Effects of fasting and refeeding in the rat on adipocyte metabolic functions and response to insulin.
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Adipose Tissue↗
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On the relationship between ketonuria and natriuresis during fasting and upon refeeding in obese patients.
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Adult↗
Increased glucagon secretion in protein-fed rats: effects of refeeding a normal diet.
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Animals↗
The effect of refeeding after various periods of undernutrition on the morphology of purkinje cells in the cerebellum of the rat.
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Aging↗
Dietary fatty acids on the control of glucose-6-phosphate dehydrogenase and malic enzyme in the starved-refed rat.
The role of dietary unsaturated fat in the control of hepatic glucose-6-phosphate dehydrogenase (G6PD) (EC 1.1.1.49) and malic enzyme (ME) (EC 1.1.1.40) was studied in rats subjected to one or two cycles of starvation-refeeding. Rats starved and refed a control (5% corn oil) diet showed a threefold increase in G6PD activity and a twofold increase in ME activity compared to ad libitum-fed rats. After a second cycle of starvation-refeeding G6PD and ME activities showed fourfold and threefold increases, respectively, as compared to ad libitum-fed rats. Feeding rats diets containing 8% linoleic acid (as triglycerides) prevented the increase in G6PD and ME activities upon starvation-refeeding, diets with oleic, palmitic, and stearic acis when fed did not prevent this increase. Feeding rats various combinations of linoleic, linolenic and oleic acids following starvation prevented the additional increase in G6PD and ME activities after a second starvation-refeeding cycle; however, linoleic acid fed alone during the first refeeding prevented the additional increase in ME activity but not in G6PD activity. It is suggested that the dietary control of these enzymes involves one or more specific polyunsaturated fatty acids.
Animals↗
Prevention of dietary induction of rat liver glucose-6-phosphate dehydrogenase by cyclic adenosine 3'.5'-monophosphate and its elimination by glucose prefeeding.
Glucagon, epinephrine and cyclic adenosine 3',5'-monophosphate (cyclic AMP) prevented the induction of liver glucose-6-phosphate dehydrogenase (G6PD) by refeeding a glucose-casein mixture to starved rats. The prevention by these agents occurred without any change in the amount of diet consumed. When the injection of cyclic AMP and the refeeding of glucose-casein diet were initiated simultaneously, there was an inhibiton of G6PD induction depending upon the dose and frequency of cyclic AMP administration during the period of refeeding, while when cyclic AMP was given later than 12 h of the refeeding, the lag period for induction of this enzyme, there was no preventive effect. A glucose prefeeding was also found to counteract the inhibitory effect of cyclic AMP on G6PD induction by the subsequent glucose-casein refeeding. The present data together with the elimination of actinomycin D effect by the glucose prefeeding suggest that the inhibitory effect of cyclic AMP on the induction of G6PD dehydrogenase is exerted at the level of transcription.
Animals↗
Changes in fatty acid synthesis and lipogenic enzymes in adipose tissue from fasted and fasted-refed steers.
Controls of fatty acid synthesis in bovine adipose tissue were investigated. Six Brown Swiss steers were fasted for 8 days and then refed for 56 days. Biopsy samples of backfat adipose tissue were taken during the fasting and refeeding periods. Rates of acetate incorporation into fatty acids (FAS), activities of acetyl CoA carboxylase (CBX), glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, and NADP:isocitrate dehydrogenase, and plasma free fatty acids (FFA) and plasma acetate were determined. FAS decreased 60% after 1 day of fasting and 99% after 8 days. FAS did not increase until day 3 of refeeding when energy intake was above maintenance, then returned to normal by 14 days. CBX followed a pattern similar to FAS, except its activity did rise above the control rate during refeeding. Plasma FFA increased 350% and acetate decreased 67% during fasting. After 4 days of refeeding, FFA returned to normal, and acetate increased to 156% of initial concentration, then returned to normal by 21 days. These data suggest that CBX limits FAS in adipose tissue of cattle.
Acetates↗
Stoppage of glycogenesis and "over-shoot" of induction of lipogenesis and its related enzyme activities in the liver of fasted-refed rats.
To elucidate the causes of changes of carbohydrate metabolic pathways, the time course of utilization of dietary [U-14C]sucrose and induction of enzyme activities in the livers of rats were investigated. Adult male rats of BHE strain were refed after a fast of 2 days. The nutritionally complete refeeding diet contained 60% sucrose as the only source of carbohydrate. [U-14C]Sucrose was included in the diet on either day 1 or day 2, or both of refeeding. During the first day of refeeding, the radioactivity was incorporated mainly into liver glycogen which rose to over 100 mg/g. During the second day, little 14C appeared in the liver glycogen, which decreased sharply while glucose-6-phosphatase activity increased. The glycogenic pathway thus appeared to be blocked. On the other hand, 14C incorporation in the liver fat was minimal during the first day, but was quite extensive during the second day of refeeding. The enhanced lipogenesis was accompanied by large increases of activities of glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase and NADP-malic dehydrogenase. Results clearly indicate that the carbohydrate load in the liver of intact animals was initially metabolized by the glycogenic pathway. When glycogenesis stopped, carbohydrate was metabolized differently. The enhanced incorporation of [U-14C]sucrose into liver lipids indicates an increased formation of acetyl CoA and an accelerated formation and use of NADPH, probably from increasing dehydrogenase activities. Our data suggest that the blockage of synthesis of glycogen with the continuation of carbohydrate load was a primary cause in over-shooting induction of hepatic dehydrogenase activities and lipogenesis.
Adipose Tissue↗
Dietary fat-dependent changes in hepatic cholesterogenesis and the activity of 3-hydroxy-3-methylglutaryl-CoA reductase in fasted-refed rats.
Effects of various dietary fats on the activity of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase and sterol and fatty acid synthesis from [1-14C]acetate and [2-14C]mevalonate were examined in the liver from fasted-refed rats. Rats fasted for 2 days were refed a fat-free diet or diets containing various fats (tricaprylin, trilaurin, trimyristin, tristearin, camellia oil, or safflower oil) at the 10% level for 1, 3, or 7 days. The activity of HMG-CoA reductase was restored to about one-half of the pre-fasting levels in all groups after refeeding for 1 day and increased to above the pre-fasting levels after 3 days, with the exception of safflower oil, the rise was especially noticeable when fat-free, tricaprylin, and tristearin diets were fed. After 7 days, the activity of HMG-CoA reductase, except for rats refed tristearin, was decreased to levels that were far below those observed after 1 day-refeeding. This was particularly marked with tricaprylin, trilaurin, and camellia oil. The response of sterogenesis resembled that of the reductase. Dietary fat-dependent modification of fatty acid synthesis from [1-14C]acetate was first demonstrated after 7 days. Hepatic esterified cholesterol tended to accumulate and the deposition was marked after 3 days of refeeding. However, fat-dependent alterations of this parameter were remarkable on day 7. The concentration of plasma cholesterol also showed dietary fat-dependent changes after refeeding. Dietary fats appear to play an important role not only in the regulation of hepatic HMG-CoA reductase and sterol synthesis, but also in the overall processes of cholesterol dynamics.
Animals↗
Effect of starvation on tRNA synthesis, amino acid pool, tRNA charging levels and aminoacyl-tRNA synthetase activities in the posterior silk gland of Bombyx mori L.
Changes in the translational machinery components of the Bombyx mori posterior silk gland were analysed during starvation and refeeding and compared to the regularly fed larvae. During starvation, tRNA and ribosomal RNA synthesis are stopped. The amounts of different RNA classes and of the different tRNA species slow down at the same rate. Thus various tRNA show similar half-lifes and the preexisting tRNA adaptation to fibroin mRNA translation persists during starvation. Similarly, the tRNA/rRNA ratio is constant during starvation and refeeding (12 tRNA molecules for one ribosome) as in silk glands of control animals. Aminoacyl-tRNA synthetases and tRNA charging levels are decreased during starvation. The maximal tRNA charging level obtained during maximal protein synthesis in control animals is regained after 24 h refeeding of starved larvae. Changes observed in the free amino acid pool are not similar from one amino acid to another and levels reached after starvation do not differ strongly from the controls. Our results suggest that the production of translation apparatus components is coordinated and adjusted to the protein synthesis activity. Whether this coordination occurs in the silk gland is discussed on the basis of the "metabolic regulation", primarily described in prokaryotes and Yeast. Transfer RNA charging levels seem to play a key role in the process of regulation and could be implicated in the mechanism of tRNA adaptation if this phenomenon results as expected from a transcriptional control.
Amino Acids↗
The effects of dietary self-selection upon the overshoot phenomenon in starved-refed rats.
The food intake, liver composition and hepatic activity of pyruvate kinase (PK), glucose-6-phosphate dehydrogenase (G6P-DH), malic enzyme (ME) and acetyl CoA carboxylase (AcCoA Cx) were studied in starved-refed rats. When rats were refed a mixed diet for 3 days, food intake significantly increased (by 33%) from day 1 to 3 and the glycogen accumulation was maximal after 24 hours, but decreased significantly by day 3 (by 34%). In contrast, liver triglycerides sharply increased (10-fold) from day 1 to 3. Furthermore, during refeeding a large increase of G6P-DH, ME and AcCoA Cx was reached on day 3 when the average activity was 5.5- to 6.5-fold higher than before fasting. When rats were refed under conditions of self-selection (carbohydrates, lipids and proteins) total food intake was the same each day, but lipid and carbohydrate intakes varied reciprocally: lipid intake decreased whereas carbohydrate consumption increased during the 3 day refeeding period. Liver glycogen level was unchanged and both the triglyceride accumulation and the overshoot of lipogenic enzymes were highly attenuated: on day 3, they reached 50% of values observed in mixed diet refed rats. Administration of 8-azaguanine during refeeding under self-selecting conditions lowered food intake but had no effect on the pattern of food intake on the first day. In the following days, lipid intake fell dramatically. Azaguanine does not alter liver glycogenesis, but prevents both liver triglyceride accumulation and the overshoot of lipogenic enzymes.
Animals↗
The regulation of erythropoiesis in protein-energy-malnutrition.
The erythropoietin (ESF) content of plasma and urine has been studied in children with protein-energy-malnutrition (PEM) living in the Kivu province at an altitude of 1467--2000 m. On admission, packed cell volume (PCV) was moderately reduced; after 2 months of refeeding PCV had increased but was still lower than in the controls. Plasma ESF was increased on admission and in patients refed for 2 months. The expected positive correlation between serum and urine ESF levels was found after refeeding but not on admission; the last finding could not be explained by the presence of erythropoiesis inhibiting factor(s) in the urine. In spite of the normal 2,3-DPG and P50 previously described in PEM in Kivu, the anaemia associated with this disease is not merely an adaptation to lowered oxygen consumption and there must be some disturbances in the responsiveness of bone marrow to ESF. The high ESF values observed after 2 months of refeeding confirm that the restoration of the red cell volume proceeds slowly.
Adolescent↗
Failure of short-term nutritional convalescence to reverse the adverse hemodynamic effects of protein-calorie malnutrition in dogs.
We previously reported that protein-calorie malnutrition (PCM) exerts adverse hemodynamic effects on left ventricular (LV) structure and function. In the present experiments, we tried to determine the duration of these adverse effects by inducing significant weight loss in matched beagle dogs followed by a short-term course of nutritional repletion. Following restitution of initial body weight, the animals were placed on total cardiopulmonary bypass and an isovolumetric LV preparation was established to determine baseline LV function compared with matched animals that remained normally-nourished, and with a third group in which the effects of PCM were not reversed. Decreases in LV compliance persisted following refeeding as did the decreases in the first derivative of LV pressure (LV dp/dt). Although animals re-fed ordinary diets following acute weight loss restored normal concentrations of myocardial glycogen, cardiac abnormalities persited for more than one month following refeeding. These results suggest that the adverse effects of semistarvation on LV functions cannot be completely reversed by short-term refeeding.
Animals↗
Effect of cholesterol-rich diet on the content of nicotinamide nucleotides, adenine nucleotides and acetyl-CoA in the liver, the vascular wall and the kidney of spontaneously hypertensive rats (SHR).
The liver content of NAD and of adenylic nucleotides of normally fed spontaneously hypertensive rats (SHR) is lower than in normotensive rats. The cholesterol-rich diet does not change the liver NAD level. However it decreases adenine nucleotides and increases the level of acetyl-CoA and of NADP. Normal refeeding after a long-term cholesterol-rich diet induces an increase in the low levels of the coenzymes (moth NAD and adenine nucleotides). The liver coenzyme changes caused by the cholesterol-rich diet and by the normal refeeding of SHR are opposite to those established in normotensive rats. Vascular wall nicotinamide coenzymes in SHR are lower than in ulistar rats. The vascular wall of SHR reacts to the cholesterol-rich diet by a rise in NAD, i.e. conversely to the reaction observed in the liver of SHR and vascular wall of normotensive rats. Normal refeeding induces a further increase in the content of coenzymes. These results show that the effect of cholesterol-rich diet on the coenzyme content in the SHR is opposite to that in normotensive rats. The renal redox-system NAD+-NAD-H is more sensitive to the cholesterol-rich diet than the liver one, and its coenzyme changes indicate a greater reduction state, a reaction pattern which is typical for renal hypoxia. The results suggest that the cholesterol-rich diet influences the metabolism of the liver, the kidney and the vascular wall in a different way and to a different degree. SHR have a specific type of reaction to this cholesterol-rich diet.
Acetyl Coenzyme A↗
The effect of protein depletion on the rate of protein synthesis in rat liver.
In order to understand the mechanism of decreased protein synthesis in the liver of rats fed a protein-free diet, the average polypeptide chain assembly time (tc) was measured by the method of Mathews et al. (J. Biol. Chem. (1973) 248, 1329). For rats fed a normal diet, tc in liver in vivo was 1.28 min. A 10-day period of protein depletion led to a value of tc = 2.08 min, corresponding to a 38% depression in polypeptide elongation rate. Protein depletion caused an extensive breakdown of hepatic polysomes and refeeding of a complete mixture of amino acids resulted in rapid recovery of polysomal profile. But tc in the liver of the refed animals gave still depressed value of 1.95 min. The amount and size distribution of poly(A)-containing mRNA in the liver, as determined by [3H]poly(U) hybridization, were the same for normal and depleted groups. These results suggest that both initiation and elongation steps of protein synthesis are depressed in the liver of protein-depleted rats. Refeeding of amino acid mixture rapidly restores initiation but not elongation activity.
Animals↗
Differential response of rat brown and white adipose tissue to environmental or nutritional stress.
1. In vivo fatty acid synthesis by brown adipose tissue was enhanced in rats exposed to cold (5 degrees C) or altitude (4300 m) for 7 days but was unaltered in rats exposed to heat (35 degrees C) for an equivalent period. In vivo fatty acid synthesis by white adipose tissue was depressed by cold exposure while altitude and heat exposure had no effect. 2. In vitro, CO2 production and lipid synthesis were elevated in brown adipose tissue from rats fasted for 4 days. Refeeding (4 days) such rats reversed these effects, leading to depressed values relative to those of control rats. In contrast, these metabolic events in white adipose tissue were decreased by fasting and increased compared to controls during subsequent refeeding.
Adipose Tissue↗
Amenorrhoea, body weight and serum hormone concentrations, with particular reference to prolactin and thyroid hormones in anorexia nervosa.
Twenty women with anorexia nervosa were investigated at varying stages during weight gain. Basal prolactin and TSH and prolactin responses to TRH were normal and unrelated to body weight. LH, FSH and 17 beta oestradiol were low in emaciated patients and rose with weight gain. There was no correlation between serum gonadotrophin and prolactin concentrations. T3 and T4 concentrations were low but T3 rose with weight gain during refeeding over 4-6 weeks, whereas T4 remained low. A positive correlation was found between the TSH response to TRH and body weight. The abnormalities in the hypothalamic-pituitary-thyroid axis were similar to those seen in a variety of chronic illnesses and appear to be unrelated to the amenorrhoea. The failure of restoration of normal function at least after short-term refeeding requires further investigation. It was concluded that the amenorrhoea in anorexia nervosa is not associated with changes in prolactin secretion but is determined primarily by changes in the hypothalamic-pituitary-gonadal axis. These changes are induced largely by nutritional factors but psychological factors may also be involved.
Adolescent↗
Glycerokinase in rat and human adipose tissue: response to hormonal and dietary stimuli.
Glycerokinase activity was measured in homogenates of rat and human adipocytes. Human adipocyte glycerokinase activity was not altered by various dietary and hormonal treatments. In contrast, glycerokinase activity in rat adipocytes was decreased by fasting 48 hr and returned toward normal levels after refeeding for 36 hr. This increase in enzyme activity during refeeding was blocked by prior administration of uromycin. Glycerokinase activity was also significantly increased following prolonged incubation of rat adipocytes with dexamethasone in vitro. This stimulation of glycerokinase was further augmented by the simultaneous addition of insulin. Glycerokinase activity in rat and human adipocytes was also dependent on the body weight of the respective tissue donor. Other data presented indicate that glycerokinase is not involved in the "anti-lipolytic" action of insulin. The possible metabolic significance of glycerokinase in adipose tissue is discussed.
Adipose Tissue↗