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Vendor differences in starvation-induced gastric ulceration.

The incidence of starvation-induced gastric lesions was observed in Sprague-Dawley rats obtained from four different vendors (ARS/Sprague-Dawley, Hilltop, Holtzman, and Charles River). Food was withheld for 5 days from rats weighing 150, 200, 260 or 330 g. Glandular lesions occurred in 150 g rats; rumenal lesions occurred in 200+ rats. ARS/Sprague-Dawley rats developed more glandular lesions, whereas Hilltop rats developed more rumenal lesions.

Animals↗

Starvation and respiratory rhythmic behavior in groups of light-dark synchronized Sprague-Dawley rats.

Twenty adult male SPF Sprague-Dawley rats, grouped by 5 and synchronized by a light (L)-dark (D) 12:12 alternation, were deprived of food and water for 7 days; 20 other rats were taken as controls. Continuous measurement of emitted carbon dioxide (VCO2), which was taken as an index of respiratory and metabolic exchanges, shows that starvation significantly (p less than 0.001) decreases the amplitudes of the circadian VCO2 rhythms (by 42.5% during L and 35.6% during D) and also the L----D photic VCO2 responses (by 9.2%; p less than 0.05). Concerning ultradian rhythms of mean and great periods (40 min less than tau less than 24 hr), food and water suppression diminishes their amplitudes (by 58.4% in L and 32.4% in D) and changes their phases (by a 1.29 radian advance in L and a 0.68 radian delay in D). Rats recovered their prestarvation circadian and ultradian VCO2 rhythms 6-7 days after food and water had been given back to them.

Activity Cycles↗

Effect of starvation on endocrine cells in the rat stomach.

The influence of food deprivation on gastric G- and D-cells and on parietal cells was studied in the rat. In fed controls and groups of rats fasted for 12 and 96 h G-, D- and parietal cell densities, somatostatin and gastrin concentration in antral and fundic specimens and serum gastrin were compared. Gastrin in antral mucosa, serum gastrin, G-cell density as well as antral D-cell density decreased in long-term fasted rats by 52%, 90%, 58% and 42%, respectively. Fundic D-cell density remained unchanged. After 96 h starvation somatostatin concentration slightly increased in antral mucosa (+35%; P less than 0.05), but decreased in fundic mucosa (-40%; P less than 0.05). Parietal cell density was not influenced by prolonged fasting. These findings demonstrate that changes in D-cell morphology and mucosal somatostatin content are not parallel and that the rat gastric D-cell is less dependent on food in the gastric lumen than the G-cell. The unaltered fundic D-cell density reflects the functional activity of gastric D-cell which has also been shown to be independent of the presence or absence of food.

Animals↗

Effect of starvation and diabetes on the activity of the eukaryotic initiation factor eIF-2 in rat skeletal muscle.

The ability of the initiation factor eIF-2 in skeletal muscle extracts to form ternary initiation complexes ([Met-tRNA(f).eIF-2.GDP]) is decreased by either starvation or diabetes. These conditions also impair the ability of muscle extracts to dissociate [eIF-2.GDP], suggesting inhibition of the guanine nucleotide exchange reaction essential for eIF-2 recycling. We could not, however, detect any change in the phosphorylation state of the alpha subunit of eIF-2. This suggests that eIF-2 activity may be regulated in this system by a mechanism not involving its phosphorylation.

Animals↗

On the energy fuel in voles during their starvation.

Starved voles derive energy predominantly from endogenous carbohydrates, unlike small laboratorial rodents which use free fatty acids as fuel during their fasting. This seems the reason why deep hypoglycemia is developed in fasting voles. The rate of gluconeogenesis in starved voles is rather high while oxidation of carbohydrates in that state is more rapid than their formation. Utilization of fat in fasted voles is relatively small. Voles can die after starvation still having a lot of fats in their bodies. Oxygen consumption in starved voles decreases to a small extent.

Animals↗

Weight loss and catabolic adaptations to starvation in grey seal pups.

Five grey seal pups lost from 18 to 32% of their initial body weight during a 21 day starvation period. Blubber fat mass density was 0.93 +/- 0.03 g/cm3. A considerable loss of blubber fat was recorded, but analysis of the weight loss and body size data indicated that blubber fat was retained for thermoregulatory reasons, particularly in the lean, smaller seals. It is possible that phocid seals during periods of negative energy balance have a higher rate of protein catabolism than normal for terrestrial mammals.

Adaptation, Physiological↗

Serum cortisol, glucose and lipids in plaice (Pleuronectes platessa L.) exposed to starvation and aquarium stress.

Plaice were maintained in the aquarium (11-12 degrees C) during May for 15 days without feeding. Within 48 hr, there was a decline in serum total lipids (P less than 0.001), phospholipids (P less than 0.01), triglycerides (P less than 0.001), cortisol (P less than 0.01) and glucose (P less than 0.001), but an increase in nonesterified fatty acids (NEFA; P less than 0.01). There was a significant inverse correlation between NEFA and glucose over 15 days (P less than 0.001) and between NEFA and cortisol over the first 5 days (P less than 0.01). Cortisol and glucose showed a significant correlation over 15 days (P less than 0.01). Serum cortisol and glucose were not apparently affected by starvation. Only cortisol provided a sensitive indicator of aquarium disturbance. Exposure of the fish to agitation or reduced O2 for 1 hr significantly elevated cortisol (P less than 0.001) but only the latter treatment elevated glucose (P less than 0.01); neither treatment affected the lipids.

Animals↗

Suppression of Ehrlich ascites tumor growth in mice by starvation and streptozotocin-induced diabetes.

Starvation-induced hypoglycaemia and streptozotocin-induced diabetes suppressed the growth of Ehrlich ascites tumor in mice. The suppression of tumor growth by diabetes was alleviated by administration of insulin. The number of glucose carriers on tumour cells was found to be reduced in diabetes and partial resumption of glucose carriers was observed in tumour cells of diabetes after insulin administration. Insulin had no direct effect on tumour growth in vivo and did not affect the number of glucose carriers on tumour cells in vitro. The physiological significance of these observations is discussed.

Animals↗

Acute starvation decreases acetylcholinesterase activity in different regions of rat brain.

The activity of acetylcholinesterase (AChE) was assayed spectrophotometrically in four brain regions of rats that had been deprived of food for 96 h. A significant decrease in the total AChE activity (by 4-45%) as well as in its specific activity (by 14-28%) was observed in the supernatant and total particulate fractions from cerebral hemispheres, cerebellum, brainstem and diencephalon + basal ganglia. Similarly, blood glucose, body weight and protein content of subcellular fractions from most brain regions showed decreases after starvation.

Acetylcholinesterase↗

Effect of starvation and a protein diet on the amino acid metabolism enzyme activities of the organs of domestic fowl hatchlings.

The activities of alanine and aspartate transaminases, adenylate deaminase, glutamine synthetase and glutamate and xanthine dehydrogenases have been measured in liver, yolk sac membrane, intestine and breast and leg muscle of domestic fowl hatchlings receiving for 3 or 5 days either a standard diet or hard boiled eggwhite as well as in 3 or 5 days starved animals. The patterns of activation of amino acid metabolism enzymes were fully comparable in protein-fed and starved groups with respect to fed controls; the differences with respect to the latter became more marked in 5- than in 3-days old chicks. In 5-days old chicks intestine alanine transaminase activity increased in parallel to that of liver in protein-fed animals but not in those starved, in agreement with an enhanced alanine transfer between both organs under this situation. Both, starvation and protein-feeding, induced a general decrease in the amino acid metabolizing ability of muscle. Glutamine (but not alanine) synthetizing capabilities were enhanced.

AMP Deaminase↗

Glucose dehydrogenase, glucose-6-phosphate dehydrogenase and hexokinase in liver of rainbow trout (Salmo gairdneri). Effects of starvation and temperature variations.

1. Activities of trout liver glucose dehydrogenase (GDH, EC 1.1.1.47) and glucose-6-phosphate dehydrogenase (G6PD, EC 1.1.1.49) were increased after a sudden drop in water temperature, but not in long-time cold acclimated as compared with warm acclimated trout. 2. Possibly, the activities of GDH and G6PD were temporarily increased in connection with metabolic adaptation to the lower temperature. 3. The activities of GDH and G6PD were not changed by the stress of handling. 4. Partially purified trout liver GDH has a lower activation energy with glucose than with glucose-6-phosphate as substrate, and the Km (glucose) decreases with decreasing assay temperature. 5. At low temperatures, the activity of trout liver GDH with glucose as substrate may be comparable to that of glucose-6-phosphate. 6. Partially purified beef liver GDH has a high activation energy with glucose as substrate, and the Km (glucose) does not change with the assay temperature. 7. Hexokinase (HK, EC 2.7.1.1) and GDH activities were unchanged when trout were deprived of food for 4 weeks. Apparently, the trout liver glucose utilization did not adapt to the starvation.

Acclimatization↗

Energy metabolism in the brain, adaptation towards starvation.

It is hypothesized that the brain's incapacity to utilize energy sources other than glucose and ketone bodies, constitutes a mechanism of protecting it from self degradation, at the expense of the rest of the body, during periods of starvation. This protection is based upon the brain's inability to catabolize substances of which it is built, for energy production.

Adaptation, Physiological↗

Mobilization of stored hexachlorobenzene and p,p-dichlorodiphenyldichloroethylene during partial starvation in rats.

Hexachlorobenzene (HCB) and p,p'-dichlorodiphenyldichloroethylene (p,p'-DDE) kinetics were compared in rats before, during and after partial starvation. Food restriction produced a drastic mobilization of the residues stored in the adipose tissue resulting in symptoms of neurotoxicity. The redistribution was reversible and did not produce a significant reduction in the chemicals body burden. HCB and p,p'-DDE, although both highly lipophilic, showed important differences in their blood transport and distribution pattern, with more HCB being transported by red blood cells and with a greater facility for HCB to reach the liver and the brain.

Adipose Tissue↗

Depletion of brain serotonin does not alter 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced starvation syndrome in the rat.

We have previously reported a series of biological events in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-intoxicated rats which resulted in elevated brain serotonin (5-HT) levels, offering a possible explanation of the acute toxicity (reduced feed intake and death) in these animals. It was thus hypothesized that depletion of central 5-HT stores should alter the TCDD-induced starvation syndrome. Brain 5-HT was selectively depleted by intracerebroventricular infusions of the neurotoxin 5,7-dihydroxytrytamine (5,7-DHT). Subsequently the animals were given a lethal dose of TCDD. In rats treated with 5,7-DHT hypothalamic 5-HT was depleted up to 90% compared to control animals, yet TCDD induced the expected reduction of bodyweight and feed intake. These results suggest that although TCDD increases central 5-HT levels as a result of increased plasma tryptophan, this may not be the main cause for reduced feed intake and lethality in these animals.

5,7-Dihydroxytryptamine↗

Effect of age, starvation and circadian rhythm on the ascorbic acid content and succinic dehydrogenase activity of the kidney of male garden lizard, Calotes versicolor.

Both ascorbic acid content and SDH activity of kidney reached peak levels during sexual maturity and then declined. Starvation stress (21 days) induced low levels of ascorbic acid content and SDH activity of the kidney. Nocturnal levels of ascorbic acid content and SDH activity were significantly lower than the diurnal values.

Age Factors↗

Nutritional deficiency, starvation, and tissue antioxidant status.

Tissue antioxidant status may be compromised under conditions of dietary restriction, either as the result of a deficiency in a specific cofactor required by a particular antioxidant enzyme or of more complex alterations of a generalized nature triggered by metabolic responses to starvation. Many similarities exist between insulin-reversible abnormalities in tissue antioxidant enzyme activities seen in experimental diabetes and in animals subjected to food deprivation-induced weight loss which is associated with hypoinsulinemia. The complex alterations in tissue antioxidant enzyme activities resulting from nutritional deficiency states, disease or drug administration may have important clinical consequences. Free radical-related processes have been implicated in the pathology of certain conditions in which weight loss is frequently recommended (e.g., diabetes and atherosclerosis). It will be important to investigate the possible adverse effects of this intervention on the underlying disease process involved. Glutathione-dependent hepatic detoxification processes are impaired under conditions of nutritional deficiency. This finding not only has important clinical implications but the standard practice of fasting small laboratory animals overnight to ensure reliable drug absorption can markedly influence the results of pharmacological/toxicological experiments. Further studies of the influence of nutritional status on free radical-related processes are likely to yield valuable information which may be applicable to a variety of research and clinical problems.

Animals↗

Starvation-sensitive UCP 3 protein expression in thymus and spleen mitochondria.

To date, UCP 3 has only been associated with skeletal muscle and brown adipose tissue (BAT). Using RT-PCR/PCR methodology, we show that human spleen and human thymus contain UCP 3. In addition, using peptide antibodies, previously demonstrated to be selective for UCP 3, we show that UCP 3 protein is present in mitochondria isolated from rat thymus and mitochondria isolated from reticulocytes, monocytes and lymphocytes of rat spleen. UCP 3 protein expression is also starvation-sensitive. UCP 3 abundance is augmented in mitochondria isolated from thymus and mitochondria isolated from lymphocytes of the spleen from fasted rats when compared to fed controls. The results are consistent with a role for UCP 3 in developing lymphocytes, thymus atrophy and fatty acid utilisation in spleen and thymus.

Animals↗