Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxidation in vivo of [14C]triolein to 14CO2 was significantly lower in obese (fa/fa) Zucker rats as compared with their lean (+/?) controls. In response to a 24 h starvation period, both lean and obese rats showed an enhanced rate of [14C]triolein oxidation. There were, however, no changes in the rate of intestinal absorption of [14C]triolein between the lean and obese animals. Conversely, the total tissular [14C]lipid accumulation was significantly higher in white adipose tissue, carcass and plasma in the obese animals, whereas that of brown adipose tissue was lower. This was associated with a marked hyperinsulinaemia and hypertriglyceridaemia in the fa/fa animals. Starvation dramatically decreased [14C]lipid accumulation in white adipose tissue of the lean Zucker rats, but had no effect in the obese rats. The lipogenic rate of the obese rats was significantly higher than that of lean rats in liver, white adipose tissue, skeletal muscle and carcass. Lipoprotein lipase activity (per g of tissue) was significantly lower in both white and brown adipose tissue of obese versus lean rats; however, total activity was higher in both tissues. Starvation significantly lowered perigenital-adipose-tissue lipoprotein lipase activity in the lean groups, and had no effect in the obese ones. These results demonstrate that the tissue capacity of exogenous lipid uptake is involved, but cannot be the only factor influencing the maintenance of obesity in these animals. Thus, in the adult fa/fa rat, the large increase in obesity is not solely dependent on a deviation of energy-producing substrate metabolism towards the storage of lipids in white fat. Other factors, such as a low rate of oxidation, a high lipogenic rate and decreased brown-adipose-tissue activity are involved in the perseverance of the obesity syndrome.
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PMID:Lipid metabolism in the obese Zucker rat. Disposal of an oral [14C]triolein load and lipoprotein lipase activity. 201 94

Female rats were mated and thyroidectomized on the same day. Some animals were kept without treatment and killed on day 12 or 21 of gestation (T). Others were subsequently treated daily with 1.8 micrograms L-T4/100 g BW for either the first 12 days and then not treated from that time until day 21 [T+T4(I+0)] or else not treated for the first 12 days and then treated from days 12-21 [T+T4(0+II)]. A final group received treatment during the entire 21-day study [T+T4(I+II)] and was used as the control. The net maternal body weight increased until day 12 of gestation in T+T4(I+II) rats, but not in T animals. On day 21 net maternal body weight was significantly lower in T and T+T4(0+II) than in T+T4(I+II) rats. Lipoprotein lipase activity in the lumbar fat pads increased from days 0 to 12 of gestation and decreased on day 21, whereas in the heart the change was in the opposite direction, and these changes were greater in T+T4(I+II) rats than in T rats. Incorporation of [U-14C]glucose administered in vivo into liver [14C]fatty acids or [14C]glycogen was significantly lower in T rats than in T+T4(I+II) on either the 12th or 21st day of gestation. The response of plasma triglyceride, glycerol, or beta-hydroxybutyrate levels to 24 h of starvation was similar in 12-day pregnant rats regardless of whether they were treated with T4, whereas on day 21 the change was greater in T+T4(I+II) or T+T4(I+0) animals than in T or T+T4(0+II) animals. Results show that maternal hypothyroidism during the first half of gestation impaired the anabolic events occurring during this phase and compromised the normal catabolic response during late gestation even when T4 treatment was restored. However, once maternal metabolic stores were built up normally during the first half of gestation, maternal hypothyroidism during late gestation did not affect the mother's normal metabolic adaptation, including the accelerated response to starvation.
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PMID:Maternal hypothyroidism during the first half of gestation compromises normal catabolic adaptations of late gestation in the rat. 205 83

Technological advances in the intensive care of low birth weight (LBW) infants have resulted in major increases in their survival. New challenges in meeting their nutritional needs have emerged. Very low birth (VLBW) weight infants have very little body fat or glycogen reserves at birth, making them susceptible to starvation. If fed enterally, they require at least 120 calories/kg per day for growth. Numerous immaturities in the gastrointestinal tract and liver limit protein digestion, absorption, and metabolism. Several amino acids not considered essential to the older child or adult are essential to the VLBW infant. Supplying a high protein load with an inappropriate amino acid composition may lead to metabolic imbalances. The digestion and absorption of fats differs from the older child or adult. Lingual and gastric lipases are important, and the lack of bile acids limits fat absorption. Lipoprotein lipase deficiency causes problems when too much fat or fat of incorrect composition is provided. There are controversies regarding the most appropriate carbohydrate source, but research shows that lactose remains an important carbohydrate source for most of these infants. Calcium, magnesium, and phosphorus requirements pose questions in both enterally and parenterally nourished infants. Studies of iron usage suggest that VLBW infants fed either human milk or formula should receive iron supplements. Vitamin E may be helpful in preventing oxygen toxicity. Vitamin D deficiency contributes to bone demineralization and rickets. Controversy exists regarding the correlation between vitamin A nutrition and development of chronic lung disease. Guidelines have been developed for recommended intakes, but much needs to be learned to provide a sound scientific basis upon which to provide optimal nourishment for the high risk, LBW infant.
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PMID:Scientifically-based strategies for nutrition of the high-risk low birth weight infant. 212 45

To determine to what extent lipoprotein lipase activity in the liver of the newborn rat depends on milk ingestion, its changes were studied during different nutritional conditions. Newborns were placed with nurse rats with or without ligated nipples and they were killed at 0,8 or 24 h of life. Lipoprotein lipase in newborns liver was characterized by its inhibition in the presence of 1.0 M NaCl, its specific elution at 1.5 M NaCl on heparin-Sepharose 4B column and its requirement for serum in the assay mixture to manifest its activity. In fed animals lipoprotein lipase activity and triacylglycerol content in liver as well as circulating triacylglycerols and ketone bodies increased progressively after birth. When newborns were kept starved the change in enzyme activity was significantly enhanced, whereas the increase found after birth in the other parameters disappeared. Starvation produced reduction in circulating RIA-insulin levels in the newborn rats. Results show that liver lipoprotein lipase activity in the newborn rat is controlled by a mechanism which resembles that of the enzyme in the adult heart and indicate that its presence facilitates the uptake by the liver of fatty acids from circulating triacylglycerols for their oxidation rather than deposit.
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PMID:Starvation enhances lipoprotein lipase activity in the liver of the newborn rat. 388 51

1. The effects of dietary modification, including starvation, and of corticotropin injection on the activities of acyl-CoA synthetase, glycerol phosphate acyltransferase, dihydroxyacetone phosphate acyltransferase, phosphatidate phosphohydrolase, diacylglycerol acyltransferase and lipoprotein lipase were measured in adipose tissue. 2. Lipoprotein lipase activities in heart were increased and those in adipose tissue were decreased when rats were fed on diets enriched with corn oil or beef tallow rather than with sucrose or starch. The lipoprotein lipase activity was lower in the adipose tissue of rats fed on the sucrose rather than on the starch diet. 3. Rats fed on the beef tallow diet had slightly higher activities of the total glycerol phosphate acyltransferase in adipose tissue than did rats fed on the sucrose or starch diet. The diacylglycerol acyltransferase and the mitochondrial glycerol phosphate acyltransferase activities were higher for the rats fed on the tallow diet than for those fed on the corn-oil diet. 4. Starvation significantly decreased the activities of lipoprotein lipase (after 24 and 48 h), acyl-CoA synthetase (after 24 h) and of the mitochondrial glycerol phosphate acyltransferase and the N-ethylmaleimide-insensitive dihydroxyacetone phosphate acyltransferase (after 48 h) in adipose tissue. The activities of the microsomal glycerol phosphate acyltransferase, diacylglycerol acyltransferase and the soluble phosphatidate phosphohydrolase were not significantly changed after 24 or 48 h of starvation. 5. The activities of lipoprotein lipase and phosphatidate phosphohydrolase in adipose tissue were decreased 15 min after corticotropin was injected into rats during November to December. No statistically significant differences were found when these experiments were performed during March to September. These differences may be related to the seasonal variation in acute lipolytic responses. 6. These results are discussed in relation to the control of triacylglycerol synthesis and lipoprotein metabolism.
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PMID:The activities of lipoprotein lipase and of enzymes involved in triacylglycerol synthesis in rat adipose tissue. Effects of starvation, dietary modification and of corticotropin injection. 628 Jun 82

Lipoprotein lipase (LPL) activities of skeletal muscles, heart and adipose tissue were investigated during feeding, prolonged food restriction, and refeeding. The influence of the duration of starvation on adipose tissue LPL activity was to cause it to decrease throughout starvation, whereas heart LPL activity increased during the first 24 hours of fasting and then declined for the remainder of the fast. Starvation of 10-week-old female, lean and obese rats to 80% of initial body weight required 5 and 9 days, respectively. In fed controls, no differences between phenotypes were found for any tissue in the LPL activities expressed per gram tissue. However, obese rats exhibited significantly smaller muscle mass and a resulting 29% lower total skeletal muscle LPL activity. No phenotype differences were detected for tissue LPL activities during starvation or refeeding. During caloric restriction, the LPL activities were reduced in heart (-18%) and adipose (-52%) tissues, but skeletal muscle was unchanged except for the slow-twitch, oxidative soleus muscle, which was increased approximately two-fold. After refeeding to initial body weight, the LPL activity of heart returned to normal, but adipose tissue was dramatically increased (+300%) for both lean and obese Zucker rats. These data suggest that reduced skeletal muscle mass with normal LPL activity per gram tissue may contribute to an increased availability of plasma triglyceride fatty acids to adipose tissue of the genetically obese rat.
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PMID:The influence of starvation and refeeding on the lipoprotein lipase activity of skeletal muscle and adipose tissue of lean and obese Zucker rats. 685 9

Lipoprotein lipase (EC 3.1.1.34) extracted from adipose tissue of glucose-fed rats with 5 mM-sodium barbital, pH 7.5, containing 20% (v/v) glycerol and 0.1% (v/v) Triton X-100, was partially purified by affinity chromatography on heparin linked to Sepharose 4B. Sodium dodecyl sulphate/polyacrylamide-gel electrophoresis of the partially purified enzyme preparation revealed the presence of two major Coomassie-staining bands (mol.wts. 62 000 and 56 000) as well as a number of minor bands. Treatment of partially purified enzyme with [1,3-3H]di-isopropyl fluorophosphate resulted in the incorporation of radiolabel into the band of mol.wt. 56 000, but not into the band of mol.wt. 62 000. Both the amount of the 56 000-mol.wt. polypeptide and the incorporation of [1,3-3H]di-isopropyl fluorophosphate into this band were greatly reduced in the enzyme preparations isolated from adipose tissue of 48 h-starved rats. whereas the amount of the 62 000-mol.wt. polypeptide was unaffected by starvation. Purification of lipoprotein lipase from adipose tissue of glucose-fed rats was also carried out using affinity chromatography on Sepharose 4B linked to heparin with low affinity for antithrombin-III. This procedure resulted in the presence of a single band of mol.wt. 56 000 on sodium dodecyl sulphate/polyacrylamide-gel electrophoresis. These results suggest that the polypeptide of mol.wt. 56 000 corresponds to the subunit of lipoprotein lipase, whereas the 62 000-mol.wt. polypeptide probably represents antithrombin-III.
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PMID:Purification and characterization of rat adipose tissue lipoprotein lipase. 716 5

Lipoprotein lipase (LPL) activities in parametrial and interscapular adipose tissue, soleus and adductor longus muscles and hearts of female rats were measured during progressive starvation, chow re-feeding after 24 h starvation and throughout dark and light phases in rats permitted unrestricted access to chow. Adipose-tissue LPL activities declined by 50% after 6 h starvation and continued to fall as the starvation period was extended to 24 h. Skeletal-muscle LPL activities dramatically increased between 9 and 12 h of starvation. Cardiac LPL activities increased 2.5-fold within 6 h of starvation, reaching a maximum after 12 h of starvation. Adipose-tissue LPL activities increased rapidly within 2 h of re-feeding chow ad libitum after 24 h starvation, achieving 'fed ad libitum' values after 6 h. Oxidative-skeletal-muscle LPL activities also increased after 2 h of refeeding and exceeded 'fed ad libitum' values throughout the 6 h re-feeding period. Cardiac LPL activities remained up-regulated for the 6 h of re-feeding. Adipose-tissue LPL activities exceeded those of cardiac or skeletal muscle throughout both light and dark phases. The lowest adipose-tissue LPL activities were observed at 9 h into the light phase. In contrast, cardiac LPL activity declined throughout the dark phase, with a minimum at 9 h into the dark phase. No such variation was observed for skeletal-muscle LPL activities. A diurnal nadir in plasma triacylglycerol (TG) concentrations coincided with the peak in cardiac LPL activities. The results demonstrate that, during unrestricted feeding and re-feeding after prolonged starvation, changes in skeletal-muscle and adipose-tissue LPL activities are neither reciprocal nor co-ordinate. Regulation of cardiac LPL activity during the diurnal cycle may be an important aspect of both of cardiac fuel selection and whole-body TG metabolism.
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PMID:Changes in lipoprotein lipase activities in adipose tissue, heart and skeletal muscle during continuous or interrupted feeding. 850 37

Since during pregnancy the mother switches from an anabolic to a catabolic condition, the present study was addressed to determine the effect of 48 h food deprivation on days 7, 14 and 20 of pregnancy in the rat as compared to age matched virgin controls. Body weight, free of conceptus, decreased with food deprivation more in pregnant than in virgin rats, with fetal weight (day 20) also diminishing with maternal starvation. The decline of plasma glucose with food deprivation was greatest in 20 day pregnant rats. Insulin was highest in fed 14 day pregnant rats, and declined with food deprivation in all the groups, the effect being not significant in 7-day pregnant rats. Food deprivation increased plasma glycerol only in virgin and 20 day pregnant rats. Plasma NEFA and 3-hydroxybutyrate increased with food deprivation in all groups, the effect being highest in 20 day pregnant rats. Food deprivation decreased plasma triacylglycerols in 14 day pregnant rats but increased in 20 day pregnant rats. In 20-day fetuses, plasma levels of glucose, NEFA and triacylglycerols were lower than in their mothers when fed, and food deprivation caused a further decline in plasma glucose, whereas both NEFA and 3-hydroxybutyrate increased. Liver triacylglycerols concentration did not differ among the groups when fed, whereas food deprivation caused an increase in all pregnant rats and fetuses, the effect being highest in 20-day pregnant rats. Lipoprotein lipase (LPL) activity in adipose tissue was lower in 20 day pregnant rats than in any of the other groups when fed, and it decreased in all the groups with food deprivation, whereas in liver it was very low in all groups when fed and increased with food deprivation only in 20 day pregnant rats. A significant increase in liver LPL was found with food deprivation in 20 day fetuses, reaching higher values than their mothers. Thus, the response to food deprivation varies with the time of pregnancy, being lowest at mid pregnancy and greatest at late pregnancy, and although fetuses respond in the same direction as their mothers, they show a specific response in liver LPL activity.
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PMID:Differential metabolic response to 48 h food deprivation at different periods of pregnancy in the rat. 1243 82