Search PubMed⌕ Search

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.

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

At least 1,261 records · Page 70Linked to original sources
PubMed1977

Diet and starvation on the composition and calculated density of fat-free body mass.

The density of the fat-free body mass (FFM) was calculated from carcass composition and density of body components in 148 growing rats under different dietary conditions. These conditions were controlled feeding with 20% and 5% casein diets during 6 and 9 wk, followed by 5 days of starvation, and after starvation with 2 wk refeeding with 20 and 5% casein diets. The results showed that the density of FFM was fairly constant. The means and standard deviations for all conditions were 1.0965 +/- 0.0057 and 1.0956 +/- 0.0075, for the 20% and 5% casein groups, respectively, with a grand mean of 1.0960 +/- 0.0066. It was concluded that the assumption of a constant density of FFM holds very well for many dietary and experimental conditions.

Animals↗
PubMed1985

Effects of starvation on lung mechanics and biochemistry in young and old rats.

Two groups of rats (young and old) were food-deprived for 3 wk and were compared with age-matched fed groups. Final body weight and dry and wet weights of lungs were significantly reduced in both young and old starved rats. As determined by saline volume-pressure (VP) curves, lungs of young starved rats accepted significantly less volume at all pressure levels compared with lungs of young fed rats. When expressed as a percent of maximum lung volume, the VP curve in young starved rats was significantly shifted upward at low lung volumes. In the old rats, the VP curves were similar in fed and starved rats. Total lung content of protein, DNA, crude connective tissue, hydroxyproline, and elastin were significantly reduced in young starved compared with young fed rats, whereas in old starved rats only protein and DNA contents were lower than those in old fed animals. It appears that in rapidly growing young rats starvation leads to growth retardation, loss of connective tissue components, and possibly reduction in tissue elastic forces at low lung volumes, whereas starvation has no significant effects on lung mechanics and connective tissue in old rats.

Age Factors↗
PubMed1989

Effects of starvation and refeeding on elastase-induced emphysema.

Adult rats received pancreatic elastase (75 U/100 g) intratracheally and were divided into three groups: fed, starved, and refed. Starved rats received one-third of their measured daily food consumption until they lost 40% body weight. The refed group was fed after 40% weight loss. A control group received saline intratracheally. Saline volume-pressure curve was shifted more significantly to the left of the control group in starved than in fed rats and was superimposed in refed and fed groups. Mean linear intercept was larger and alveolar surface area was smaller in starved than in fed rats compared with the control group; both were similar in fed and refed rats. Protein and hydroxyproline content of the lung were higher in fed than in control and in starved groups; after refeeding these returned to the control values. We conclude that starvation aggravates elastase-induced injury and that refeeding results in the complete recovery of the mechanical but only partial recovery of the morphometric changes induced by starvation.

Animals↗
PubMed2000

Starvation, leptin and epithelial cell proliferation in the gastrointestinal tract of the mouse.

BACKGROUND/AIMS: Leptin, the ob/ob gene product, is a recently discovered peptide hormone, secreted by adipocytes, which can act as a satiety factor to regulate food intake. Its levels thus will be related to the presence of food in the lumen of the gut, and food intake is one of the most potent stimuli for intestinal epithelial cell proliferation. Leptin has a variety of other actions and the aim of this study was to see if one of these was to stimulate mucosal growth. METHODS: Three groups of mice were fed ad libitum, starved for 48 h or starved for 48 h and given twice-daily intraperitoneal injections of recombinant leptin (1 microg/g). RESULTS: Starvation led to a 20% decrease in body weight and a similar decrease in the weights of the intestines. Starvation also markedly inhibited intestinal epithelial cell proliferation. Leptin had little effect on the small intestine and did not stimulate proliferation. However, in the hind gut it was associated with small but significant decreases in caecal weight, distal colon mitotic counts (p = 0.036) and in colonic crypt area (approximately 20%, p<0.001). CONCLUSION: Leptin did not stimulate intestinal cell proliferation, however it did have a paradoxical inhibitory action on the caecum and colon.

Animals↗
PubMed1998

Effect of three days starvation on the phagocytic activity of rat peritoneal macrophages.

To examine the effect of starvation on the phagocytic activity of rat peritoneal macrophages, 8 animals were kept for 3 days on water supply only. The cells showed an increased capacity for superoxide anion production and a marked decrease in their ability to engulf latex particles. The corticosterone level of the fasting animals was markedly increased, an observation suggesting that the alteration of macrophage function could be hormonally mediated. The findings in the present study indicate that the decreased phagocytic capacity of peritoneal macrophages following starvation may be one of the factors responsible for the increased susceptibility to infections in malnourished individuals.

Animals↗
PubMed1976

Effect of starvation on pituitary growth hormone cells and blood growth hormone and prolactin levels in the rat.

Growth hormone (GH) cells of rats were studied on days, 2, 4 and 7 of starvation. Immunoperoxidase staining for light microscopy confirmed the presence of GH in the pituitaries of all groups of animals. Electron microscopy revealed crinophagy in the cytoplasm of GH cells on days 4 and 7. By ultrastructural morphometry, volume density and the diameter of secretory granules in the cytoplasm of GH cells remained unchanged. Blood GH determinations showed a significant decrease on day 4 of the starvation period. On day 7 most of the values were in the range of the controls. Blood prolactin levels fell significantly on day 7. It appears that the pituitary is capable of secreting GH even in rats completely deprived of exogenous nutrients.

Animals↗
PubMed1982

Effects of starvation and refeeding on lung biochemistry in rats.

Adult rats received one fifth of their measured daily food consumption until they lost 40% body weight. Some of these rats were then refed until they reached their initial body weight. We measured the following in fed, starved, and refed animals: (1) disaturated phosphatidylcholine (DSPC) content of lung tissue and of lavage fluid, (2) protein content of lung tissue and of lavage return, and (3) DNA and RNA content of lung tissue. In starved lungs, tissue and lavage DSPC content, total protein and RNA contents, and RNA/DNA ratios were significantly lower than in fed rats. After refeeding, DSPC values returned completely to normal, whereas protein, DNA, and RNA contents were significantly higher than in fed rats. The RNA/DNA ratio was similar in the fed and refed groups. Changes in lavage DSPC are consistent with the increased surface elastic forces in starvation and their return to normal with refeeding reported by us previously. It appears that starvation leads to a reduction in cell size without changes in cell number and that refeeding is associated with a more significant increase in cell number than in cell size.

Animals↗
PubMed2005

Leptin corrects host defense defects after acute starvation in murine pneumococcal pneumonia.

RATIONALE: Leptin is an adipocyte-derived hormone that declines dramatically during fasting and plays a pivotal role in the neuroendocrine response to starvation. Previously, we employed leptin-deficient (ob/ob) mice to identify an important role for leptin in the host defense against Klebsiella pneumonia. OBJECTIVES: To assess the effects of fasting on the innate immune response against pneumococcal pneumonia and to determine the effects of maintaining circulating leptin levels on host defense in fasted mice. METHODS: C57BL/6 mice were either fed ad libitum or fasted for 48 h and given an intraperitoneal injection of saline or recombinant leptin (1 microg/g of body weight) twice daily for 48 h before bacterial challenge. Mice were challenged with 10(5) cfu of Streptococcus pneumoniae via the intranasal route. MEASUREMENTS AND MAIN RESULTS: Lung homogenate S. pneumoniae burden was nearly 20-fold greater in the fasted as compared with fed mice. The impairment in bacterial clearance observed in fasted animals was associated with reduced bronchoalveolar lavage neutrophil counts and interleukin-6 and macrophage inflammatory protein-2 levels. Alveolar macrophages from fasted animals also exhibited defective phagocytosis and killing of S. pneumoniae and reduced calcium-ionophore-stimulated leukotriene B(4) synthesis in vitro. In contrast, the provision of exogenous leptin to fasted animals restored bacterial clearance, bronchoalveolar lavage levels of neutrophils and cytokines, alveolar macrophage bacterial killing, and leukotriene B(4) synthesis. CONCLUSIONS: These results suggest that reduced leptin levels substantially contribute to the suppression of pulmonary antibacterial host defense during starvation and that administration of this adipokine may be of therapeutic benefit clinically.

Acute Disease↗
PubMed1969

Liver and kidney metabolism during prolonged starvation.

This study quantifies the concentrations of circulating insulin, growth hormone, glucose, free fatty acids, glycerol, beta-hydroxybutyrate, acetoacetate, and alpha amino nitrogen in 11 obese subjects during prolonged starvation. The sites and estimated rates of gluconeogenesis and ketogenesis after 5-6 wk of fasting were investigated in five of the subjects. Blood glucose and insulin concentrations fell acutely during the 1st 3 days of fasting, and alpha amino nitrogen after 17 days. The concentration of free fatty acids, beta-hydroxybutyrate, and acetoacetate did not reach a plateau until after 17 days. Estimated glucose production at 5-6 wk of starvation is reduced to approximately 86 g/24 hr. Of this amount the liver contributes about one-half and the kidney the remainder. Approximately all of the lactate, pyruvate, glycerol, and amino acid carbons which are removed by liver and kidney are converted into glucose, as evidenced by substrate balances across these organs.

Acetoacetates↗
PubMed1974

The effect of adrenergic blockade on the glucagon responses to starvation and hypoglycemia in man.

In an attempt to ascertain whether the sympathetic nervous system modulates glucagon release in man during starvation and hypoglycemia, the influence of alpha and beta adrenergic blockade on glucagon responses was studied in young, healthy men subjected to fasting and insulin-induced hypoglycemia. Six volunteers fasted for 84 h on three separate occasions. Plasma immunoreactive glucagon (IRG), measured initially at 12 h, climbed gradually from mean levels of 54 pg/ml to a zenith of 124 pg/ml at 48 h, with maintenance of these levels for the duration of the fast. The infusion of propranolol or phentolamine throughout the terminal 24 h of the second and third fasts failed to alter the pattern of IRG release. After an overnight fast, five volunteers received insulin intravenously, which evoked a mean rise in plasma IRG levels from 63 pg/ml to a maximum of 256 pg/ml at 30 min. The concurrent administration of propranolol or phentolamine did not modify the glucagon responses to insulin-induced hypoglycemia. These data suggest that the augmented glucagon release in man during starvation or after hypoglycemia is not significantly regulated by signals from the adrenergic nervous system.

Adolescent↗
PubMed1975

Hepatic mitochondrial function in ketogenic states. Diabetes, starvation, and after growth hormone administration.

The study was designed to evaluate hepatic mitochondrial function during ketotic states. The ketogenic models studied were streptozotocin-induced diabetic ketoacidosis, 48 h of starvation, and after growth hormone administration. In the last-mentioned model we observed increased free fatty acids but not ketonemia. Oxidative phosphorylation was measured using the citric acid cycle substrates pyruvate and succinate, the amino acid glutamate, a ketone body beta-hydroxybutyrate, and a long-chain fatty acid palmitoyl-l-carnitine. State 3 (ADP stimulated) and state 4 (ADP limited) respiration, respiratory control ratio (state 3/state 4), and the ADP/O ratios were normal in the controls and the experimental groups. Uncoupled respiration produced by dinitrophenol with a variety of substrates was unchanged in the experimental groups compared to the controls. Fatty acid oxidation was studied in detail. The rate of utilization of palmitoyl-l-carnitine by controls or experimental groups did not depend on the product formed (citrate, acetoacetate). No significant changes were observed in the oxidation of palmitoyl-CoA (+ carnitine) or with an intermediate-chain fatty acid hexanoate. The specific activity of hepatic mitochondria carnitine palmitoyltransferase did not change in any of the three experimental groups. It is concluded that during diabetic ketoacidosis, starvation, and growth hormone administration, there is (a) no alteration in hepatic mitochondrial function; (b) no change in the intrinsic capacity of hepatic mitochondria to oxidize fatty acids; and (c) no change in the specific activity of mitochondrial carnitine palmitoyltransferase. The mechanism by which the body restrains flux through the mitochondrial oxidative machinery remains to be fully determined.

Acidosis↗
PubMed2001

MtnK, methylthioribose kinase, is a starvation-induced protein in Bacillus subtilis.

BACKGROUND: Methylthioadenosine, the main by-product of spermidine synthesis, is degraded in Bacillus subtilis as adenine and methylthioribose. The latter is an excellent sulfur source and the precursor of quorum-sensing signalling molecules. Nothing was known about methylthioribose recycling in this organism. RESULTS: Using trifluoromethylthioribose as a toxic analog to select for resistant mutants, we demonstrate that methylthioribose is first phosphorylated by MtnK, methylthioribose kinase, the product of gene mtnK (formerly ykrT), expressed as an operon with mtnS (formerly ykrS) in an abundant transcript with a S-box leader sequence. Although participating in methylthioribose recycling, the function of mtnS remained elusive. We also show that MtnK synthesis is boosted under starvation condition, in the following decreasing order: carbon-, sulfur- and nitrogen-starvation. We finally show that this enzyme is part of the family Pfam 01633 (choline kinases) which belongs to a large cluster of orthologs comprizing antibiotic aminoglycoside kinases and protein serine/threonine kinases. CONCLUSIONS: The first step of methylthioribose recycling is phosphorylation by MTR kinase, coded by the mtnK (formerly ykrT) gene. Analysis of the neighbourhood of mtnK demonstrates that genes located in its immediate vicinity (now named mtnUVWXYZ, formerly ykrUVWXYZ) are also required for methylthioribose recycling.

Bacillus subtilis↗
PubMed1981

Fetal and neonatal cerebral metabolism following maternal canine starvation.

Pregnant dogs were starved for 72 hr before a term delivery. Maternal (1.68 +/- 0.39 versus 0.74 +/- 0.20 mM) and fetal (0.39 +/- 0.03 versus 0.22 +/- 0.07) circulating free fatty acids and maternal (2.99 +/- 0.79 versus 1.04 +/- 0.84) and fetal (2.53 +/- 0.35 versus 1.01 +/- 0.32) ketones were elevated whereas blood glucose values remained unchanged at the time of delivery. After birth, pups born to starved mothers had significantly lower blood glucose values during 3, 6, 9, and 24 hours of neonatal fasting. Intracerebral glucose concentrations paralleled those in the blood as they were depressed at 3, 6, and 9 hours of age. Cerebral glycogen content was lower in pups born to starved mothers at 6 (2.72 +/- 0.43 versus 4.32 +/- 0.56 mumoles/g) and 24 (2.31 +/- 0.17 versus 3.48 +/- 0.39 mumoles/g) hr, whereas UDP-glucose concentrations were significantly elevated in these pups during fetal, 3, 9, and 24 hr of age. Phosphoenolpyruvate was higher after maternal starvation in the fetus and at 6 and 9 hr, whereas cerebral pyruvate concentrations were elevated at 3, 6, and 9 hr of age. The elevation of pyruvate with no alteration of lactate concentration resulted in an elevated cytoplasmic NAD/NADH ratio at 3 hr of age (1381 +/- 194 versus 792 +/- 198). Cerebral alpha-ketoglutarate and calculated oxaloacetate concentrations were elevated throughout the day after maternal starvation whereas malate concentrations were depressed at 3 and 9 hr of age. Cerebral energy charge was unaffected, whereas the calculated energy reserve was lower at 3, 6, and 24 hours. Cerebral amino acids demonstrated elevated aspartate concentrations at 3 and 6 hr. Cerebral glutamine concentrations were lower during fetal stage (7.86 +/- 0.52 versus 10.01 +/- 0.41 mumoles/g) and 3, 6, and 9 hr of life.

Adenine Nucleotides↗
PubMed1985

The effect of short-term starvation on mucosal barrier function in the newborn rabbit.

The compromised human newborn frequently presents with overwhelming feeding problems which lead to inadequate intake. These problems may affect the development of the small intestine, especially mucosal barrier function, leading to increased infections and susceptibility to allergens. To study this, an animal model was established using neonatal rabbits deprived of nutrients from birth until 72 h. Mucosal barrier function was compared in deprived and control (naturally fed 72-h-old animals) rabbits by measuring immunoreactive bovine serum albumin in serum 4 h after intragastric infusion of crystalline bovine serum albumin (200 mg/100 g body weight). Trypsin activity was measured in rinse fluid obtained from the small intestine. Representative sections of jejunum from control and experimental animals were formalin fixed and stained with hematoxylin and eosin for morphologic comparison. Following the bovine serum albumin feeding, a significantly increased serum immunoreactive bovine serum albumin and significantly decreased trypsin-like activity of the small intestinal rinse fluid was noted in starved animals compared to controls. In addition, the enterocytes of malnourished animals were more cuboidal and contained fewer and smaller supranuclear granules on microscopic examination than the enterocytes of controls. This study suggests that short-term starvation in newborns affects mucosal barrier function. Acute starvation may place newborns at increased risk for infections and allergic disease.

Acute Disease↗
PubMed1978

Antiserum to somatostatin reverses starvation-induced inhibition of growth hormone but not insulin secretion.

The role of SRIF in starvation-induced inhibition of GH and insulin secretion was assessed by passive immunization with anti-SRIF serum. Six-hour secretory profiles obtained from chronically cannulated male rats deprived of food for 72 h showed marked suppression of GH secretory bursts and significant depression of plasma insulin levels. Administration of 1 ml SRIF antiserum (SRIF AS) iv to starved rats resulted in rapid (within 15 min) restoration of high amplitude GH pulses (600-800 ng/ml) and sighificant elevation of GH trough values. The mean 6-h GH level of starved SRIF, AS-treated rats (189.2 +/- 23.9 ng/ml) was significantly higher than that of starved, normal sheep serum-treated control animals (62.8 +/- 5.8 ng/ml) (P less than 0.005). In contrast to the effects on GH, plasma insulin levels in starved rats administered SRIF AS remained low. No significant difference was observed in the mean 6-h plasma insulin level of starved-SRIF, AS-treated rats when compared to starved, normal sheep serum-treated controls. These findings suggest that circulating SRIF is a physiological regulator of starvation-induced GH suppression but is not involved in mediating the inhibition of insulin.

Animals↗
PubMed1999

Starvation: early signals, sensors, and sequelae.

To identify the sequences of changes in putative signals, reception of these and responses to starvation, we sampled fed and starved rats at 2- to 6-h intervals after removal of food 2 h before dark. Metabolites, hormones, hypothalamic neuropeptide expression, fat depots, and leptin expression were measured. At 2 h, insulin decreased, and FFA and corticosterone (B) increased; by 4 h, leptin and glucose levels decreased. Neuropeptide Y messenger RNA (mRNA) increased 6 h after food removal and thereafter. Adrenal and plasma B did not follow ACTH and were elevated throughout, with a nadir at the dark-light transition. Leptin correlated inversely with adrenal B. Fat stores decreased during the last 12 h. Leptin mRNA in perirenal and sc fat peaked during the dark period, resembling plasma leptin in fed rats. We conclude that 1) within the first 4 h, hormonal and metabolic signals relay starvation-induced information to the hypothalamus; 2) hypothalamic neuropeptide synthesis responds rapidly to the altered metabolic signals; 3) catabolic activity quickly predominates, reinforced by elevated B, not driven by ACTH, but possibly to a minor extent by leptin, and more by adrenal neural activity; and 4) leptin secretion decreases before leptin mRNA or fat depot weight, showing synthesis-independent regulation.

Adipose Tissue↗
PubMed1978

Effect of starvation on the production and peripheral metabolism of 3,3',5'-triiodothyronine in euthyroid obese subjects.

The effect of starvation on the peripheral metabolism of rT3 was evaluated in four obese euthyroid patients. During starvation, the serum rT3 concentration increased by 69% while the MCR of rT3 decreased in all four patients from control values of 96 +/- 23 (mean +/- SD) to 68 +/- 17 liters/70 kg . day, resulting in a slight increase in the mean production rate of rT3. These findings are in contrast to the marked decrease in T3 production rate associated with fasting, indicating that inner and outer ring deiodination of T4 can be varied independently.

Female↗
PubMed1980

Indomethacin and aspirin prevent the starvation-induced fall in plasma insulin.

To investigate whether prostaglandins (PGs) play a role in the regulation of insulin secretion during starvation, we have studied the effects of two inhibitors of PG synthesis, indomethacin (INDO) and acetylsalicylic acid (ASA), on plasma insulin during a 72-h fast. Five lean males and six obese females were given 200 mg INDO daily throughout a 72-h fast during which plasma glucose was maintained at normal postabsorptive levels by a continuous infusion of glucose. In addition, four obese females were treated with 3 g ASA in a similar protocol. Another six lean males and six obese females served as a control group, receiving only iv glucose during the fast. In both the lean and obese control subjects, a significant decrease in plasma insulin was noted by 72 h (lean, 53 +/- 8% of basal insulin; obese, 69 +/- 6%; P less than 0.02). By contrast, aspirin and INDO administration prevented the decline in plasma insulin in both lean (INDO, 92 +/- 5%) and obese (INDO, 109 +/- 11%; ASA, 111 +/- 17%) subjects. These data suggest that endogenous PG production may be a controlling factor in insulin secretion during starvation.

Adult↗