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PubMed1983

Interaction of glucocorticoid and thyroxine in the responses of rats to starvation-refeeding.

The interaction of glucocorticoid (GC) and thyroxine (T4) in the generation of the hepatic enzyme overshoot and lipid response to starvation-refeeding was studied. Male Sprague-Dawley rats were either left intact, or treated with propylthiouracil (PTU), or adrenalectomized (ADX), or ADX and/or PTU treated and treated with GC and/or T4. One-half of each of these treatment groups was fed a 65% glucose diet while the remaining rats were starved for 48 hours and refed the glucose diet for 48 hours. After decapitation, hepatic lipid and glucose-6-phosphate dehydrogenase (G6PD) activity were determined. Rats treated with only PTU had less of an enzyme overshoot than nontreated rats, and the full overshoot response was restored with T4 treatment. ADX rats did not have the typical enzyme overshoot response to starvation-refeeding. However, ADX rats had their overshoot response restored with GC. PTU-treated ADX rats had more of an overshoot response than did ADX rats. When T4 was administered to PTU-treated ADX rats there was less of an enzyme overshoot; however, when both T4 and GC were administered to the PTU-treated ADX rats, the overshoot response was fully restored. The liver lipid response to starvation-refeeding followed a similar pattern except that in PTU-treated rats the liver lipid levels were significantly higher in the starved-refed rats than in the ad libitum-fed rats. These results indicate that T4 and GC play a role in the G6PD and liver lipid response to starvation-refeeding.

Adrenalectomy↗

PubMed1984

Ornithine decarboxylase induction in rat colon: synergistic effects of intrarectal instillation of sodium deoxycholate and starvation-refeeding.

Starvation-refeeding, intrarectal instillation of the suspected colon tumor promoter sodium deoxycholate (NaDOC), and a combination of the treatments were compared for their effects on ornithine decarboxylase (ODC) activity in the colon of male Sprague-Dawley rats. Starvation (48 hours) and refeeding (12 hours) led to a fivefold increase in ODC levels compared to ad libitum-fed controls, while NaDOC instillation led to a threefold rise. The combination of the two treatments gave a synergistic 16-fold increase over controls. The synergism observed in colon may indicate that the two treatments used act via different mechanisms to induce ODC, possibly by an increase in general macromolecular synthesis after starvation-refeeding and a specific increase in ODC synthesis after NaDOC treatment. Since this starvation-refeeding regimen is quite similar to the "starve and gorge" feeding pattern exhibited by pair-fed control animals, the use of pair-fed controls may not be appropriate for examining either ODC levels or processes, such as tumor promotion, which may be linked to ODC levels. The synergistic enhancement of tumor promoter-related ODC induction by a dietary pattern (rather than a dietary component) suggests a new area for investigation of potential nutrition-cancer interactions.

Animals↗

PubMed1985

Reduced and compensatory growth: endocrine and metabolic changes during food restriction and refeeding in steers.

Effects of food restriction, followed by refeeding, on energy and nitrogen metabolism, growth rates and blood levels of hormones and metabolites were studied in steers. During the restriction period, which lasted for almost 5 mo, allowance for energy and nitrogen were close to maintenance requirements. Heat production and growth rates were markedly lowered. In response to reduced food intake concentrations of thyroxine (T4), 3,5,3'-triiodothyronine (T3), insulin (IRI), glucose and alpha-amino-acid nitrogen (AAN) were reduced, those of growth hormone (GH) and nonesterified fatty acids (NEFA) were elevated, whereas 3,3',5'-triiodothyronine (rT3) and albumin were not different from levels measured in nonrestricted animals. During refeeding heat production and energy balances increased, nitrogen balances were transiently elevated and the animals exhibited compensatory growth. In response to refeeding, concentrations of T4, T3 and IRI increased within days. In contrast, GH decreased whereas rT3 did not change. Within 2 d of refeeding there was a rapid fall of NEFA, and an increase of glucose, and beta-hydroxybutyrate within 2 and 12 d, respectively. The data demonstrate the ability of growing ruminants to adapt rapidly to variations in food intake by closely linked metabolic and endocrine changes, which are associated with shifts in energy and nitrogen metabolism and, finally, by reduced or compensatory growth.

3-Hydroxybutyric Acid↗

PubMed1995

Liver glucose-6 phosphatase activity is inhibited by refeeding in rats.

This study was conducted to determine whether inhibition of hepatic glucose-6 phosphatase is involved in the mechanism of suppression of hepatic glucose production during the postprandial period. We studied the time course of changes in the enzyme activity by refeeding food-deprived rats with nonpurified diet. The Vmax of the enzyme, assayed in homogenates from livers freeze-clamped in situ in anesthetized 48-h unfed rats (12.3 +/- 0.15 U/g wet liver, mean +/- SEM, n = 6) was progressively decreased upon refeeding: 11.1 +/- 0.5, 8.5 +/- 0.4 and 7.9 +/- 0.5 U/g, in rats refed for 90, 180 (P < 0.01) and 360 min (P < 0.01), respectively. The Km of the enzyme was not affected by refeeding. No inhibition of the enzyme was observed in microsomes purified from these homogenates, suggesting a metabolite-induced inhibition mechanism. To assess the role of insulin in the inhibition, we assayed the glucose-6 phosphatase activity in similarly processed liver homogenates from food-deprived rats perfused with insulin at physiological and supraphysiological concentrations, whereas plasma glucose was maintained at the basal level by adapted glucose perfusion (euglycemic clamps). No inhibition of glucose-6 phosphatase was found under these conditions, suggesting that insulin cannot by itself account for the inhibition observed in the refeeding experiments. These data constitute the first demonstration of the inhibition of glucose-6 phosphatase activity during the postprandial period.

Animals↗

PubMed1996

Muscle and liver protein synthesis adapt efficiently to food deprivation and refeeding in 12-month-old rats.

Our aim was to analyze mechanisms involved in the adaptation of protein metabolism to food deprivation and refeeding in adult rats. Twelve-month-old rats, which had been food-deprived for 113 h and refed for 6 h, were injected subcutaneously with a flooding dose of valine (with 50% [1-13C]-L-valine) to measure in vivo protein synthesis in tibialis anterior, soleus and liver. Protein and RNA contents were also measured. In both muscles, protein mass was maintained during food deprivation. Due to a drop in protein synthetic capacity (Cs), total and myofibrillar protein synthesis rates were reduced in food-deprived rats and were not stimulated by a 6-h refeeding. In contrast, protein levels were maintained lower than RNA levels in liver during food deprivation, and Cs was higher than in fed rats. Protein synthesis rates and ribosomal efficiency were reduced in food-deprived rats. Due to maintenance of protein synthetic capacity, there was a rapid stimulation of liver protein synthesis with refeeding, which induced a significant rise in protein mass (also related to an inhibition of protein degradation). In conclusion, coordinated responses of liver and muscles allowed a sparing of muscle proteins during food deprivation and a rapid recovery of liver proteins during refeeding. Control of ribosome quantity could play a critical role in these adaptations in tissue protein synthesis in adult rats.

Aging↗

PubMed1998

Neuropeptide Y and corticotropin-releasing hormone concentrations within specific hypothalamic regions of lean but not ob/ob mice respond to food-deprivation and refeeding.

Leptin is proposed to control food intake at least in part by regulating hypothalamic neuropeptide Y (NPY), a stimulator of food intake, and corticotropin-releasing hormone (CRH), an inhibitor of food intake. Ob/ob mice are leptin-deficient and would thus be expected to exhibit alterations in hypothalamic NPY and CRH. We therefore measured concentrations of NPY and CRH in discrete regions of the hypothalamus (i.e., ARC, arcuate nucleus; PVN, paraventricular nucleus; VMH, ventromedial nucleus; DMH, dorsomedial nucleus; and SCN, suprachiasmatic nucleus) of 6.5-7-wk-old ob/ob and lean mice with free access to stock diet, 24 h after food deprivation, and 1 h after refeeding. Fed ob/ob mice had 55-75% higher concentrations of NPY in the ARC, VMH and SCN than lean mice. Food deprivation increased NPY concentrations approximately 70% in the ARC, PVN and VMH of lean mice, and refeeding lowered NPY concentrations approximately 70% in the PVN of these mice. NPY in these hypothalamic regions of ob/ob mice was unresponsive to food deprivation or refeeding. The most pronounced change in CRH concentrations within the regions examined (i.e., ARC, PVN and VMH) occurred in the ARC of lean mice where refeeding lowered CRH concentrations by 75% without influencing ARC CRH concentrations in ob/ob mice. The hypothalamic concentrations of two neuropeptides involved in body weight regulation (i.e., NPY and CRH) in leptin-deficient ob/ob mice respond abnormally to abrupt changes in nutritional status.

Animals↗

PubMed1977

Fasting and refeeding: cell kinetic response of jejunum, ileum and colon.

Following a period of fasting, feeding a normal diet results in a burst of DNA synthesis in the crypts of the colonic epithelium. This is due largely to a prompt entry of cells, blocked in G1, into S. Peak levels of S cellularity exceed 4 times the fasting, and 2 times the normal fed control values. Refeeding a low residue diet (soluble casien, glucose and corn oil) results in a return to control levels of proliferative activity, but no hyperplasia. However, in jejunum and ileum, refeeding is followed by a return to near control levels of proliferation with only a slight overshoot in S phase cellularity. During the fasting period, the ileal crypt proliferative compartment (Pc-zone) and total crypt cellularity decline significantly. These changes are accompanied by an increase in the total cycle time, due to an equivalent lengthening of the G1 and S phase. Following refeeding, there is a reduction in the cycle time and a gradual return to the control values for the Pc-zone size and cellularity. In the colon, fasting has no effect on the Pc-zone size or total crypt cellularity. There is an approximate doubling of the cycle time due solely to an increase in G1. Following refeeding there is an increase in the Pc-zone size and crypt cellularity and a marked shortening of the cycle time. Evidence that a G1 cycle blockade is induced in the colon by fasting is given by a lenghening of the G1 period and by stathmokinetic studies employing vincristine.

Animals↗

PubMed2003

NPY ablation in C57BL/6 mice leads to mild obesity and to an impaired refeeding response to fasting.

Neuropeptide Y (NPY) is an orexigenic (appetite-stimulating) peptide that plays an important role in regulating energy balance. When administered directly into the central nervous system, animals exhibit an immediate increase in feeding behavior, and repetitive injections or chronic infusions lead to obesity. Surprisingly, initial studies of Npy(-/-) mice on a mixed genetic background did not reveal deficits in energy balance, with the exception of an attenuation in obesity seen in ob/ob mice in which the NPY gene was also deleted. Here, we show that, on a C57BL/6 background, NPY ablation is associated with an increase in body weight and adiposity and a significant defect in refeeding after a fast. This impaired refeeding response in Npy(-/-) mice resulted in a deficit in weight gain in these animals after 24 h of refeeding. These data indicate that genetic background must be taken into account when the biological role of NPY is evaluated. When examined on a C57BL/6 background, NPY is important for the normal refeeding response after starvation, and its absence promotes mild obesity.

Adipose Tissue↗

PubMed1987

Decreased myofibrillar proteolysis after refeeding requires dietary protein or amino acids.

Previous studies have demonstrated that brief fasting augments and refeeding a complete diet diminishes the breakdown of myofibrillar proteins in rat skeletal muscle. The purpose of the present study was to determine which dietary component(s) was responsible for this effect and to determine the role of insulin and amino acids. Myofibrillar proteolysis was evaluated by measuring the release of 3-methylhistidine by perfused rat muscle of 1-day fasted rats and 1-day fasted rats refed for 4-24 h with a complete, protein-free, or lipid meal. For comparison, tyrosine release by perfused muscle was measured in the absence and presence of cycloheximide to evaluate net and total proteolysis, respectively. Refeeding of either diet increased plasma insulin. Despite this, myofibrillar proteolysis decreased only when protein or amino acids was included in the test meal. On the other hand, the complete or protein-free meal decreased tyrosine release in the absence but not in the presence of cycloheximide, suggesting that either diet enhanced muscle protein synthesis. Most amino acids in plasma and muscle decreased after refeeding the protein-free meal, whereas after the complete meal some amino acids in plasma and muscle increased, whereas other decreased or changed little. These results indicate that decreased myofibrillar proteolysis in muscle after refeeding of food-deprived rats requires dietary protein or amino acids. They also suggest that hormonal and/or nutritional factors other than insulin and amino acids may orchestrate this response. However, a role of amino acids cannot yet be excluded, because it is conceivable that changes in specific amino acids in plasma instead of muscle may signal diminished proteolysis.

3-Hydroxybutyric Acid↗

PubMed1990

Protein metabolic effects of a prolonged fast and hypocaloric refeeding.

In a study of the mechanism of adaptation to protein deficiency, 10 moderately obese women underwent a 3-wk fast followed by random allocation to a 1-wk refeeding regimen providing 80 g carbohydrate or protein. Protein metabolism was studied by means of nitrogen (N) balance, urinary 3-methylhistidine excretion, and postabsorptive plasma leucine flux using L-[1-13C]leucine infusions. After the 3-wk fast, plasma leucine flux and 3-methylhistidine excretion both decreased by 31% from control diet values (P less than 0.01), and N balance was -5.9 g/day. After protein refeeding, N balance was positive (+1.7 g/day, P less than 0.05) whereas leucine flux was unchanged from prolonged fasting values. After carbohydrate refeeding, N balance improved to -3.1 g N/day, whereas leucine flux decreased by a further 18% (P less than 0.05). Protein and carbohydrate refeeding were associated with further 23 and 31% reductions of 3-methylhistidine excretion compared with prolonged fasting (P less than 0.05). The results support the hypothesis that improved efficiency of protein retention in starvation is intimately associated with a decreased rate of protein turnover.

3-Hydroxybutyric Acid↗

PubMed1990

Adipocyte lactate production remains elevated during refeeding after fasting.

The metabolic state occurring with refeeding after fasting is characterized by the rapid restoration of hepatic glycogen. Recent evidence suggests that a main substrate for glycogenesis is lactate. Because adipose tissue is an active site of lactate production that increases with fasting, we examined the magnitude and duration of lactate production by isolated adipocytes from three adipose depots of rats fasted for 48 h and then refed for up to 96 h. The data show that 48 h of fasting results in a markedly elevated rate of adipocyte lactate production, which increased from 3-9% of total glucose metabolized in the fed state to 49-60% in the fasted state. During the refeeding period, lactate production remained elevated for 12-24 h and then declined. Mesenteric adipocytes had a higher rate and more prolonged elevation in lactate production than cells from the other two depots. We conclude that, with refeeding after a fast, adipocyte glucose conversion to lactate remains elevated during the time of hepatic glycogen restoration. This suggests that adipose tissue may actively produce lactate for glycogenesis during refeeding.

Adipose Tissue↗

PubMed1999

Changes in the circulating IGF system during short-term fasting and refeeding in rats.

There is little information on free insulin-like growth factor I (IGF-I) and its regulatory proteins during fasting and refeeding. Therefore, we examined rats during fasting (0, 1, 2, and 3 days) and refeeding (3, 6, and 12 h and 1, 2, 3, and 7 days) (n = 6-9). Serum was analyzed for insulin, C-peptide, growth hormone (GH), free and total IGF-I, IGF-binding protein (IGFBP)-1 and -3, and the acid-labile subunit (ALS). Additionally, liver mRNA for IGF-I, IGFBP-1, and ALS was determined. Fasting reduced serum levels of GH, free and total IGF-I, IGFBP-3, and ALS, whereas IGFBP-1 was increased (P < 0.0001). Refeeding normalized IGFBP-1 at 3 h and GH at 12 h. Free IGF-I changed in parallel with total IGF-I, ALS, and IGFBP-3, being normalized at 48 h of refeeding. IGFBP-1 (peptide and mRNA) correlated inversely with insulin and C-peptide (P < 0.001). The correlation between peptide and mRNA was relatively strong for IGFBP-1 (r(2) = 0.36; P < 0.0001), moderate for IGF-I (r(2) = 0.18; P < 0.0005), and insignificant for ALS. In conclusion, insulin appears to regulate IGFBP-1 in fasted and refed rats. However, the normal inverse relationship between free IGF-I and IGFBP-1 was absent, and free IGF-I changed in parallel with total IGF-I and thus ALS and IGFBP-3. Finally, the regulation of the hepatic synthesis of IGF-I, IGFBP-1, and ALS seems to differ substantially.

Animal Feed↗

PubMed1986

Effect of refeeding on polyamine biosynthesis in isolated enterocytes.

Ornithine decarboxylase (ODC) activity has been found to be preferentially associated with small intestinal villus cells rather than crypt cells in the rat. In the present study, ODC, S-adenosylmethionine decarboxylase (SAMDC), and polyamines were measured in isolated enterocytes to determine which cell populations increased polyamine biosynthetic activity after refeeding. Two hours following refeeding, significant increases in ODC were observed in villus tip (10 times) and midvillus (20 times) enterocytes. No increase in ODC activity was found in isolated crypt cells. A similar pattern was observed for SAMDC. Enzyme activity increased in villus tip (2 times) and midvillus (27 times) cells but not in crypt enterocytes. Putrescine contents were increased following refeeding in midvillus enterocytes (P less than 0.05) and in crypt cells (P less than 0.05). The accumulation of putrescine in midvillus cells occurs via ODC-induced biosynthesis, whereas in crypt enterocytes it may be due to putrescine uptake. The lack of induction of ODC and SAMDC in crypt enterocytes following acute refeeding suggests these enzymes are apparently not involved in the initiation of cell proliferation known to occur under this condition.

Adenosylmethionine Decarboxylase↗

PubMed1994

Temporal pattern of rat small intestinal gene expression with refeeding.

Studies were carried out to elucidate the molecular mechanisms underlying small intestinal epithelial growth. Adult rats were fasted for 4 days and then refed a chow diet for up to 48 h. Histological examination confirmed the sequential occurrence of mucosal atrophy and hyperplasia. Northern blot analyses of RNA derived from small intestinal mucosal scrapings revealed a striking pattern of alterations in the expression of two different categories of genes. There were very early increases in the expression of c-fos and c-jun, reflecting the mitogenic response to refeeding that occurs within the crypt compartment. Studies using the protein synthesis inhibitor cycloheximide suggest that c-fos and c-jun are part of the "immediate-early" response of the small intestine. At later time points after the refeeding stimulus, differential changes occurred in the expression of the brush-border enzymes, lactase, and intestinal alkaline phosphatase (IAP). Refeeding caused a decrease in lactase gene expression and an increase in the expression of the 3.0-kb IAP mRNA species, reflecting a return of the villus phenotype to the normal fed state. Thus we have demonstrated a complex and temporally related pattern of gene expression within the small intestinal epithelium upon refeeding. The results provide insight into the relationship between the processes of intestinal growth and differentiation.

Animals↗

PubMed1991

Effects of fasting and refeeding on the proliferative response of rat aorta to injury.

To explore the interplay between the mitotic activity of arterial smooth muscle cells and the variations of plasma glucose and insulin concentrations, we have studied over 14 days the response of thoracic aorta to injury with a balloon catheter in rats submitted to fasting and refeeding. Animals were fasted from the day before until the third day after injury. The proliferative reaction of intima-media was assessed 2, 3.5, 4, 6, 8, and 14 days after injury, comparing freely fed with fasted-refed rats. Fasting decreased plasma glucose and insulin concentrations and DNA synthesis by intima-media, whereas refeeding increased these three variables transiently. The DNA content of intima-media at any time during the response to injury and the intimal thickening on day 14 were not influenced by the sequence of fasting and refeeding, which suggests that the early decrease in DNA synthesis induced by fasting had been compensated for by the later increase in DNA synthesis induced by refeeding. In conclusion, besides hormonal influences (such as insulin), metabolic influences (such as the availability of energetic fuels) are likely to act on the proliferative response of arteries to injury.

Animals↗

PubMed1984

Effects of fasting and restricted refeeding on utilization of ingested energy in rats.

Ingested metabolizable energy was partitioned into 3 components--storage, cost of storage, and maintenance--to study energy utilization during 20 days of refeeding following a 3-day fast in adult male Wistar rats. During the refeeding period, one experimental group was refed ad libitum, whereas two others were restricted to approximately 75 and 50%, respectively, of prefast food intake. Energy utilization in the experimental groups was compared with that in nonfasted controls. Energy conservation occurred in all experimental groups during refeeding, and the primary form of that conservation was a decrease in the energy required for maintenance. The decreased requirement for maintenance allowed a greater proportion of ingested energy to be used for restoration of carcass energy. The degree of energy conservation was, in general, proportional to the degree of food restriction during refeeding.

Adipose Tissue↗

PubMed1991

New adipocyte formation in mice during refeeding after long-term deprivation.

Cell kinetic characteristics of the epididymal adipose tissue of mice were examined during refeeding after prolonged food deprivation. Mature mice were given a glucose-electrolyte solution for 20-40 days, and subsequent to a body weight loss of 35%, they were given normal mouse food ad libitum. After refeeding, their body weight and adipose tissue weight returned to the levels before the deprivation. We examined the formation of new adipocytes in the epididymal adipose tissue with [3H]thymidine autoradiography. Flash labeling experiments revealed that cell proliferation was most active on the 6th day after refeeding and decreased thereafter until the 13th day when few labeled cells were seen. Cumulative labeling experiments showed that replicated poorly differentiated mesenchymal cells developed into adipocytes by storing fat droplets. New adipocyte formation was observed in adult mice during refeeding after long-term deprivation.

Adipose Tissue↗

PubMed2005

[Refeeding syndrome. A review].

Refeeding syndrome is a complex clinical picture that encompass all those alterations that can occur as a consequence of the nutritional support (oral, enteral or parenteral) in malnourished patients. Refeeding syndrome is classically characterized by neurological alterations, respiratory symptoms, cardiac arrhythmias and heart failure few days after beginning of refeeding, with life-threatening outcome. Its pathogenesis includes alterations in the corporal fluids, and in some electrolytes, minerals and vitamins. In this article a review of refeeding syndrome pathogenesis and clinical manifestations is carried out, with a final series of recommendations for lowering the risk of this syndrome and for facilitate the early diagnosis and the treatment.

Humans↗