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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Carrier-mediated beta-D-hydroxybutyrate transport in brush-border membrane (maternal-sided) vesicles prepared from trophoblast rat placenta was studied. The existence of a carrier-mediated transport system for beta-D-hydroxybutyrate in brush-border membrane vesicles was substantiated by the strong inhibitory effect of the protein modifier p-chloromercuriphenyl sulfonic acid and by the saturability of beta-D-hydroxybutyrate uptake as a function of beta-D-hydroxybutyrate concentration. beta-D-hydroxybutyrate uptake was stimulated by the presence of an inward-directed proton gradient but not by an inward-directed Na+ gradient. The mechanism for transport of beta-D-hydroxybutyrate seems to be a beta-D-hydroxybutyrate/H+ symport and not a beta-D-hydroxybutyrate/OH- antiport because beta-D-hydroxybutyrate transport was not sensitive to 4,4-diisothiocyano-2,2'-stilbenedisulfonic acid or furosemide. The Km, Vmax, and kd calculated by applying the iteration procedure to the data were 16 mM, 58 nmol.mg-1.10 s-1, and 0 nL.mg-1.s-1, respectively. The beta-D-hydroxybutyrate transport system might be shared by other monocarboxylic acids, and the carrier shows reversibility and exchange properties. There were no significant changes in the kinetic parameters of the beta-D-hydroxybutyrate transport system during the last 3 d of gestation. Nevertheless, there was a significant increase in the capacity of the beta-D-hydroxybutyrate transport system in brush-border membrane vesicles prepared from fasted pregnant rats, suggesting that the rise in maternal ketone body levels occurring as a consequence of maternal starvation is concurrent with the stimulation of the activity of the beta-D-hydroxybutyrate placental carrier to supply the fetus with ketone bodies.(ABSTRACT TRUNCATED AT 250 WORDS)
Pediatr Res 1992 Sep
PMID:Carrier-mediated beta-D-hydroxybutyrate transport in brush-border membrane vesicles from rat placenta. 140 69

Undernutrition may exacerbate hyperoxia-induced lung injury, a finding that may be of significance in the early clinical management of the premature human infant. Addressing this specific problem, we found that 72 h of food restriction in guinea pig pups delivered 3 days preterm increased mortality rates among pups exposed to 95% oxygen (8/18) and yet had no effect on 21% oxygen (air)-exposed pups (0/10). Reduced tolerance of hyperoxic conditions was not, however, associated with increased lung injury, assessed as pulmonary microvascular leakage. Pulmonary antioxidant enzyme activities [Cu,Zn superoxide dismutase (SOD), Mn SOD, glutathione peroxidase, and catalase] were unaltered by starvation or hyperoxia. Lung glutathione concentration was slightly decreased after food restriction, whereas hyperoxic exposure did not change either lung or bronchoalveolar lavage fluid glutathione concentrations or lung antioxidant enzyme activities. Increased susceptibility to the lethal effects of oxygen in the starved preterm guinea pig pup could not be attributed to a deficiency of pulmonary antioxidant defenses.
Am J Physiol 1992 Sep
PMID:Effect of food restriction on hyperoxia-induced lung injury in preterm guinea pig. 141 61

Metabolic acidosis immediately after surgical operation is followed by metabolic alkalosis. Hormonal change by surgical stress and anaerobic glucolysis due to tissue ischemia cause initial lactic acidosis. Later alkalosis may be caused by secondary aldosteronism and bicarbonate production from lactate and citrate supplied by massive infusion and transfusion. Postoperative complications, such as respiratory insufficiency, renal failure and hypovolemic or septic shock, cause acidosis. In the gastrointestinal surgery, acidosis can be caused by starvation and loss of bicarbonate contained in bile, pancreatic juice or intestinal fluid, and alkalosis can be caused by loss of HCl in gastric juice. Severe acidosis can be caused by extracorporeal circulation, hypothermia, low output syndrome or declamping shock in cardioaortic surgery.
Nihon Rinsho 1992 Sep
PMID:[Acid-base disturbances in surgical operation]. 143 18

Effects of starvation on thyroid function were studied in 5- to 6-week-old (R x U) F1 rats. Starvation lowered plasma TSH in female, but not in male rats. Plasma T4 and T3 levels decreased, whereas the dialysable T4 fraction increased during starvation. Free T4 (FT4) levels decreased rapidly in females, but only after prolonged fasting in male rats. Glucose decreased, and free fatty acid levels increased during starvation. Peripheral TRH levels did not change during food deprivation. Since effects of starvation were most apparent in young female rats, such rats were used to study hypothalamic TRH release during starvation and subsequent refeeding. Basal in vitro hypothalamic TRH secretion was less in starved rats than in control or refed animals. In vitro hypothalamic TRH release in medium with 56 mM KCl increased 3-fold compared to basal release, and in these depolarization conditions TRH release was similar between hypothalami from control, starved and refed rats. In rats starved for 2 days, TRH level in hypophysial portal blood was lower than that of controls. Thus, diminished thyroid function during starvation may at least in part be caused by a reduced hypothalamic TRH release.
Neuroendocrinology 1992 Sep
PMID:Effect of starvation and subsequent refeeding on thyroid function and release of hypothalamic thyrotropin-releasing hormone. 143 73

In order to delineate the roles of lignin and manganese peroxidases in the degradation of polycyclic aromatic hydrocarbons by Phanerochaete chrysosporium, the biodegradation of phenanthrene (chosen as a model for polycyclic aromatic hydrocarbons) was investigated. The disappearance of phenanthrene from the extracellular medium and mycelia was determined by using gas chromatography. The disappearance of phenanthrene from cultures of wild-type strains BKM-F1767 (ATCC 24725) and ME446 (ATCC 34541) under ligninolytic (low-nitrogen) as well as nonligninolytic (high-nitrogen) conditions was observed. The study was extended to two homokaryotic (basidiospore-derived) isolates of strain ME446. Both homokaryotic isolates, ME446-B19 (which produces lignin and manganese peroxidases only in low-nitrogen medium) and ME446-B5 (which totally lacks lignin and manganese peroxidase activities), caused the disappearance of phenanthrene when grown in low- as well as high-nitrogen media. Moreover, lignin and manganese peroxidase activities were not detected in any of the cultures incubated in the presence of phenanthrene. Additionally, the mineralization of phenanthrene was observed even under nonligninolytic conditions. The results collectively indicate that lignin and manganese peroxidases are not essential for the degradation of phenanthrene by P. chrysosporium. The observation that phenanthrene degradation occurs under nonligninolytic conditions suggests that the potential of P. chrysosporium for degradation of certain environmental pollutants is not limited to nutrient starvation conditions.
Appl Environ Microbiol 1992 Sep
PMID:Degradation of phenanthrene by Phanerochaete chrysosporium occurs under ligninolytic as well as nonligninolytic conditions. 144 13

We have studied the changes in concentration of glycogen, glucose and the bisphosphorylated sugars, glucose 1,6-P2 and fructose 2,6-P2, in several rat brain regions during 72 h of starvation. The animals were killed by focused microwave irradiation. The activities of glycogen metabolizing enzymes in the different areas were measured. A large decrease in glycogen and glucose concentration was observed in all areas. The concentrations of bisphosphorylated sugars changed, suggesting that an increase in glycolysis could take place at the beginning of starvation, with blood glucose as a major energy source. Differences in metabolite concentration before starvation disappeared after 72 h. The activities of glycogen synthase, glycogen phosphorylase and glycogen phosphorylase kinase were similar in all areas, and they did not change during starvation.
Brain Res 1992 Sep 25
PMID:Effect of starvation on glycogen and glucose metabolism in different areas of the rat brain. 144 41

Obesity is characterized by a high risk for glucose intolerance and cardiovascular disease. Since magnesium deficiency or depletion have often been associated with both pathologies, is of interest to study magnesium status in severely obese subjects before any form of treatment. Negative magnesium balances have been described in overweight persons submitted to total starvation, hypocaloric diets, and obesity surgery. For this reason 80 non-diabetic obese men and 118 age-matched obese women were studied. Serum and erythrocyte magnesium concentrations were significantly higher in the male population but the mean values were not suggestive of a magnesium deficit before any form of treatment was started. Since metabolic abnormalities and cardiovascular risk are greater in patients with upper body fat distribution (UBFD) both sexes were subdivided according to "waist-to-hip" circumference ratio. No difference could be shown in the obese men but in women, UBFD subjects showed higher basal insulin levels and increased erythrocyte magnesium concentration as compared to those with classical gynoid fat distribution. A 75 g oral glucose tolerance test enabled the subjects to be subdivided into those with normal or impaired glucose tolerance (IGT). The IGT group in both sexes was older and more obese. Mean values of serum magnesium and erythrocyte magnesium were not decreased despite the more pronounced insulin resistance in the IGT group. However a significant negative correlation was found between fasting blood sugar/insulinaemia and erythrocyte magnesium, showing that this middle-aged obese population can maintain normal circulating levels of magnesium, in contrast to type II diabetics or older subjects where for other reasons (urinary losses or decreased intake) magnesium status is interfered with.
Magnes Res 1992 Sep
PMID:Magnesium and obesity: influence of gender, glucose tolerance, and body fat distribution on circulating magnesium concentrations. 146 56

Homicide by starvation is a very rare occurrence, especially when the victim is ambulant. This paper presents a case where the death of the individual went undiscovered for more than 3 weeks. A successful conviction for murder ensued. The paper also discusses social and pathological problems associated with this crime.
Am J Forensic Med Pathol 1992 Sep
PMID:Homicide by starvation. 147 37

Zinc deficiency, whether a result of an acquired or inherited abnormality of zinc metabolism, is associated with characteristic cutaneous findings. The inherited variety is known as acrodermatitis enteropathica. We present a case of zinc deficiency secondary to starvation induced by anorexia nervosa. Since the cutaneous stigmata of zinc deficiency and anorexia nervosa can initially be subtle and occasionally overlap, we believe that screening zinc levels in patients with anorexia nervosa with prominent cutaneous findings should be considered.
Pediatr Dermatol 1992 Sep
PMID:Acquired zinc deficiency in association with anorexia nervosa: case report and review of the literature. 148 78

The spontaneous reversion to His+ of the Salmonella typhimurium alleles hisD3052 and hisG46 was investigated. In fluctuation tests, the expected "jackpot" distribution of His+ revertants was not observed. The experimental distributions were close to Poisson distribution. The redistribution test showed no significant differences in the His+ colony counts between spread and unspread plates. An attempt at indirect selection of His+ revertants in fluid medium failed. It was also shown that the mean number of His+ reversion events and the mean number of revertants per plate were similar. At the same time, kanamycin-resistant mutants had jackpot distribution. Selection for His+ revertants (histidine starvation) did not increase mutation to Kanr.
Res Microbiol 1992 Sep
PMID:The origin of His+ revertants of Salmonella typhimurium obtained on selective medium. 148 55


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