then refed. Cartilage growth activity was measured by the incorporation of SO4 by costal cartilage incubated in vitro. Serum somatomedin activity was measured by the ability of sera to stimulate the incorporation of SO4 in vitro by cartilage from hypophysectomized rats or normal young pigs. Cartilage growth activity was unchanged after 24 h of fasting, but decreased significantly to hypopituitary levels after 72 h. The decrease in cartilage growth activity could not be attributed to a decrease in the ability of cartilage to respond to somatomedin, since fasted rat cartilage incubated in vitro had significantly greater stimulation from the addition of normal rat serum (normal somatomedin) than from the addition of hypophysectomized rat serum (low somatomedin). A decrease in serum somatomedin preceded the decrease in growth activity; somatomedin was significantly decreased after 24 h of fasting, and fell to hypopituitary levels after 72 h of fasting. The decrease in somatomedin could not be attributed to growth hormone deficiency, since treatment with bGH did not prevent the fall in somatomedin. The direct addition of fasted rat serum to normal rat serum did not inhibit the somatomedin activity of the normal serum. The refeeding of 72h-fasted rats was associated with an increase in serum somatomedin which was significant after 6 h, and comparable to control levels after 24 h of refeeding. The increase in somatomedin was followed by an increase in cartilage growth activity, which was significant after 12 h, and comparable to control levels after 48 h of refeeding. We conclude that adequate food intake appears to be required for the maintenance of normal levels of somatomedin; the processing of nutrients may modulate the generation of somatomedin.

Animal Nutritional Physiological Phenomena↗

PubMed2003

Adiponectin gene expression in subcutaneous adipose tissue of obese women in response to short-term very low calorie diet and refeeding.

Adiponectin is an adipocyte-derived protein suggested to be involved in energy homeostasis and in lipid and glucose metabolism. Little is known regarding the consequence of acute changes in energy balance on adiponectin mRNA expression in human adipose tissue. Using a real-time RT-PCR assay, we investigated the effects of 2-d very low calorie diet (VLCD) and subsequent refeeding on adiponectin mRNA expression in sc adipose tissue of morbidly obese women. Basal adiponectin mRNA abundance of the obese women showed a wide distribution (2.6-14.3 mRNA/18S rRNA; coefficient of variation, 51.2%) and was significantly lower than that of lean controls (P < 0.001). In the obese group, the VLCD caused a 33% rise (P < 0.01) in the average level of mRNA, whereas refeeding caused a 32.8% fall (P < 0.05). In contrast, the change in leptin mRNA expression with either VLCD or refeeding was not statistically significant. The obese subjects who showed an acute adiponectin mRNA response to the changes in energy intake had a higher basal level of adiponectin mRNA (P = 0.02) and a borderline-significantly lower body mass index compared with the subjects who showed no or weak adiponectin mRNA response. Insulin sensitivity of the responder subgroup significantly increased by 89% (P = 0.008) after the VLCD, whereas insulin sensitivity of the nonresponder subgroup only increased by 24% (P = 1.56). This study indicates that adiponectin mRNA in sc adipose tissue can acutely respond to short-term energy changes in some obese subjects. Both the levels of adiposity and insulin sensitivity may contribute to the variation in adiponectin gene expression in response to acute energy changes.

Adiponectin↗