SEARCH · Search PubMed

Results for “STARVATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 307 records · Page 17Linked to original sources

PubMed2006

Alcohol alters skeletal muscle heat shock protein gene expression in rats: these effects are moderated by sex, raised endogenous acetaldehyde, and starvation.

Alcoholic myopathy is a common pathology characterized by wasting due to reduced protein synthesis, although the mechanisms involved remain unclear. Women are particularly sensitive and malnutrition exacerbates the myopathy. This study aimed to address (i) whether long-term alcohol feeding alters expression of heat shock proteins (HSPs) in male and female rats; (ii) the effect of immediate alcohol dosing with or without raised levels of endogenous acetaldehyde; and (iii) the effect of starvation. To address this, (i) male and female rats were fed alcohol in the long-term (6-7 weeks as 35% of energy in a liquid diet) and compared to controls fed the same diet with isoenergetic glucose; (ii) male rats given an immediate bolus (75 mmol ethanol per kilogram body weight intraperitoneally) 2.5 hours before sacrifice and compared to controls given a dose of saline (with or without pretreatment with cyanamide-an acetaldehyde dehydrogenase inhibitor which raises endogenous acetaldehyde); (iii) male rats starved for 1 or 2 days then immediately dosed with alcohol. Protein levels of HSP 27, HSP 60, and HSP 70 were measured in muscles of male rats fed alcohol and pair-fed control rats by SDS-PAGE and Western blotting in study I. Levels of HSP 27, HSP 60, HSP 70, and HSP 90 mRNA were analyzed in hind limb skeletal muscle by reverse transcription-polymerase chain reaction with an endogenous internal standard, glyceraldehyde-3-phosphate-dehydrogenase. (i) Long-term alcohol dosage reduced HSP 27 in male rats but not in females, whereas HSP 90 mRNA increased in long-term alcohol-fed female rats but not in male rats. These changes were reflected by a similar trend in HSP protein content, although statistical significance was not achieved. (ii) There was no effect on any of the HSP mRNAs in rats dosed immediately with alcohol or in combination with cyanamide. (iii) Starvation per se for 2 days was associated with an increase in HSP 27 mRNA. Alcohol administration after 2 days starvation caused a blunting of the increased HSP 27 mRNA in starvation alone. This suggests that long-term alcohol exposure affects HSP gene expression and that this effect is moderated by sex and starvation. This may contribute to, or reflect, the biochemical lesion in alcoholic myopathy.

Acetaldehyde↗

PubMed2006

Effect of starvation on Fos and neuropeptide immunoreactivities in the brain and pituitary gland of Xenopus laevis.

In mammals complex interactions between various brain structures and neuropeptides such as corticotropin-releasing factor (CRF) and urocortin 1 (Ucn1) underlay the control of feeding by the brain. Recently, in the amphibian Xenopus laevis, CRF- and Ucn1-immunoreactivities were shown in the hypothalamic magnocellular nucleus (Mg) and evidence was obtained for their involvement in food intake. To gain a better understanding of the brain structures controlling feeding in X. laevis, the effects of 16 weeks starvation on neurones immunoreactive (ir) to Fos and neuropeptides in various brain structures were quantified. In the Mg, compared to controls, starved animals showed fewer neurones immunopositive for Fos (-55.9%), Ucn1 (-44.0%), cocaine and amphetamine-regulated transcript (CART) (-94.3%) and metenkephalin (ENK) (-65.0%), whereas CRF-ir neurones were 2.1 times more numerous. These differences were mainly apparent in the ventral part of the Mg, followed by the medial and dorsal part of the nucleus. In the neural lobe of the pituitary gland a 22.5% lower optical density of CART-ir was observed. In the four other brain structures investigated, starvation had different effects. The dorsomedial part of the suprachiasmatic nucleus showed 5.9 times more NPY-ir cells and in the ventromedial thalamic area a lower number of NPY-ir cells (-33.6%) was found, whereas the Edinger-Westphal nucleus contained fewer CART-ir cells (-42.2%); no effect of starvation was seen in the ventral hypothalamic nucleus. Our results support the hypothesis that in X. laevis, the Mg plays a pivotal role in feeding-related processes and, moreover, that starvation also has neuropeptide- and brain structure-specific effects in other parts of the brain and in the pituitary gland, suggesting particular roles of these structures and their neuropeptides in physiological adaptation to starvation.

Animals↗

PubMed2000

Developmental changes in the response of larval Manduca sexta fat body glycogen phosphorylase to starvation, stress and octopamine.

Fasting or starvation of 1(st)- and 2(nd)-day fifth instar Manduca sexta larvae leads to rapid activation of fat body glycogen phosphorylase. Under feeding conditions, 21-29% of the phosphorylase was found in the active form. However, after only one hour of starvation, the active form increased to 55-65%. In larvae on the 3(rd)-day there was a slower increase in the activation, requiring three hours of starvation to reach a maximum of 60-65%. No activation was observed in 4(th)-day larvae after three hours of starvation. When 1(st)- or 2(nd)-day larvae were decapitated, the time-course of activation of glycogen phosphorylase was very similar to that observed in intact insects. However, activation of glycogen phosphorylase following decapitation was only observed in 1(st)- and 2(nd)-day larvae. In 2(nd)-day larvae, octopamine promoted activation of glycogen phosphorylase and 100-pmol of octopamine promoted maximum activation. Higher amounts of injected octopamine caused a decrease in activation. The injection of 100 pmol of octopamine caused a 50-55% activation of phosphorylase within 30 minutes. The simultaneous injection of the alpha-adrenergic receptor antagonist phentolamine with octopamine blocked the octopamine effect in 1(st)- and 2(nd)-day feeding larvae. However, the activation of glycogen phosphorylase observed in ligated/decapitated larvae on the 1(st)- and 2(nd)-day was not abolished by injection of phentolamine. All of these data suggest that factors other than adipokinetic hormone and octopamine may be involved in the activation of glycogen phosphorylase during fasting or starvation in the early part of the fifth larval stage of M. sexta.

Animals↗

PubMed2000

Hormones and metabolites of arctic foxes (Alopex lagopus) in response to season, starvation and re-feeding.

Svalbard's arctic foxes experience large seasonal variations in light, temperature and food supply throughout the year, which may result in periods of starvation. The aim of this work is to investigate if there are seasonal variations in post-absorptive plasma thyroid hormones (free thyroxin (fT(4)), free triiodothyronine (fT(3)) and reverse triiodothyronine (rT(3))) and metabolites (free fatty-acids (FFA) and beta-hydroxybutyrate (beta-OHB)) with season and their response to starvation and re-feeding. The concentrations of post-absorptive free triiodothyronine were significantly higher in November than May, while those of thyroxin, reverse triiodothyronine, free fatty-acids and beta-hydroxybutyrate remained unchanged. Possible explanations for the seasonal variations in free triiodothyronine are discussed. There were no significant changes from post-absorptive concentrations of thyroxin and reverse triiodothyronine in starved and re-fed foxes. However, free triiodothyronine concentrations decreased during starvation and increased again with re-feeding both in May and November. Starvation induced high levels of free fatty acids in both May and November, indicating increased lipolysis. There was a significant increase in beta-hydroxybutyrate in November only, indicating that arctic foxes are capable of protein conservation during starvation.

3-Hydroxybutyric Acid↗

PubMed1994

Brain metabolism during short-term starvation in humans.

During prolonged starvation, brain energy requirements are covered in part by the metabolism of ketone bodies. It is unknown whether short-term starvation of a few days' duration may lead to reduced brain glucose metabolism due to the change toward ketone body consumption. In the present study we measured the cerebral metabolism of glucose and ketone bodies in nine healthy volunteers before and after 3.5 days of starvation. Regional glucose metabolism was measured by dynamic positron emission tomography using [18F]2-fluoro-2-deoxy-D-glucose. The mean value of K1* in gray and white matter increased by 12% (p < 0.05), whereas k2* and k3* were unchanged compared with control values. Regional glucose metabolism in cortical gray matter was reduced by 26% from 0.294 +/- 0.054 to 0.217 +/- 0.040 mumol g-1 min-1 (p < 0.001). White matter glucose metabolism decreased by 27% (p < 0.02). The decrease was uniform in gray and white matter with regional decreases ranging from 24 to 30%. A determination using Fick's principle confirmed the reduction in glucose metabolism yielding a decrease of 24% from 0.307 +/- 0.050 to 0.233 +/- 0.073 mumol g-1 min-1 (p < 0.05), whereas CBF did not change (0.57 +/- 0.07 vs. 0.57 +/- 0.06 ml g-1 min-1). The global net uptake of beta-hydroxybutyrate increased 13-fold from 0.012 +/- 0.024 to 0.155 +/- 0.140 mumol g-1 min-1 (p < 0.05). Net uptake of acetoacetate and net efflux of lactate and pyruvate did not change significantly during starvation. The present study shows that the human brain adapts to the changes in energy supply as early as 3 days following initiation of starvation, at which time ketone bodies account for approximately one-fourth of the cerebral energy requirements.

Adult↗

PubMed1983

The effect of starvation and refeeding on lipogenic enzymes in mammary glands and livers of lactating rats.

Lactating rats were starved for 48 h and refed a high-carbohydrate diet for a further 48 h. Starvation stops milk secretion, which resumes shortly after refeeding. Three lipogenic enzymes, fatty acid synthase, glucose 6-phosphate dehydrogenase (EC 1.1.1.49) and 'malic' enzyme (EC 1.1.1.40) all decrease in the mammary gland during starvation and are restored to the pre-starvation levels 48 h after refeeding. The same enzymes in liver also decrease during starvation, but increase to values significantly higher than those for the normal fed rats after refeeding the high-carbohydrate diet. For the fatty acid synthase these values were four times the pre-starvation values. Serum insulin and prolactin concentrations also increased upon refeeding the high-carbohydrate diet.

Animals↗

PubMed1987

Acyl-CoA dehydrogenase activity in the riboflavin-deficient rat. Effects of starvation.

Riboflavin deficiency in weanling rats causes a metabolic disorder characterized by failure to oxidize fatty acids. The disorder is similar to that seen in several human diseases, some of which are responsive to pharmacological doses of riboflavin. Previous analysis of the riboflavin-deficient rat has shown that the failure of fatty acid oxidation is due to a decrease in the activity of the acyl-CoA dehydrogenases of beta-oxidation. The activity of these flavoenzymes in liver rapidly decreases when a riboflavin-deficient diet is initiated. The objectives of these experiments were to analyse the effects of starvation on liver mitochondria isolated from the riboflavin-deficient rat. Our studies show that the decreased mitochondrial fatty acid oxidation induced by riboflavin deficiency is partially reversed by starvation. The extent of this reversal is proportional to the duration of starvation. The starvation-associated increase in fatty acid oxidation is mediated by an increase in the mitochondrial short-chain acyl-CoA dehydrogenase activity. The activity of this enzyme is increased such that the ratio of short-chain acyl-CoA dehydrogenase apoenzyme to holoenzyme does not change. We conclude that short-chain acyl-CoA dehydrogenase activity is limiting for fatty acid oxidation when its activity falls below a critical point. The increased mitochondrial specific activity of short-chain acyl-CoA dehydrogenase during starvation may result from an increased availability of flavin coenzyme or an increase in enzyme catalytic efficiency.

Acyl-CoA Dehydrogenase↗

PubMed1987

Effect of total starvation and very low calorie diets on intestinal permeability in man.

1. The effect of total starvation for 4-5 days on the intestinal uptake and urinary excretion of markers from an orally administered mixture of mannitol (5g), [14C]mannitol (0.5 microCi), lactulose (10 g) and 51Cr-labelled ethylenediaminetetra-acetate (51Cr-EDTA) (30 microCi), was assessed in five lean (group 1) and four obese (group 2) subjects. The effect of a very low calorie diet for 1 week and of a subsequent 5 day period of total starvation on intestinal permeability was assessed in a similar way in another group of obese subjects (group 3). Transit time from mouth to caecum of the fastest component of the oral mixture was assessed by the appearance of hydrogen in breath (all subjects), and the configuration of the transit spectrum through various segments of the gastrointestinal tract, was assessed by a radionuclide scan method (group 2 subjects only). The effect of starvation on plasma/renal clearance of these markers in subjects of group 2 was assessed with the use of a bolus intravenous injection of a mixture of mannitol (2 g). [14C]mannitol (10 microCi), lactulose (0.1 g) and 51Cr-EDTA (5 microCi). 2. The uptake and urinary excretion of orally administered mannitol was decreased by total starvation. The mean decrease was 47% in the lean subjects (P less than 0.025), 33% in group 2 obese subjects (P less than 0.05) and 41% in group 3 obese subjects P greater than 0.05). In contrast, starvation produced no significant change in either the excretion of 51Cr-EDTA or lactulose.(ABSTRACT TRUNCATED AT 250 WORDS)

Creatinine↗

PubMed1994

Short-term starvation alters the free amino acid content of the human intestinal mucosa.

1. The effects of short-term starvation and refeeding on the free amino acid concentrations of the intestinal mucosa were characterized in male subjects (n = 6), using endoscopically obtained biopsy specimens from the duodenum and from all four segments of the colon. 2. The alterations in the amino acid concentrations in response to short-term starvation were overall uniform in both duodenal and colonic mucosa as well as in plasma. Most amino acids decreased, whereas branched-chain amino acids increased. 3. In the colon, glutamic acid and glutamine decreased during the starvation period, whereas they remained unaltered in the duodenum. This was the major difference in response to short-term starvation between the amino acid concentrations in the intestinal mucosa of the duodenum and colon. 4. Refeeding for 3 days normalized the amino acid concentrations except for glutamic acid, asparagine and histidine, which remained low in the colon, and threonine, which showed an overshoot in both parts of the intestine. 5. The changes in mucosal amino acid concentrations seen in response to starvation and refeeding were uniform in the four segments of the colon. This suggests that sampling from the rectum/sigmoid colon will give representative values for the free amino acid concentrations of the entire large intestine.

Adult↗

PubMed2001

The effect of short-term starvation or water deprivation on caffeine pharmacokinetics in calves.

The aim of this study was to determine the effect of short-term starvation or water deprivation on the pharmacokinetics of caffeine in calves. The experiment was carried out on 30 Holstein-Friesian calves (10 calves in a control group, 10 calves in a 'starved' group and 10 calves in a 'water-deprived' group) aged 24-25 days. Control group calves were given caffeine at 24-25 and 28-29 days of age. In the experimental groups caffeine studies were performed before and after 4 days of starvation or water deprivation. In the control group no significant differences between the pharmacokinetic parameters of caffeine in 24-25 and 28-29 day-old calves were observed. Starvation for 4 days was associated with an increase in the mean residence time (MRT) of caffeine in each subject. The increase was statistically significant (P < 0.01). After starvation the total plasma clearance of caffeine decreased (about 20 per cent). The decrease was statistically significant (P < 0.05). The volume of caffeine distribution (V(ss)) was slightly but not significantly increased. Similarly, water deprivation was associated with significant increase in the mean residence time of caffeine in each subject. The total plasma clearance of caffeine decreased (about 30 per cent). This decrease was statistically significant (P < 0.01). The volume of caffeine distribution was slightly but not significantly decreased. Results obtained in this study indicate that short-term (for 4 days) starvation or water deprivation leads to a general inhibition of hepatic P450 enzymatic system and may impair the elimination of drugs that undergo metabolism by these enzymes.

Animals↗

PubMed1984

Interaction of cold and starvation in the regulation of plasma corticosterone levels in the male rat.

Plasma corticosterone levels were determined in serial samples obtained from 3 groups of rats: 1) starved, 2) cold-treated (4 degrees C), and 3) starved and cold treated (4 degrees C). Starvation resulted in an increase of plasma corticosterone on the 3rd day and the increase henceafter was linear with the number of days of treatment up to day 13 whereas upon cold exposure, the plasma corticosterone levels first increased on day 1 up to day 3, and then declined on day 9. Cold and starvation in combination led to a greater elevation of plasma corticosterone level than cold or starvation alone. It is concluded that the increase of plasma corticosterone during starvation or cold may be related to altered metabolism under such circumstances, and that the effect of cold and starvation are synergistic and may be mediated by different neural mechanisms.

Animals↗

PubMed1981

Changes in the concentrations of the minor constituents of goat's milk during starvation and on refeeding of the lactating animal and their relationship to mammary gland metabolism.

1. Changes in the concentrations of the minor constituents of goat's milk were observed during 48 h starvation and on refeeding. 2. The concentrations of hexose phosphate and UDP-hexoses increased during starvation and decreased on refeeding. 3. The concentrations of phosphoenolpyruvate and glycerate 3-phosphate decreased during starvation and increased on refeeding. 4. Isocitrate:2-oxoglutarate increased during starvation and decreased on refeeding. 5. Changes in the minor constituents of milk can be explained in terms of the metabolic changes occurring in the mammary gland during starvation. It is proposed that changes in the concentrations of these metabolites in milk reflect changes in their concentrations in the cytosol or Golgi vesicles of the mammary gland.

Animals↗

PubMed1986

Starvation increases the solubility of volatile anaesthetics in rat liver.

We evaluated the effect of starvation on anaesthetic solubility in tissues involved in lipid transport (blood) or metabolism (liver) and in a tissue not involved in either (brain). The liver/gas partition coefficients of isoflurane, enflurane, halothane and methoxyflurane in rats increased by 15-20% after 6 h of starvation and reached a maximum increase of 35-42% after 24 h of starvation. After 48 h of starvation the coefficients had returned to control values. Blood/gas and brain/gas partition coefficients were not changed or were inconsistently changed by starvation. The maximum change in blood or brain solubility was 14% (at 6 h), and 29 of 32 mean values changed less than 10%.

Anesthetics↗

PubMed1978

Starvation and refeeding in rats: effect on organismic respiration, cytoplasmic constituents of liver, and succinic dehydrogenase activity in liver, kidney, and heart.

An analysis of starvation and starvation followed by refeeding was undertaken to characterize some organismic, organ, and mitochondrial responses to these two circumstances. Body weight, organismic respiration as well as weight protein and succinic dehydrogenase activity for liver, kidney, and heart were determined over the course of 6 days of starvation and 5 days refeeding for adult male rats. Assays of marker enzyme activities for mitochondria (cytochrome oxidase), lysosomes (acid phosphatase), endoplasmic reticulum (glucose-6-phosphatase), and plasma membranes (5'-nucleotidase) were conducted for liver in addition to quantitations of mitochondrial protein. All enzyme determinations were done on whole tissue homogenates and reported as total organ activity. Liver mitochondria were harvested quantitatively directly from whole liver homogenates by zonal centrifugation for determination of mitochondrial protein. Starvation resulted in a major loss of body weight, organ weight, and organ protein; liver greater than kidney greater than heart. These changes were accompanied by a major reduction in organ succinic dehydrogenase activity; liver greater than kidney. In heart, succinic dehydrogenase was doubled in activity at day 2 of starvation and subsequently diminished to values not significantly lower than controls. In liver, mitochondrial mass (protein) was severely diminished. From analysis of marker enzyme activities, it appeared that lysosomes, endoplasmic reticulum, and plasma membrane were also decreased. Refeeding restored the greatest part of these losses within 5 days.

Animals↗

PubMed1988

Synthesis of membrane and periplasmic proteins during starvation of a marine Vibrio sp.

Changes in membrane and periplasmic protein profiles induced by starvation conditions in the marine Vibrio sp. S14 were examined by one-dimensional gel electrophoresis. Analysis by densitometry resolved at least six periplasmic proteins, nine outer membrane proteins, and four cytoplasmic membrane proteins induced at various times during 120 h of nutrient and energy starvation. Eight of these were also synthesized by heat- and/or ethanol-shocked cells. Pulse-labelling indicated that the starvation-induced proteins were not products of degradation, and that their synthesis was differently modulated during starvation. The most pronounced changes occurred during the initial hours of nutrient and energy deprivation. The correlation between the initial changes in protein composition and utilization of the intracellular energy reserve poly-beta-hydroxybutyrate is discussed. The rate of proteolysis during the initial hours of starvation was approximately 16 times greater than that during exponential growth.

Bacterial Outer Membrane Proteins↗

PubMed1983

Dopamine blockade inhibits starvation ketosis in man.

The effects of dopamine blockade on the endocrine and metabolic response to starvation have been investigated by administration of metoclopramide, 30 mg daily, or placebo to five normal subjects fasted for sixty hours on two occasions. Blood glucose and alanine concentrations fell with starvation and metoclopramide had no further effect. Concentrations of the other gluconeogenic precursors, lactate and pyruvate, were also unaffected by metoclopramide. The rise in circulating ketone body concentrations with fasting was impaired by metoclopramide, significantly from 44 h onwards (blood total ketone body concentration at 60 h, 3.42 +/- 0.94 mmol/l with placebo; 2.08 +/- 0.67 mmol/l with metoclopramide, P less than 0.05). Blood glycerol and plasma non-esterified fatty acids (NEFA) levels rose with starvation, and metoclopramide had no further effect. Serum insulin concentrations remained low with fasting, while circulating glucagon and growth hormone levels rose. Similar changes were noted with both metoclopramide and placebo. Serum prolactin concentrations during starvation were elevated two to four fold by metoclopramide. The inhibitory effect of dopamine blockade on ketosis thus occurred despite hyperprolactinaemia, and did not result from measurable alterations in insulin, glucagon or growth hormone secretion. The data suggest a stimulatory role for endogenous dopamine on starvation ketonaemia in man.

Acidosis↗

PubMed1995

The effect of starvation on leucine, alanine and glucose metabolism in obese subjects.

The relationship between changes in ketone concentrations and leucine metabolism (seven obese subjects), glucose and alanine metabolism (seven obese subjects) was investigated using radioisotopic techniques after 12 h, 60 h and 2 weeks starvation. Leucine metabolism was also measured in five lean subjects after 12 h and 60 h starvation. In the obese subjects leucine concentration increased after 60 h starvation and leucine metabolic clearance rate, glucose and alanine concentration decreased (P < 0.05). Glucose and alanine production rate (Ra) decreased after 2 weeks (P < 0.05) but there was no change in leucine Ra after 60 h or 2 weeks. In the lean subjects leucine concentration, production rate and oxidation rate were increased after 60 h (P < 0.005, P < 0.05, P < 0.05). Ketone concentration was inversely related to alanine Ra (r = -0.51, P < 0.02) but was not related to measurements of protein metabolism in the obese subjects. This study demonstrates that the effect of short-term starvation on protein metabolism differs in lean and obese subjects. The decrease in glucose Ra during long-term starvation may be in part due to a decreased supply of alanine for gluconeogenesis.

Adult↗

PubMed1997

Carbon starvation of Salmonella typhimurium does not cause a general increase of mutation rates.

Mutation rates in bacteria can vary depending on the genetic target studied and the specific growth conditions of the cells. Here, two different methods were used to determine how rates of mutation to antibiotic resistance, auxotrophy, and prototrophy were influenced by carbon starvation on agar plates. The rate of mutation to rifampin resistance was increased by starvation as measured by fluctuation tests, similar to what has been reported previously for Escherichia coli. In contrast, the rates of mutation to various types of auxotrophy were unaffected or decreased as measured by both fluctuation tests and a repeated-streaking procedure. Similarly, the rates of reversion to prototrophy of his and lac nonsense and missense mutations were unaffected by starvation. Thus, mutation rates of different genetic targets can be affected differently by starvation and we conclude that carbon starvation is not generally mutagenic in Salmonella typhimurium.

Drug Resistance, Microbial↗