Gene/Protein Disease Symptom Drug Enzyme Compound
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1. Rates of total protein turnover, synthesis and breakdown were measured in five children before and after recovery from severe protein-energy malnutrition and while receiving 0.6 g of protein and 397 kJ day-1 kg-1. 2. Thes rates were calculated after giving doses of [15N]glycine every 2 h along with the feeds and measuring the rate of excretion of [15N]urea in urine. 3. Malnourished children had significantly lower rates of protein turnover, synthesis and breakdown than after they had recovered. 4. During recovery from protein-energy malnutrition, two children on a daily intake of 1.2 g of protein and 605 J/kg body weight, had rates of protein turnover, synthesis and breakdown that were twice as great as those found on admission and higher than after recovery. 5. On the study diet the malnourished children maintained their weight while the recovered children lost weight; the apparent nitrogen balance was more positive in the malnourished children. 6. In recovered children, the rate of protein synthesis was unchanged over a wide range of protein intake, whereas the rate of protein breakdown appeared to rise with a reduction in protein intake.
Clin Sci Mol Med 1977 Nov
PMID:Protein turnover, synthesis and breakdown before and after recovery from protein-energy malnutrition. 41 38

1. Young Wistar rats were used as an experimental model to determine the effects of protein-energy malnutrition on glucose tolerance and insulin release. 2. Malnourished rats presented some of the features commonly found in human protein-energy malnutrition, such as failure to gain weight, hypoalbuminaemia, fatty infiltration of the liver and intolerance of oral and intravenous glucose loads. 3. The rate of disappearance of glucose from the gut lumen was greater in the malnourished rats but there was no significant difference in portal blood glucose concentration between normal and malnourished rats 5 and 10 min after an oral glucose load. 4. Insulin resistance was not thought to be the cause of the glucose intolerance in the malnourished animals since these rats had a low fasting plasma insulin concentration with a normal fasting blood glucose concentration and no impairment in their hypoglycaemic response to exogenous insulin administration. Furthermore, fasting malnourished rats were unable to correct the insulin-induced hypoglycaemia despite high concentrations of hepatic glycogen. 5. Malnourished rats had lower peak plasma insulin concentrations than normal control animals after provocation with oral and intravenous glucose, intravenous tolbutamide and intravenous glucose plus aminophyllin. This was not due to a reduction in the insulin content of the pancreas or potassium deficiency. Healthy weanling rats, like the older malnourished rats, had a diminished insulin response to intravenous glucose and intravenous tolbutamide. However, their insulin response to stimulation with intravenous glucose plus aminophyllin far exceeded that of the malnourished rats. Thus the impairment of insulin release demonstrated in the malnourished rats cannot be ascribed to a 'functional immaturity' of the pancreas.
Clin Sci Mol Med 1976 Mar
PMID:Glucose tolerance and insulin release in malnourished rats. 81 69

1. Total body potassium was estimated by 40-K measurement with a high-sensitivity whole body counter in normal individuals over a wide age range and in patients who were obese or were grossly wasted as a result of various conditions which restricted food intake. 2. Potassal males and females, but when individuals of different age groups were matched for height, a significant fall in total body potassium with increasing age was observed only in males. Total body potassium of females was about 75% that of males of similar height when young, the sex difference decreasing with ageing. In the normal population, total body potassium was significantly correlated with height and with weight; regression equations for various relationships are given. 3. Fat-free mass was estimated from total body potassium, values of 65 and 56 mmol of potassium/kg fat-free mass being used for males and females respectively. Body fat estimated by this method correlated well with skinfold measurements over a wide range of body weight but in malnourished individuals having inadequate food intake there was considerable fat-free mass from total body potassium appear unsatisfactory in malnutrition. Considerable differences between expected and observed values of total body potassium were found in muscular individuals and in normal individuals who were thin but whose body weight was relatively constant. 4. The patients with malnutrition were low both in body fat as estimated by skinfold thcikness and in total body potassium estimated on the basis of height. Plasma potassium was, however, normal and potassium supplements did not increase the total body potassium. 5. Total body potassium of obese individuals was not significantly different from that of normal weight individuals on the basis of height. Total body potassium fell on weight reduction with a very low energy diet of 1260 kJ (300 kcal.) daily but changed little with a 3300 kJ (800 KCAY POTASSIUM WAS BEST PREDICTED FROM THE INDIVIDUAL'S HEIGHT. For those whose body weight was less than expected, the use of weight gave the best prediction but the error was considerable when the weight deviation was large.
Clin Sci Mol Med 1975 May
PMID:Total body potassium and body fat estimation in relationship to height, sex, age, malnutrition and obesity. 112 34

Malnutrition has been associated with changes in cardiac metabolism and performance. We have previously reported a diabetic-type cardiomyopathy associated with chronic food restriction and weight loss. Because the creatine-phosphocreatine-creatine kinase system is important in the contractile process, we studied the components of this system in rats fed a food-restricted diet (33% of control animal intake). After 4 weeks of food restriction, total creatine kinase (CK) activities were reduced by 28% in ventricles and by 38% in atria. The CK isoenzymes in the heart were not equally affected. The BB isoenzyme was decreased by 77% and 78%, the MB isoenzyme by 45% and 43%, the MM isoenzyme by 22% and 19% and CKmito by 16% and 15% in ventricles and atria, respectively. In contrast, brain CK activity which is predominantly the BB isoenzyme, was slightly higher in the food-restricted than in control rats. Further studies on ventricular tissue from food-restricted rats revealed a 27% decline in myofibrillar CR activity and a 58% decline in myofibrillar ATPase activity. Phosphocreatine and creatine concentrations were not changed by food restriction, however, ATP was decreased by 23% in ventricles from rats on the restricted diet. Cardiac mitochondrial oxidative phosphorylation was also impaired. State 3 respiration with alpha-ketoglutarate was reduced 20% in the food-restricted heart. These changes are compared to those which we previously observed in the diabetic rat heart and the significance of these findings is discussed.
J Mol Cell Cardiol 1992 Aug
PMID:Effect of food restriction on the phosphocreatine energy shuttle components in rat heart. 143 12

The hypermodified base 2-methylthio-N6-isopentenyladenosine (ms2i6A) at position 37 occurs frequently in tRNAs that read codons starting with uridine. Here we have studied how ms2i6A affects the accuracy of poly(U) translation in vitro. Deficiency leads to a higher rejection rate of tRNA4(Leu) by more aggressive proofreading on the wild-type ribosome, but with the initial selection step unchanged. Our data indicate that ms2i6A has no effect on codon-anticodon interactions on wild-type ribosomes as long as aminoacyl-tRNA is in ternary complex with EF-Tu and GTP. ms2i6A deficiency in the cognate poly(U) reader tRNA(Phe) leads to increased misreading when the near-cognate competitor tRNA4(Leu) is wild-type. ms2i6A deficiency in tRNA4(Leu) gives a decreased error level in competition with wild-type tRNA(Phe).
J Mol Biol 1991 Dec 20
PMID:ms2i6A deficiency enhances proofreading in translation. 176 49

Deficiency of argininosuccinate synthetase causes arginine auxotrophy in lower organisms and causes citrullinemia in humans and cattle. Previously, seven missense mutations, four mutations associated with an absence of an exon in mRNA, and one splicing mutation have been identified in human neonatal citrullinemia. Reverse transcription of mRNA, amplification of cDNA and sequencing of cDNA clones were used to identify two additional missense mutations causing citrullinemia. One mutation involves substitution of leucine for serine at position 18 (S18L) and the other a substitution of cysteine for arginine at position 86 (R86C). Both of these mutations represent C----T transitions in CpG dinucleotides, and eight of nine missense mutations causing human citrullinemia involve similar transitions in CpG dinucleotides. The nucleotide coding sequence and deduced amino acid analysis are available for four mammalian species, yeast and three bacterial species. Six of nine missense mutations in humans occur in amino acid positions that are completely conserved in these organisms. Mutations causing human citrullinemia are extremely heterogeneous, and all non-consanguineous individuals studied to date are compound heterozygotes.
Mol Biol Med 1991 Feb
PMID:Additional mutations in argininosuccinate synthetase causing citrullinemia. 194 92

Escherichia coli K-12 strains completely lacking catalase activity due to mutations in katG, katE, and katF genes were constructed in order to assess the role of hydrogen peroxide in mutagenesis. Mutagenesis was monitored by selecting forward mutations to L-arabinose resistance. Lethality was measured at experimental conditions equivalent to those of the mutant yield by using a mixed culture of pairs of isogenic strains distinguished by their differential nutritional requirements. Deficiency in katG, katE, and katF genes leads to an enhanced spontaneous mutation rate as well as an enhanced sensitivity to both the lethal and mutagenic effects of hydrogen peroxide or an H2O2-generating mixture of compounds, such as coffee. To compare further the responses of the catalase-deficient bacteria to those of catalase-proficient counterparts, other genotoxins were analyzed. Both catalase-deficient and catalase-proficient strains were equally mutated by MMS, 4-NQO, and ultraviolet light. It is concluded that the bacterial strains and the mutagenicity tests described in the paper represent a useful tool to study the role of H2O2 in mutagenesis.
Environ Mol Mutagen 1990
PMID:Mutagenesis in Escherichia coli lacking catalase. 219 82

A mutation in the gene IRA1 (formerly called PPD1) was originally characterized as a deficiency of a phosphoprotein phosphatase. The IRA1 gene has been cloned and sequenced. A large open reading frame (8,817 base pairs) which can encode a protein of 2,938 amino acids was found. Northern (RNA) blot analysis detected a message of about 10 kilobases, and nuclease S1 protection demonstrated mRNA start points at 97 and 98 base pairs upstream from the putative initiator ATG codon. Disruption of the IRA1 gene resulted in sensitivity to nitrogen starvation and heat shock. Diploids homozygous for the disrupted IRA1 gene were deficient in sporulation. Disruption of the IRA1 gene suppressed the lethality of the cdc25 mutation but did not suppress the lethality of either the ras1 ras2 or the cyr1 mutations. Deficiency of the phosphoprotein phosphatase was not reproducible in the disruption mutant of the IRA1 gene. Moreover, the ira1 mutant showed an increased level of cyclic AMP. Our results suggest that the IRA1 protein inhibits the function of the RAS proteins in a fashion antagonistic to the function of the CDC25 protein in the RAS-cyclic AMP pathway in Saccharomyces cerevisiae.
Mol Cell Biol 1989 Feb
PMID:IRA1, an inhibitory regulator of the RAS-cyclic AMP pathway in Saccharomyces cerevisiae. 254 Apr 26

In the present study, the effects of intratracheal administration of bleomycin have been examined on daily food intake and on plasma levels of glucose, cortisol, and insulin, and on lung levels of calmodulin, calcium, and collagen in hamsters. Since bleomycin treatment caused nutritional deficiency leading to loss of body weight, we have included pair-fed and control-fed as control groups in order to rule out the nutritional deficiency-related effects on these measurements. Bleomycin-treated animals showed a dramatic decrease in daily food intake and body weight as compared to control-fed animals. Bleomycin-treated animals were hyperglycemic when compared to nutritionally comparable pair-fed animals and had plasma glucose levels similar to those of control-fed animals. Plasma cortisol levels in bleomycin-treated and pair-fed animals showed a time-dependent increasing trend, whereas plasma insulin levels in both groups tended to decrease. The lung levels of calmodulin and calcium in bleomycin-treated animals were significantly increased when compared with the pair-fed or control-fed group. Bleomycin-treated animals had significantly higher levels of lung collagen than pair-fed or control-fed at 7 and 13 days after treatment. The lung collagen content in pair-fed animals was significantly less than that of control-fed at 13 days. It was concluded that a disturbance in carbohydrate metabolism and increased lung levels of calmodulin and calcium might be somehow involved in fibroproliferative changes of the lung in bleomycin-treated animals.
Exp Mol Pathol 1985 Apr
PMID:Effects of intratracheal administration of bleomycin or saline in pair-fed and control-fed hamsters on daily food intake and on plasma levels of glucose, cortisol, and insulin, and lung levels of calmodulin, calcium, and collagen. 257 45

We have previously reported that the heart retains its pumping performance despite loss of contractile mass during tumor disease and malnutrition. This adaptation is associated with increased agonist affinity of the beta-receptor. The present study was undertaken to evaluate if increased beta-receptor agonist affinity has a physiologic counterpart which may contribute to the remained function in hypotrophic hearts. The isolated, perfused, working rat heart was used as a model. Hearts from tumor-bearing rats showed an increased sensitivity and reactivity to graded isoproterenol stimulation compared to freely-fed control animals. Starved and protein-calorie malnourished (PCM) control animals had a similar response of heart rate, left ventricular peak pressure and contractility as the tumor-bearing group. This increased response to beta-adrenergic stimulation thus seems to be a general adaptation to loss of contractile mass and not to a tumor-specific reaction. Tumor-bearing animals had lower myocardial content of norepinephrine and epinephrine compared to starved, PCM and freely-fed control rats. Oxygen consumption was higher in hearts from tumor-bearing animals compared to freely-fed controls during all experimental conditions. Starved and PCM rats, in contrast, had decreased oxygen consumption compared to the freely-fed controls. The heart might thus be one of the organs contributing to the increased energy expenditure seen in malignant tumor disease possibly due to a changed adrenergic regulation in the tumor state compared to uncomplicated undernutrition.
J Mol Cell Cardiol 1987 Jul
PMID:Cardiac sensitivity and responsiveness to beta-adrenergic stimulation in experimental cancer and undernutrition. 282 95


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