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PubMed2000

The effect of severe undernutrition, and subsequent refeeding on digestive function in human patients.

BACKGROUND: Severe undernutrition may adversely affect gut function. AIMS: To investigate the effects of severe undernutrition and subsequent refeeding on human digestive function. METHODS: Severely undernourished patients (body mass index (BMI) < 17 kg/m2) were studied before, and after a period of intensive nutritional support. Standard intestinal absorption tests (faecal fat and urinary xylose excretion), pentagastrin-stimulated acid secretion, and cholecystokinin octapeptide (CCK-8)-stimulated pancreatic enzyme secretion tests were performed. In addition, duodenal biopies were taken to assess gut mucosal morphology. Findings were evaluated in comparison to a group of normal healthy volunteers. RESULTS: Mean BMI of the patients prior to nutritional support was 13.41 kg/m2, with improvement to 16.12 kg/m2 after. Duodenal histology showed evidence of villous atrophy in six of 14 (43%) undernourished patients. Mean xylose excretion following a 5 g oral dose was 0.62 g/5 h in the group of undernourished patients prior to nutritional support (normal > 1 g/5 h), with improvement to 1.40 g/5 h (P < 0.01) after feeding. Maximal gastric acid output was significantly impaired in the undernourished group, as compared to the controls (6.94 mEq/l vs 25.53 mEq/l, P < 0.02), with a significant improvement to 12.30 mEq/l (P < 0.05) following nutritional support. Pancreatic enzyme output was significantly reduced (amylase 830.9 U/h vs 2304 U/h, P < 0.01; lipase 38.0 U/h vs 118.6 U/h, P < 0.01; trypsin 119.7 U/h vs 341.4 U/h, P < 0.01). Following a period of nutritional support there was a significant improvement in amylase and lipase outputs to 1819 U/h and 85.5 U/h, respectively (P < 0.01). These levels were not significantly different from the normal controls. Trypsin output, however, remained significantly impaired at 174.3 U/h (P < 0.01). CONCLUSIONS: Severe undernutrition is associated with significant impairment of digestive function, with improvement occurring following nutritional support. These changes may affect initial tolerance to enteral feeding, particularly in those patients with co-existent gut disease.

Cachexia↗

PubMed1978

An iron requirement for the synchronous progression of colonic cells following fasting and refeeding.

Evidence is presented to show dietary iron to be a major co-factor in the colonic hyperplasia observed following fasting and refeeding. The iron component serves to remove a fasting induced colonic G1 cycle block and produce the resultant synchronous progression of cells through the cycle. Deleting iron from the refed diet results in no colonic hyperplasia and/or synchronous progression of cells. The results are discussed from the viewpoint of colonic steady state cell renewal and as a possible tool for the study of in vivo steady state cell renewal.

Animals↗

PubMed2005

Hypophosphataemia in old patients is associated with the refeeding syndrome and reduced survival.

OBJECTIVES: Previous studies found that hypophosphataemia (HP) a common finding in hospitalised patients associated with unfavourable outcome, but they did not focus on old patients. The aim of the current study was to determine the prevalence, associated risk factors and potential clinical consequences of HP detected during hospitalisation in a geriatric medical centre. DESIGN: Case-control study. SETTING: A total of 312-bed geriatric division. SUBJECTS: We compared 325 patients aged >or=65 years with at least one episode of HP-group defined by serum phosphate <or=0.77 mmol L(-1) with 326 patients without HP (non-HP group). MEASUREMENTS: Evaluation included baseline anamnesis, demographic and laboratory data. Patients in both groups were followed up to 2.7 years and clinical outcome recorded included length of hospitalisation, in-hospital and long-term survival. RESULTS: About 14.1% of 2307 elderly had HP. Patients in the HP-group compared with the non-HP group had significantly more weight loss, lower albumin levels, more sepsis and received threefold more glucose-containing infusions and twofold more food supplementations (P < 0.0001). HP was detected on average on the 10.9 +/- 21.5 days of hospitalisation. Patients in the HP-group compared with the non-HP group, had significantly longer hospitalisation period (P < 0.0001) and reduced long-term survival (P = 0.003) with threefold increased mortality rates. In a multivariate analysis, HP was not found to be an independent predictor of mortality. CONCLUSIONS: The HP was common among old hospitalised patients. Clinical characteristics of the HP-group, the time-course and strong association with glucose and food supplementation, are compatible with the refeeding syndrome, described previously in malnourished patients. HP was associated with significantly reduced survival.

Aged↗

PubMed1987

Effects of an elemental diet, inert bulk and different types of dietary fibre on the response of the intestinal epithelium to refeeding in the rat and relationship to plasma gastrin, enteroglucagon, and PYY concentrations.

Refeeding starved rats with an elemental diet resulted in a marked increase in crypt cell production rate (CCPR) in the proximal small intestine but not in the distal regions of the gut. Little effect on CCPR was noted when inert bulk (kaolin) was added to the elemental diet. Addition of a poorly fermentable dietary fibre (purified wood cellulose) had little effect on intestinal epithelial cell proliferation except in the distal colon where it significantly increased CCPR. A more readily fermentable fibre (purified wheat bran) caused a large proliferative response in the proximal, mid, and distal colon and in the distal small intestine. A gel forming fibre only significantly stimulated proliferation in the distal colon; the rats in this group, however, did not eat all the food given. There was no significant correlation between CCPR and plasma gastrin concentrations, but plasma enteroglucagon concentrations were significantly correlated with CCPR in almost all the sites studied. Plasma PYY concentrations also showed some correlation with CCPR, especially in the colon. Thus while inert bulk cannot stimulate colonic epithelial cell proliferation fermentable fibre is capable of stimulating proliferation in the colon, and especially in the distal colon: it can also stimulate proliferation in the distal small intestine and it is likely that plasma enteroglucagon may have a role to play in this process.

Animals↗

PubMed1988

Effects of fasting and refeeding on somatostatin concentration and binding to cytosol from rabbit gastric mucosa.

Somatostatin like immunoreactivity and the density of somatostatin binding sites were measured in stomach (fundus and antrum) from either fed, 12 to 96 hours fasted, or 96 hours fasted plus 48 hours refed rabbits. The somatostatin concentration increased in fundic and antral mucosa after 24 h and reached its highest value after 96 h of fasting. The number of specific somatostatin binding sites with high and low affinity decreased with the duration of fasting. Refeeding of fasted animals resulted in a normalisation to control values of gastric mucosal somatostatin and somatostatin binding.

Animals↗

PubMed1989

Protein metabolism during nutrient deprivation and refeeding of neonatal heart cells.

Pathological conditions or nutrient deprivation in the heart cause an imbalance between rates of protein synthesis and degradation, often resulting in a severe depletion of cardiac protein. We used cultured neonatal rat heart cells, a model system exhibiting positive nitrogen balance, to examine the effects of 10 h of starvation on myocardial glucose and protein metabolism. Cellular capacity for glucose utilization was depressed after starvation, as evidenced by lower hexokinase and other glycolytic enzyme activities and a 21% decrease in glucose usage. A 21.0% decrease in protein synthetic rate and an increase in protein degradation rate combined to yield a 29.5% decrease in total cellular protein during starvation. Degradation rates increased 29.0, 46.7, and 59.6% in 2-, 24-, and 96-h prelabeled cells, respectively, indicating that lability increased with half-life of proteins. During refeeding of starved, cultured cells, at least three proteins were synthesized at a lower rate. At the same time, proteins with approximate molecular masses of 45, 84, 92, and 174 kDa exhibited increased synthesis.

Animals↗

PubMed2004

Hormonal responses to fasting and refeeding in chronic renal failure patients.

To study anorexia in chronic renal failure (CRF) patients, we measured appetite-related hormones in seven CRF patients and four controls. Plasma concentrations and fractional changes from baseline (values from day 1, 0800) are listed as control vs. CRF (means +/- SE). Leptin, although higher in CRF (5.6 +/- 1.7 and 34 +/- 17 ng/ml), was suppressed after fasting; decrements were -51 +/- 9 and -55 +/- 8%. Nocturnal surge present during feeding was abolished upon fasting in both groups. Neuropeptide Y (NPY) was elevated in CRF (72 +/- 12 vs. 304 +/- 28 pg/ml, P = 0.0002). NPY rhythm, reciprocal to that of leptin, was muted in CRF. Basal cortisol was similar in both groups (17 +/- 3 and 17 +/- 2 microg/dl). In the controls, cortisol peaked in the morning and declined in the evening. CRF showed blunted cortisol suppression. Decrements were -61 +/- 3 and -20 +/- 9% at 1800 on day 1 (P = 0.008) and -61 +/- 8 and -26 +/- 8% at 2000 on day 2 (P = 0.02). Basal ACTH (25 +/- 5 and 54 +/- 16 pg/ml) as well as diurnal pattern was not statistically different between the groups. Baseline insulin was 6 +/- 1 and 20 +/- 9 microU/ml. During fasting, insulin was suppressed to -64 +/- 10 and -51 +/- 9%, respectively. Upon refeeding, increments were 277 +/- 96 and 397 +/- 75%. Thus, in our CRF patients, anorexia was not due to excess leptin or deficient NPY. Impaired cortisol suppression should favor eating. Insulin suppression during fasting and secretion after feeding should enhance both eating and anabolism. The constant high NPY suggests increased tonic hypersecretion.

Adrenocorticotropic Hormone↗

PubMed1990

Placental lactogen receptors in maternal sheep liver: effects of fasting and refeeding.

In a recent study we demonstrated that fasting of the pregnant ewe reduces the number of placental lactogen (PL) receptors in fetal sheep liver. In the present study we examined the effects of a 72-h fast on the number and affinity of PL receptors in maternal sheep liver. Fasting caused a 57% reduction in the number of hepatic ovine PL receptors; this effect was reversed by refeeding. There were no changes in the affinity of the PL receptor, the subunit structure of the receptor, or the extent of occupancy of the receptor by endogenous circulating maternal hormones. The number of hepatic PL receptors was correlated positively with the maternal plasma concentrations of glucose and insulin, suggesting that these factors may regulate PL binding to maternal tissues during pregnancy. In addition, PL receptor number was correlated positively with maternal plasma insulin-like growth factor I (IGF-I) concentrations, suggesting that a reduction in hepatic ovine PL binding may contribute to the reduction in maternal IGF-I during fasting. Fasting produced a 72% reduction in the number of ovine growth hormone receptors in maternal liver and an 83% increase in hepatic insulin binding. These findings indicate that fasting of the pregnant ewe reduces the number of PL receptors in maternal and fetal liver. The reduction in PL binding may contribute to maternal and fetal hyposomatomedinemia and may play a role in the pathogenesis of the intrauterine growth retardation that accompanies maternal nutritional deprivation.

Animals↗

PubMed1992

Hepatic metabolism during fasting-refeeding transition in conscious pregnant rabbits.

The aim of the present study was to determine changes induced by pregnancy in the hepatic handling of nutrients during the fasting-refeeding transition. Net hepatic and gut substrate fluxes were determined by the Fick principle in conscious pregnant (day 30) and nonpregnant rabbits in the 2 h after consumption of a mixed meal. Hepatic glucose production was suppressed by approximately 50% in both groups from 15 to 90 min. Pregnant rabbits returned to control levels at 120 min. Pregnant females displayed a larger gut glucose output and a greater arterial hyperglycemia. The hepatic and gut balance of lactate as well as the arterial level was almost unchanged. In pregnant females the hepatic uptake and arterial concentration of free fatty acids (FFA) remained almost unchanged, whereas these measures decreased in nonpregnant females by approximately 55 and approximately 80%, respectively, at 120 min. The decline in hepatic output of beta-hydroxybutyrate was similar in both groups. In pregnant rabbits arterial levels of beta-hydroxybutyrate did not parallel changes in the hepatic release as in nonpregnant females. Pregnant females displayed a greater hyperinsulinemia both in the portal vein and the artery over the first hour. It is concluded that, in pregnant rabbits fed a mixed meal, the ability of the liver to handle glucose is impaired because of insulin resistance. The latter brings about a greater and prolonged arterial hyperglycemia, which is reinforced by peripheral insulin resistance. Furthermore, the higher level of FFA may also contribute to the hyperglycemia. As a result, a greater amount of glucose is diverted to other sites, presumably the uterus.

3-Hydroxybutyric Acid↗

PubMed1992

Effect of fasting and refeeding on mesenteric autoregulation in conscious rabbits.

To determine whether feeding improves the efficacy of mesenteric autoregulation in conscious animals, rabbits were instrumented with pulsed-Doppler flow probes on the superior mesenteric artery and distal abdominal aorta to record mesenteric and hindquarters blood flow velocity. Hydraulic occluders were placed on the abdominal aorta (just below the celiac artery) and the thoracic vena cava to vary mesenteric and hindquarters arterial pressure (MAP), which was monitored via a catheter positioned in the distal abdominal aorta. Heart rate (HR) and lumbar sympathetic nerve activity (LSNA) were monitored as indexes of sympathetic nervous system activity. Pressure-velocity curves were obtained by aortic and caval occlusions on two consecutive days; first after a 24-h fast and after approximately 24 h of ad libitum refeeding. In the fed state, mesenteric velocity was significantly increased and MAP was decreased slightly; the slight decrease in MAP was counteracted by significant increases in HR and LSNA, whereas hindquarters perfusion was unchanged. The mesenteric and hindquarters pressure-velocity curves were all highly linear (r greater than or equal to 0.9) and showed no evidence of autoregulation in the fasted or fed state when pressure was changed by either the aortic or the caval occlusions. We conclude that autoregulation plays a minor role in the short-term regulation of mesenteric blood flow in the conscious rabbit.

Animals↗

PubMed2006

Glucokinase and hexokinase expression and activities in rainbow trout tissues: changes with food deprivation and refeeding.

The expression and activities of glucokinase (GK) and hexokinase (HK) were assessed in different tissues of rainbow trout (Oncorhynchus mykiss) under different feeding conditions (fed, fasted for 14 days, and refed for 7 days). Two different HK-I cDNAs were identified with different tissue distributions. One transcript named heart or H-HK-I was observed in the four brain regions assessed, white muscle, kidney, and gills but not in liver or erythrocytes. A second transcript named liver or L-HK-I was found in all tissues surveyed. GK mRNA was identified only in liver and the four brain regions. GK expression was altered by feeding conditions, especially in liver and hypothalamus where food deprivation decreased and re-feeding increased expression; changes in expression reflected activity changes and changes in tissue glycogen levels. In contrast, feeding conditions did not alter expression of either HK-I transcript but did alter tissue HK activities. The reduced phosphorylating capacity noted with food deprivation correlates primarily with changes in tissue HK, whereas increased capacity, as with refeeding, was associated with changes in GK; these changes fit with the different K(m) values of the GK and HK enzymes. These results provide evidence for the hypothalamus acting as a glucosensor in trout, as hyperglycemia produced increased GK expression and activity, as well as increased glycogen levels. Thus, even though trout use glucose poorly, none of the parameters tested here relate to this inability to use glucose and suggest that, at least, rainbow trout, if given an appropriate carbohydrate diet, could metabolically adjust to such a diet.

Amino Acid Sequence↗

PubMed2002

Trefoil peptide expression and goblet cell number in rat intestine: effects of KGF and fasting-refeeding.

The trefoil factor family peptides TFF1, TFF2, and TFF3 are important for gut mucosal protection and restitution. Keratinocyte growth factor (KGF) stimulates proliferation and differentiation of epithelial cells with potent effects on goblet cells. To investigate interactions between food intake and KGF, rats were fed ad libitum (control), fasted for 72 h, or fasted for 72 h and then refed for 72 h with or without KGF (3 mg. kg(-1). day(-1)). With fasting, goblet cell number in duodenum increased, TFF3 mRNA in duodenum and jejunum decreased, and TFF3 protein did not change or increased. KGF during fasting stimulated colonic growth, normalized TFF3 mRNA in duodenum and jejunum, and broadly upregulated gut goblet cell number and TFF3 protein expression. With fasting-refeeding, KGF increased small bowel and colonic mucosal growth, goblet cell number, and TFF3 protein but had variable effects on TFF3 mRNA. KGF induced TFF2 mRNA and protein in duodenum and jejunum with both nutritional regimens. We conclude that nutrient availability modifies rat intestinal goblet cell number, TFF3 mRNA, and the gut-trophic effects of KGF in a region-specific manner. KGF enhances TFF2 expression in proximal small bowel and increases goblet cell number and TFF3 protein content throughout the intestine independent of food intake.

Animals↗

PubMed1992

Food deprivation and refeeding in the camel (Camelus dromedarius).

Camels thrive in arid and semiarid areas, although food and water frequently are scarce. However, the mechanisms enabling camels to withstand food deprivation are poorly understood. In this study four female camels were totally deprived of food for 4 days. Their body weight decreased by 6%. Food deprivation caused no change in total plasma protein concentration in the camel, indicating that no alterations in plasma volume occurred. When the first meal was withheld water intake was unchanged. Next day the camels showed signs of hydration with a decreased plasma Na+ concentration and an increased excretion of diluted urine. In the afternoon water intake decreased. Urine K+ excretion fell the first day and urine volume and Na+ excretion from the third day. No activation of the renin-angiotensin-aldosterone system (RAAS) was observed. Plasma and urine urea concentration increased during food deprivation. Plasma glucose concentration and plasma cortisol and thyroxine levels did not change. Body temperature decreased during food deprivation. After refeeding, total plasma proteins increased temporarily by 12%, and a threefold increase in RAAS was seen, implying that both plasma volume and RAAs changed rapidly. Our results show that fluid balance was only slightly affected in the food-deprived camel. We suggest that strategies for the camel to endure food deprivation include maintenance of plasma volume and glucose concentration and a lowering of the body temperature.

Animals↗

PubMed1998

Behavioral changes in fasting emperor penguins: evidence for a "refeeding signal" linked to a metabolic shift.

This study examines the relationships between metabolic status and behavior in spontaneously fasting birds in the context of long-term regulation of body mass and feeding. Locomotor activity, escape behavior, display songs, body mass, and metabolic and endocrine status of captive male emperor penguins were recorded during a breeding fast. We also examined whether body mass at the end of the fast affected further survival. The major part of the fast (phase II) was characterized by the maintenance of a very low level of locomotor activity, with almost no attempt to escape, by an almost constant rate of body mass loss, and by steady plasma levels of uric acid, beta-hydroxybutyrate, and corticosterone. This indicates behavioral and metabolic adjustments directed toward sparing energy and body protein. Below a body mass of approximately 24 kg (phase III), spontaneous locomotor activity and attempts to escape increased by up to 8- and 15-fold, respectively, and display songs were resumed. This probably reflected an increase in the drive to refeed. Simultaneously, daily body mass loss and plasma levels of uric acid and corticosterone increased, whereas plasma levels of beta-hydroxybutyrate decreased. Some experimental birds were seen again in following years. These findings suggest that at a threshold of body mass, a metabolic and endocrine shift, possibly related to a limited availability of fat stores, acts as a "refeeding signal" that improves the survival of penguins to fasting.

3-Hydroxybutyric Acid↗

PubMed2000

Refeeding signal in fasting-incubating king penguins: changes in behavior and egg temperature.

This study is directed toward understanding the process of feeding stimulation ("refeeding signal") that has been suggested to operate below a body mass threshold or critical metabolic status in spontaneously fasting birds. Behavior and egg temperature (T(egg)) were continuously monitored by video monitoring and biotelemetry, respectively, in fasting-incubating king penguins kept in a pen to prevent relief by the partner until spontaneous egg abandonment. Penned birds fasted 10 days more and lost 1.2 kg more than birds relieved normally by their partner, abandoning the egg about 1 wk after reaching a critical body mass. Definitive egg abandonment was preceded by transitory abandonments of progressively increasing duration during which time the birds went further and further away from their egg. There were marked interindividual differences but on average transitory abandonments began 36 +/- 5 h before the definitive abandonment and were paralleled by resumption of display songs signaling the readiness of the bird to depart for feeding. T(egg) was maintained at around 35.7 degrees C during normal incubation but significantly decreased the last 2 days before egg abandonment. These changes are interpreted as reflecting a stimulation to refeed at a threshold body mass corresponding to a critical fat store depletion. Thus the fasting-incubating king penguin appears to be an interesting animal model for understanding the long-term metabolic control of feeding behavior in relation to energy status.

Animals↗

PubMed1991

Experimental studies on changes of neuroendocrine functions during starvation and refeeding.

Starvation resulting from famine and malnutrition remains an international concern. Malnutrition also influences the course and outcome of many diseases and when underestimated develops into a cycle of continuing dehabilitation. Thus, studies which contribute to the prevention, amelioration, or rehabilitation of the detrimental effect of starvation are warranted. Although investigations on endocrine changes related to starvation can be traced back to the early 1920s, there has been little work on the hypothalamic-pituitary axis until recently. The traditional line of thought tended to oversimplify the relationship between endocrine gland hypofunction and starvation by concluding that this hypofunction resulted from the inability of hormone production due to cellular damage and/or lack of raw materials and energy. Modern neuroendocrinology has established that neuroendocrine integration plays a major role in the body's homeostasis. The neuroendocrine system is the initial response to stress so that it is reasonable to assume that this system also plays a key role in the pathophysiological changes during starvation. This article presents a brief review of our research on: changes of anterior pituitary hormone secretions during starvation and refeeding; changes of hypothalamic neurotransmitters during starvation; and effects of modulation of central neurotransmitters on anterior pituitary hormone secretion of starved animals.

Adrenocorticotropic Hormone↗

PubMed1992

Effect of starvation and subsequent refeeding on thyroid function and release of hypothalamic thyrotropin-releasing hormone.

Effects of starvation on thyroid function were studied in 5- to 6-week-old (R x U) F1 rats. Starvation lowered plasma TSH in female, but not in male rats. Plasma T4 and T3 levels decreased, whereas the dialysable T4 fraction increased during starvation. Free T4 (FT4) levels decreased rapidly in females, but only after prolonged fasting in male rats. Glucose decreased, and free fatty acid levels increased during starvation. Peripheral TRH levels did not change during food deprivation. Since effects of starvation were most apparent in young female rats, such rats were used to study hypothalamic TRH release during starvation and subsequent refeeding. Basal in vitro hypothalamic TRH secretion was less in starved rats than in control or refed animals. In vitro hypothalamic TRH release in medium with 56 mM KCl increased 3-fold compared to basal release, and in these depolarization conditions TRH release was similar between hypothalami from control, starved and refed rats. In rats starved for 2 days, TRH level in hypophysial portal blood was lower than that of controls. Thus, diminished thyroid function during starvation may at least in part be caused by a reduced hypothalamic TRH release.

Animals↗

PubMed1979

Effects of starvation and refeeding on lung mechanics and morphometry.

Rats receiving one fifth of their usual daily food consumption for 10 days showed a significant increase in static recoil pressure of the lung (Pst[L]) due to surface forces at low lung volumes during inflation; their tissue Pst (L) decreased significantly over the entire volume-pressure loop compared to that of control rats. After 1 week of refeeding, the surface Pst (L) returned almost completely to normal, but tissue Pst (L) remained abnormally low. In starved rats, air-space enlargement with minimal loss of interalveolar septa was associated with a significant increase in mean linear intercept and volume fraction of air spaces, and with a significant decrease in corrected internal surface area and surface fraction of air space. These alterations returned partially toward normal in the refed group. We conclude that starvation increases surface elastic forces, decreases tissue elasticity of lung, and leads to air-space enlargement; redeeding leads to restoration of surface forces without the return of tissue elasticity to normal and to less severe air-space enlargement.

Animals↗