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PubMed2001

Adaptive increase in pyruvate dehydrogenase kinase 4 during starvation is mediated by peroxisome proliferator-activated receptor alpha.

Pyruvate dehydrogenase kinase isoform 4 (PDK4) is upregulated by starvation in many tissues of the body during starvation. This causes inactivation of the pyruvate dehydrogenase complex which blocks pyruvate oxidation and conserves lactate and alanine for gluconeogenesis. Enhanced PDK4 expression may be caused by the increase in free fatty acids that occurs during starvation. Free fatty acids can activate peroxisome proliferator-activated receptor alpha (PPARalpha), and activation of PPARalpha can promote PDK4 expression. This model is supported by the findings reported here that WY-14,643, a synthetic PPARalpha activator, increases PDK4 expression in wild-type mice but not in PPARalpha-null mice. Starvation likewise increases the expression of PDK4 in tissues of wild-type mice but not in tissues of PPARalpha-null mice. These findings document the functional importance of PPARalpha for PDK4 expression during starvation and suggest an important role for elevated free fatty acids in the induction.

Animals↗
PubMed1976

The effects of starvation on the planarian worm Polycelis tenuis Iijima.

Employing a combination of microscopical, biochemical and autoradiographic techniques, the primary effects of starvation on adult polycelis tenuis have been studied. Over a five week period of starvation there is on average a 32% decrease in the size of the organism. This decrease is contributed to by a reduction in mitosis and an increase in cell shrinkage autolysis and death. During starvation (following a sharp rise in RNA synthesis) there is a distinct sequence of events; four peaks of acid phosphatase activity can be resolved. The first is associated with the immediate response of the gastrodermis to feeding; the second (after 6 to 7 days) with increased autophagy and dedifferentiation in the gland cells and with muscle lysis of cells. The third peak (after 14 to 15 days) is contributed to largely by the lysis of cells in the gut and the fourth peak (after 25 to 26 days) is caused by an extensive lysis of the reproductive system. Fine structural changes involving increased intracellular vacuolation, autophagy, crinophagy, atrophy of muscle, increased intercellular space and loss of basement membrane matrix have been related to changes in enzyme pattern. Nerve cells appear unchanged throughout the first five weeks of starvation. Pigment and gland cells loose their characteristic granules, dedifferentiate and become morphologically similar to the undifferentiatied neoblasts. Dedifferentiation and the mechanisms involved in the survival of starvation are discussed.

Acid Phosphatase↗
PubMed1981

Quantitative analysis of muscle breakdown during starvation in the marine flatfish Pleuronectes platessa.

The present study describes the effects of starvation for a duration of four months on the ultrastructure of skeletal muscles from the marine flatfish (Pleuronectes platessa L.). Starvation is associated with a decrease in resting metabolic rate from 20.1 +/- 2.2 to 11.6 +/- 1.5 mg . O2/kg/h (P less than 0.05) and muscle wasting. Median fibre size fell from 700 micrometer 2 to 500 micrometer 2 in intermediate (fast oxidative) and from 1,800 micrometer 2 to 600 micrometer 2 in starved, white (fast-glycolytic) muscle fibres. In contrast, median fibre size in red (slow oxidative) muscle remained within the range 300-400 micrometer 2. The fraction of red fibre volume occupied by myofibrils (58.6%) and mitochondria (24.5%) did not change significantly with starvation. There was, however, a decrease in stored lipid 110.7% to 3.2%) and an alteration in the structure of the cristae in mitochondria from red muscle. Atrophy of white muscle fibres is associated with a decrease in both the diameter and fractional volume occupied by myofibrils (85.7% to 61.9% P less than 0.01). In a high proportion of white fibres peripheral degeneration of Z-discs is evident causing an unravelling of the thin filament lattice. It is suggested that this allows a partial decrease in myofibril diameter and hence the maintenance of contractile function in muscle from starved fish. In severely degenerating white fibres, disorganised thick and thin filaments and numerous multi-membrane lysosome-like vesicles are observed. Starvation results in an increase in the average content of mitochondria in white fibres from 2.2 to 6.7% (P less than 0.01). In fed plaice mitochondria constitute less than 1% of the volume of the white fibre in 43.5% of the fibres. The proportion of white fibres containing more than 6% mitochondria increases from 6.5% to 58% with starvation.

Animals↗
PubMed1990

Peroxisomes of the rat cardiac and soleus muscles increase after starvation. A biochemical and immunocytochemical study.

We have investigated the change of catalase activity in the homogenates of rat cardiac and skeletal muscles. After 7 days' starvation, the catalase activity of heart increased about 3-fold and that of soleus muscle enhanced 2-fold higher than that of control rats. Immunoblot analysis of catalase showed a single band in the homogenates of cardiac and soleus muscles and increase of catalase antigen after starvation. Light microscopic immunoenzyme staining showed that after starvation catalase positive granules markedly increased in both the cardiac and soleus muscle. Quantitative analysis of the staining showed that number of the granules per 100 microns 2 of tissue section was about 1.4-fold in the soleus muscle and 1.7-fold in the cardiac muscle after starvation. By electron microscopy of alkaline DAB staining, we confirmed that the granules were peroxisomes, which increased in both number and size. Furthermore, we stained the peroxisomes for catalase by a protein A-gold technique. Labeling density (gold particles/micron 2) of the cardiac and soleus muscles from the starved rat increased approximately 1.4 times as much as that of normal animal. When the numerical density is multiplied by the labeling density, the values are largely consistent with the enhancement of catalase activity. These results show that increase in the catalase activity of the muscle tissue after starvation is caused by increase in number and size of peroxisomes.

Animals↗
PubMed1978

Flux of metabolic fuels during starvation in the rat.

Rats were starved for 6 days to determine whether the "nitrogen sparing" observed during starvation in humans was also present in rats. The urinary nitrogen excretion decreased on the first day, probably due to metabolism of remaining dietary protein. From the second day of starvation to the end of the starvation period, the urinary nitrogen excretion increased progressively. The hepatic glycogen stores were depleted at the end of the first day. The blood glucose concentration remained constant throughout starvation period except for a 15% decrease on the first day. There was increased mobilization of lipid stores, starting on the first day, reflected by an increase in the blood free fatty acids, glycerol and ketone body concentrations. These metabolite concentrations began to increase on the third and fourth day which probably reflected depleted fat stores since no visible body fat was observed by the fourth day. The data indicate that the rat does not spare body protein during starvation, probably because it depletes its glycogen and fat stores rapidly and must then depend on body protein as the major fuel for energy metabolism.

Amino Acids↗
PubMedDate not supplied

Starvation-induced insulin resistance: influence on 3-O-methylglucose transport.

Starvation causes insulin resistance which is partly due to decrease of insulin action on glucose transport in target cells. Preliminary data from other authors suggest that starvation is associated with an increase of the time necessary for insulin to exert its maximum effect on glucose transport. In order to verify this finding, 3-O-methylglucose (3OMG) transport was studied in isolated rat adipocytes from starved and fed rats. The total intracellular space for 3OMG was not modified by 48h starvation. After 48h starvation, 3OMG transport into fat cells was less responsive to maximum insulin concentration than in controls: 33 +/- 2% (controls) vs 23 +/- 4% (starved) of total glucose space, p less than 0.05; the sensitivity to insulin was normal or even increased in comparison to controls: 50% of maximum effect was reached at 42 microU/ml insulin in controls and at 26 microU/ml insulin in starved animals. We could not find any effect of starvation on the time-response curves of insulin action.

3-O-Methylglucose↗
PubMed1990

Effect of acute starvation on monoamine oxidase and Na+,K(+)-ATPase activity in rat brain.

The activities of monoamine oxidase (MAO), responsible for oxidative deamination of many biogenic amines, and Na+, K(+)-ATPase, which plays a crucial role in the release mechanism of neurotransmitters, were determined in rat brain after acute starvation. They were assayed biochemically from four different regions of the brain in two subcellular fractions. Acute starvation decreased the activity of MAO, whereas the Na+,K(+)-ATPase activity was increased. An effect of starvation was also seen on the blood glucose level, body wt, and the protein content of different brain regions. Starvation or normal dietary fluctuations of certain nutrients that exert precursor influence over neurotransmitter synthesis are important to the brain, and contribute to its regulation of both neuroendocrine response and behavior. A rise in the substrate level, i.e., ATP, as a result of increased utilization of ketone bodies and low level of monoamines in the brain after acute starvation, may be the underlying factor for increasing the activity of Na+,K(+)-ATPase in rat brain. These results suggest that, probably, certain adaptive mechanisms become operative in the brain under disturbed physiological conditions.

Acute Disease↗
PubMedDate not supplied

Effects of starvation on pituitary and plasma growth hormone in rats.

The present experiments were undertaken to study the effect of complete food removal on body weight, pituitary growth hormone (GH), plasma GH and glucose concentration in male and female Wistar rats. Plasma and pituitary GH levels were measured by means of a specific radioimmunoassay. Plasma glucose concentration decrease during the initial 60 h fasting in males and 72 h in females, and remained fairly constant thereafter in both groups. Pituitary GH content was unchanged in males and females by 36 h and 60 h, respectively, after the onset of starvation. Thereafter, pituitary GH decreased progressively with increase of the starvation period. In spite of the changes in pituitary GH, plasma GH concentration in fasted male and female rats was similar to or higher than in controls. In fact, during an initial period, up to 72 h in males and 96 h in females, plasma GH levels in fasting rats were similar to control values. With longer starvation periods, plasma GH concentration rose above control values. After 24 h of refeeding 102 h fasted rats, plasma GH concentrations were comparable to control levels. In addition, after an initial loss of 10 g after 24 h fasting, body weight of both male and female animals decreased, and by the end of the starvation period it was about 50% of control weight. From these results it seems that complete food removal has a direct effect on pituitary GH. Furthermore, the fact that changes in plasma GH concentrations were evidentiated just before the period when plasma glucose was maintained at constant levels in fasted rats of both sexes supports the hypothesis that growth hormone plays a physiological role in the regulation of glucose homeostasis during starvation.

Animals↗
PubMed1983

Changes of beta-endorphin and somatostatin concentrations in different hypothalamic areas of female rats after chronic starvation.

To study the effect of starvation on hypothalamic beta-endorphin and somatostatin (SRIF) concentrations in relation to starvation induced anestrus, groups of 8 rats were fed 50% of their normal daily chow consumption. Rats were sacrificed after 4, 8, 12, and 16 days during diestrus or anestrus. beta-endorphin concentrations decreased in the preoptic suprachiasmatic area (0.52 +/- 0.13 vs 0.21 +/- 0.05 ng/mg tissue wet weight) and increased in the posterior hypothalamus (0.31 +/- 0.06 vs 0.57 +/- 0.11 ng/mg) after 4 days of starvation. No significant change occurred in the arcuate nucleus or in the median eminence. On day 8 and 12 of starvation, beta-endorphin was unaltered in all areas compared to controls. Vaginal smears showed constant diestrus in a significant number of rats (5 out of 8) after 12 days. beta-endorphin concentrations in the arcuate nuclei of these rats were significantly reduced on day 16 (1.00 +/- 0.33 vs 0.30 +/- 0.11 ng/mg). The SRIF levels changed only in the median eminence with increased concentrations on day 12 (45.2 +/- 8.4 vs 79.5 +/- 14.8 ng/mg). At this time serum levels of luteinizing hormone (LH), prolactin (PRL), and growth hormone (GH) were significantly reduced. The results indicate that changes in hypothalamic beta-endorphin accompany the events leading to starvation induced anestrus.

Anestrus↗
PubMed1976

Physiologic significance of glucocorticoids and insulin in the regulation of hepatic gluconeogenesis during starvation in rats.

The physiologic significance of glucocorticoids and insulin in the regulation of hepatic gluconeogenesis was investigated during a 48-hr starvation period by studying the factors presumed to control the rate of glucose synthesis in the final gluconeogenetic pathway. Rats were used, in which glucorticoids were removed by adrenalectomy before starvation, and in which serum insulin was kept constant before and after food withdrawal by pre-feeding with a proteinfree diet. It was found that adrenalectomized rats at constantly low serum insulin levels responded to starvation as rapidly, and to the same degree, as intact control subjects (1) by a significant increase in plasma glucagon and, consequently, in hepatic cAMP concentration; (2) by a coordinate elevation of the activities of hepatic pyruvate carboxylase, P-enolpyruvate carboxykinase, and fructose-1,6-diphosphatase; (3) by systematic alterations in the concentration of effectors of gluconeogenetic key enzymes; (4) by a shifting of the cytoplasmic NAD system towards the reduced state; (5) by a decrease in the intrahepatic concentration of glycogenic precursor substrates. These results suggest that the hepatic gluconeogenic response to starvation with respect to the regulatory factors 1-5 occurs independently from changes in the concentration of plasma glucocorticoids and insulin. The crossing over of the gluconeogenetic intermediates between pyruvate and P-enolpyruvate (PEP), which was observed in intact but not in adrenalectomized rats, supports the assumption that during starvation, glucocorticoids enhance the rate of glucose production by the liver predominantly by permitting hepatic cAMP to stimulate the yet undefined mechanism, which has been demonstrated in the isolated perfused rat liver to control the substrate flow between pyruvate and PEP.

Adenine Nucleotides↗
PubMed1978

Effect of starvation, nutriment replacement, and hypothyroidism on in vitro hepatic T4 to T3 conversion in the rat.

To evaluate the effect of starvation, oral and i.v. nutriments, and hypothyroidism on the peripheral conversion of thyroxine (T4) to 3,3', 5-triiodothyronine (T3) in the rat and mouse, an in vitro system for assessing T4 conversion to T3 by fresh liver homogenates was used. A 2-day starvation in the rat reduced hepatic T3 generation from T4 by 47% +/- 3.5% (mean +/- SE) in six separate experiments and also impaired the metabolism of 125I-r-T3. Administration of carbohydrate (CHO) and amino acids (P), but not lipid (L), significantly increased T3 generation above values observed in the starved rat. The mean serum glucose concentration was similar in all nutriment-infused groups, but serum insulin was significantly greater in the CHO- and P-infused as compared to the L-infused rats. These findings suggest that CHO and P, but not L, are important modulators of hepatic outer ring thyronine deiodination in the rat, perhaps due to increased intracellular glucose. Hypothyroidism in the rat induced by thyroidectomy and congenital secondary hypothyroidism in the dwarf mouse resulted in a striking decrease in hepatic conversion of T4 to T3. This decrease was restored to normal by the daily s.c. administration of physiologic doses of T4 (1.5 microgram/100 g) or T3 (0.5 microgram/100 g) for 14 days, and was increased above normal following treatment of normal rate with greater than physiologic doses of T4 (3microgram/100 g) or T3 (1 microgram/100g). In vitro hepatic conversion of T4 to T3 is, therefore, dependent upon thyroid function. Since 2-days starvation in the rat was associated with decreased serum concentrations of T4, T3, and TSH, and hypothyroidism resulted in decreased conversion of T4 to T3, the effect of a constant 2-day infusion of physiologic doses of T4 or T3 in the starved rat on the in vitro deiodination of T4 was assessed. Thyroid hormone replacement did not enhance the conversion of T4 to T3 in the starved rat. These observations suggest that the starvation-induced decrease in hepatic generation of T3 from T4 is not due to hypothyroidism and that the mechanism(s) of the decreased T3 production observed in starvation and hypothyroidism is different.

Amino Acids↗
PubMed1990

The effect of starvation on insulin-induced glucose disposal and thermogenesis in humans.

The effect of 48-hour starvation on glucose metabolism was studied in six non-diabetic, normal weight men using a hyperinsulinemic (100 mU/min/m2) glucose clamp (3.5 mmol/L). The rate of glucose oxidation was calculated from measurements of respiratory gas exchange, after allowing for the oxidation of ketones and of protein. During the glucose clamp, the whole body glucose disposal rate decreased from 39.8 (SEM 4.6) mumol/kg/min in the fed state to 24.1 (2.1) mumol/kg/min in the starved state (P less than .01), consistent with insulin "resistance." The glucose oxidation rate decreased from 21.8 (1.3) to 3.9 (1.4) mumol/kg/min with starvation (P less than .001), but the nonoxidative glucose disposal rate was unchanged (18.0 [3.9] mumol/kg/min normally fed, and 20.2 [1.2] mumol/kg/min starved). With starvation, the rate of glucose uptake in the forearm during the glucose clamp was reduced from 59.4 to 15.4 mumol/min/L forearm (SE 5.6, P less than .01, ANOVA). There was a significant net increase in thermogenesis during the glucose clamp in the normally fed state (0.27 [0.08] kJ/min, P less than .01, ANOVA), but not following starvation (0.11 [0.09] kJ/min, NS, ANOVA). Therefore, starvation caused decreases in oxidative glucose disposal and in forearm glucose uptake; despite the whole body nonoxidative disposal rate of glucose being unchanged, the associated net thermogenic response was diminished.

3-Hydroxybutyric Acid↗
PubMed1992

Metabolic changes during early starvation in rats fed a low-protein diet in the postweaning growth period.

Metabolic changes during the first 24 hours of starvation were studied in rats previously adapted for 3 weeks during the postweaning growth period to a low-protein diet using lactalbumin as a dietary protein source. Previous adaptation to a high-quality, low-protein diet reduced the effects of early starvation on the loss of body and liver weight. In rats fed a low-protein diet (6% lactalbumin, LP rats), free triiodothyronine (T3) concentration remained higher than in control rats (13% lactalbumin, C rats) throughout the experiment (+38%, 24 hours), and the plasma insulin concentration, which was lower than in C rats during the first 6 hours (-56%), was not different thereafter. Plasma insulin to glucagon molar ratio was lower (-54%) and liver cyclic adenosine monophosphate (cAMP) concentration was higher (+28%) in LP than in C rats in the fed state, but these were not different at 24 hours of starvation. Plasma glucose concentration was slightly lower in LP than in C rats (-15%) in the fed state, but it was not different in both groups during starvation. Whereas they were unchanged in the fed state, plasma lactate concentration was lower (-57%) and free fatty acid and total ketone body concentrations were higher (+38% and +183%, respectively) in LP than in C rats at 24 hours of starvation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Starvation stimulates pancreatic PGE content.

Recent evidence suggests that prostaglandins may exert a tonic inhibitory tone in the pancreatic beta cell during starvation. The effects of starvation on rat pancreatic prostaglandin E (PGE) content were studied. After 72 hrs of starvation, pancreatic PGE increased 250% above that of fed controls. Administration of streptozotocin, a selective beta-cell toxin, decreased pancreatic PGE significantly (p less than 0.005), but starvation partially reversed this trend. Thus, PGE may have a physiological role in modulating insulin secretion during starvation. It appears that both beta-cell and nonbeta-cell sources of PGE are involved in this phenomenon.

Animals↗
PubMed1982

The effects of starvation on muscle phosphoadenylate concentrations and adenylate energy charge of surface and cave crayfish.

1. A comparison was made of the effects of starvation on available cellular energy in two crayfish species which possess different inherent metabolic rates associated with habitat adaptations. 2. Starvation for 45 days did not significantly lower phosphoadenylate concentrations or adenylate energy charge [AEC = (ATP + 1/2 ADP)/(ATP + ADP)] in dorsal tail muscle of either the epigean (surface) crayfish. Procambarus clarkii or the cave species, Orconectes inermis inermis. 3. After 5, 15 and 30 days of starvation, P. clarkii contained greater ATP and total adenylate concentrations in dorsal tail muscle than control crayfish which were fed. 4. The greater phosphoadenylate concentrations in unfed crayfish may be associated with increased motor activity previously documented in another surface crayfish species under conditions of starvation. 5. However, starvation did not induce changes in adenylate concentrations in O. i. inermis. 6. This could be due to the lack of sufficient nutritional stress to elicit a response in this more slowly metabolizing species.

Adenine Nucleotides↗
PubMed1986

Effect of starvation and protein-feeding on blood amino acid compartmentation of domestic fowl hatchlings.

The amino acid concentrations in plasma and blood cells of 5-day old domestic fowl hatchlings that received either standard feeding, protein-feeding or were starved have been determined. The effects of 5-day starvation or protein feeding did not alter significantly the combined amino acid concentration of blood plasma, but decreased blood cell levels. The patterns of individual amino acid changes observed in starvation or protein-feeding were similar in both groups when compared with those of controls. However, starvation-induced effects were actually more marked than those observed in protein-fed animals. The patterns of change with starvation of individual amino acids in the hatchling blood compartments were very different from those observed in mammals subjected to short or medium-term starvation. The mechanisms controlling circulating amino acid concentrations act in both situations studied to maintain the plasma amino acid concentrations despite marked changes in the availability of 2-amino nitrogen energy to the animal; changes in blood amino acid compartmentation buffering plasma amino acid availability.

Amino Acids↗
PubMed1979

Variations in mitochondrial monoamine oxidase during progressive starvation in the brain of developing rats.

Effects of progressive starvation of 12, 24, 48 and 60 h upon brain mitochondrial monoamine oxidase activity were studied. The enzyme activity was determined by three different substrates: 14C-labeled tryptamine, dopamine and kynuramine. With dopamine as substrate, the enzyme activity showed decline during 24 and 48 h of starvation. Monoamine oxidase when determined by tryptamine as the substrate, showed a decrease after 60 h of starvation. The use of kynuramine as substrate also produced a decrease in enzyme activity after 48 and 60 h of starvation. Refeeding the 60-h-starved rats for the following 24 h resulted in further decrease of monoamine oxidase activity of brain mitochondria from the 60 h starved values. The results suggest that oxidative deamination of biogenic amines is greatly inhibited during progressive starvation and remains low even after feeding the 60 h starved rats for 24 h.

Animals↗
PubMed1985

Xenobiotic biotransformation in the rainbow trout liver and kidney during starvation.

Microsomal cytochrome P-450-dependent activities in the kidney of fish starved for 6 weeks were significantly lower than in fed fish whereas these activities in the liver were only depressed after 12 weeks of starvation. Hepatic cytochrome P-450-dependent activities were depressed to varying extents after 12 weeks of starvation when different substrates were used. The content of hepatic cytochrome P-450 was not affected by starvation. Hepatic UDP-glucuronosyl transferase activities were not affected by starvation. Induction of several hepatic cytochrome P-450-dependent activities by treatment of fish with beta-naphthoflavone was not influenced by starvation. In the kidneys of fish starved for 12 weeks induced levels of cytochrome P-450-dependent benzo(a)pyrene hydroxylase activities were significantly lower than in the kidneys of fed induced fish.

Animals↗