SEARCH · Search PubMed
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.
Pancreatic lipid composition was found to be altered in rats fed a protein-deficient diet for 4 wk. Increases in triglycerides and cholesteryl ester content were found in association with a decrease in phospholipids. Alterations in these lipids may adversely affect membrane function and predispose to pancreatic injury.
We experimented with a diet resembling a protein-deficient one eaten by man, having a low protein level and proteins of poor biological value. Malnutrition caused weight loss accompanied by an overall reduction of ingesta. However, the food intake, as compared to animal weight, was the same in the undernourished animals as in the controls. Bile and pancreatic juice outputs were not altered continuously and regularly but with the poor protein diet, they were lower. Refeeding a balanced diet caused these outputs to increase. When 0.6 p. 100 of methionine was added to the deficient diet, no significant difference was noted in the outputs of the rats eating the deficient diets. Enzyme activities in the juice and pancreas varied widely from one day to another during malnutrition and during refeeding. The mean values of specific activities, which masked these variations, showed that malnutrition did not significantly decrease the phospholipase A2 activity in the pancreatic juice, while potential lipase and colipase-dependent lipase activities declined. Refeeding temporarily stimulated specific phospholipase A2 and potential lipase activities the third day; colipase-dependent lipase activity was not activated. After 2 to 3 weeks of refeeding, the specific activities of the three enzymes were similar to the control values, but were no longer so at the end of refeeding. This would suggest a return to the normal, as shown by the oscillations around the control values. Protein malnutrition, as refeeding, did not in general cause the same changes in all the enzymes at the same time.
Linear discriminant functions hold promise for identifying either protein-deficient or cold-stressed calves based on blood constituents. For each of 2 yr 60 artificially bred Angus heifers were assigned randomly to a 2 x 2 factorial nutritional plan consisting of .32 or .96 kg/d of maternal CP and 8.7 or 12.2 Mcal/d of ME. The calves from these heifers were assigned randomly to environmental chambers set at either 0 or 21 degrees C in a repeated measures design. Linear discriminant functions were computed for 1 yr (training data) and then used to predict the classification of calves for the other year (validation data). Using the original data, the correct classifications of calves to the protein groups were 96, 80, 60, 59, 54, and 51% for blood samples obtained at 0, 12, 24, 36, 48, and 72 h of age, respectively. Using normalized data, corresponding correct classifications to protein groups were 94, 91, 80, 56, 54, and 52%. Results indicate that protein classification should use blood samples obtained within 12 h of age for reasonable success. For cold-stressed calves, correct classifications using original data were 47 (pre-exposure), 72, 54, 70, 67, and 66% for calves at 0, 12, 24, 36, 48, and 72 h of age, respectively. Corresponding correct classifications using normalized data were 54 (pre-exposure), 74, 70, 72, 69, and 77%. Cold stress could be detected after only 12 h of exposure; the time window for testing was much wider than for protein classification, but the classification generally was less discriminative.
Running at 0.7 km/h for 10 min every day inhibited development of osteoporosis caused by protein deficient (PD) food intake. Urine alkaline phosphatase (ALP), a marker of bone formation osteoporosis, was not elevated in rats fed PD, when the osteoporosis was inhibited by running. Estrogen supplementation increased bone-breaking energy (BBE), but did not increase bone mineral density (BMD), and did not decrease urinary ALP levels.
The effect of a low protein (4%) diet on the activity of the hydrolytic enzymes ribonuclease, deoxyribonuclease, acid and alkaline phosphatases, beta-glucuronidase and lysozyme has been studied in the spleen and thymus of weanling Wistar rats. Experimentation was carried out over 20 and 30 days, and comparisons were made with well-nourished (12% protein) controls. Body weight decreased during the terminal period in protein-deficient animals (P less than 0.001). Spleen and thymus absolute net weights also dropped significantly (P less than 0.001). In terms of organ weight relative to body weight, there was a clear decrease in thymus compared with controls (P less than 0.001). Enzyme activities expressed per total organ fell significantly. Thus, in spleen at 20 days the decrease was maximum in ribonuclease activity (91.15%) and minimum in acid phosphatase activity (44.09%). Thymus decreases ranged from 83.60% activity in beta-glucuronidase and 93.56% in ribonuclease. At 30 days decreases were accentuated; the maximum value in spleen was 92.34% lysozyme and, in thymus, 97.09% acid phosphatase. A large increase in hydrolytic activity expressed per milligram of protein was registered, especially at 30 days. This increase reached a maximum of 78.08% beta-glucuronidase in thymus and a minimum of 56.1% alkaline phosphatase; acid phosphatase and ribonuclease activities were not modified. In spleen, however, acid phosphatase (34.00%), alkaline phosphatase (62.50%), deoxyribonuclease (39.25%), and beta-glucuronidase (36.01%) increased, but lysozyme and ribonuclease enzymes decreased. We concluded that a low protein diet increases catabolism in spleen and thymus through an enhancement of lysosomal hydrolase activities.
The long-term preliminary protein deficiency in the diet gives rise to irreversible changes in sodium metabolism in experimental animals exposed subsequently to chronic salt load combined with full-value feeding. Apparently such changes do not go, however, beyond the compensatory potentialities of the body exposed to isotonic salt load, since the systolic arterial pressure does not undergo any material changes throughout the whole experiment.
BACKGROUND: Malnutrition-related diabetes mellitus is a distinct clinical entity subdivided into protein-deficient diabetes mellitus (PDDM) and fibrocalculus pancreatic diabetes (FCPD). Whereas FCPD has obvious pancreatitis manifested by pancreatic duct calculi, the evidence for involvement of the pancreas in PDDM is limited to the presence of ketosis-resistant hyperglycaemia. METHODS: We studied 10 patients with PDDM biochemically and radiologically. Endoscopic retrograde cholangiopancreatography was performed to determine if they had any evidence of chronic pancreatitis. RESULTS: Their mean faecal chymotrypsin level was low (13.2+/-5.72 microg/g), as was their basal c-peptide value (0.35+/-0.15 mmol/L). Islet cell antibodies were not detected in any of these patients. Ultrasound examination revealed pancreatic atrophy. In two patients, however, the pancreas was bulky. The ERCP showed generalized thinning of the pancreatic duct, measuring 2.4+/-0.06mm in the head, 2.01+/-0.08 mm in the body and 1.02 +/- 0.03 mm in tail region; side branches were seen but they were too sparse and thin. CONCLUSIONS: The significance of these changes is not clear, but they may represent an ongoing pancreatic disease and may, indeed, be the earliest changes of chronic pancreatitis.
The developmental toxicity of cytochalasins B (CB) and D (CD) was evaluated in protein-deprived mice. Pregnant CD-1 mice were assigned to control (26%), 16%, 8%, or 4% dietary protein groups on gestation day 1 and dosed by gavage with 0 or 1.5 mg/kg CB or CD on gestation day 8 (plug = day 1). They were killed and subjected to teratological examination on day 18. CD, but not CB, increased prenatal mortality but failed to interact significantly with dietary protein level. Fetal weights were decreased in the 4% and 8% dietary protein groups, but cytochalasin treatment did not exacerbate this effect. Cytochalasin treatment was associated with gross fetal malformations, primarily neural tube defects. Although CB and CD did not significantly increase the percentage of grossly malformed fetuses per litter, the data was suggestive of such an effect, and the incidence of affected litters was increased by cytochalasin treatment in all but the 4% protein group. Skeletal defects, such as jaw malformations, rib or sternebrae variations, and unossified skull bones appeared to be increased by both cytochalasin treatment and dietary protein deficiency. The differences from control values were nonsignificant, however, except for some cases of cytochalasin effects on skull ossification. These results show a general lack of effect of protein deprivation on the developmental toxicity of cytochalasins.
Protein-deficient ribosomal particles obtained by treatment of 50-S subunits from Escherichia coli ribosomes with 1 M NH4Cl and 50% ethanol contain less than 3% of proteins L7 and L12 and about 7% of proteins L10 and L11. Proteins L1, L5, L8/9 and L25 are also released during the treatment but in amounts accounting for less than 40%. The particles are able to form peptide bonds in different systems, such as 'fragment reaction', puromycin reaction and formation of dipeptides. They also bind N-acetylphenylalanyl-tRNA and phenylalanyl-tRNA non-enzymically but are unable to support any of the elongation-factor-dependent reactions tested. However, when methanol is present, they display up to 20% of the control EF-G-dependent GTP activities such as GTP hydrolysis and formation of the ternary complex EF-G-GuoPP(CH2)P-ribosome. The first activity is totally sensitive to the antibiotic thiostrepton while the formation of the ternary complex is unaffected by the drug. When measured by equilibrium dialysis the core particles are shown to be able to bind radioactive thiostrepton. The results show that protein L11 is not an absolute requirement either for peptidyl transferase activity or for the binding of thiostrepton, although in the last case the protein strongly enhances the ribosome affinity for the antibiotic.
Explore the source record for details and available documents.
The symptoms of E-avitaminosis against protein deficiency in the ration become manifest much earlier, i. e. in 12--16 weeks of the experiment instead of 24--36 weeks with the primary-deficient ration. This was marked by the development of the creatinuria, the falling blood serum and testes tissue tocopherol, a higher peroxidized erythrocytes hemolysis, the animals demonstrating a disturbed generative function. In the testes of the E-avitaminotic rats an appreaciably increased total activity of glucose-6-phosphate-dehydrogenase (G-6-PDG) and of the acid phosphatase (AP) was demonstrated, whereas the LDG remained essentially unchanged. An investigation of their isoenzymatic spectra revealed a considerable activity of the basic 5 G-6-PDG fractions with the appearance of additional ones, along with the disappearance of the specific LDG fraction--X-2 and a drastic fall in the activity of the specific fraction for the testes--LDG-X-1, with concurrent rise in the activity of the 5 basic fractions. In the isoenzymatic AP spectrum disappeared the AP-3 fraction of the degenerating testes tissues and a redistribution of the activity between the fractions took place.
BACKGROUND: Nucleoside-nucleotide mixture has been shown to improve gut morphology and reduce the incidence of bacterial translocation in protein deficient mice. AIMS: To compare the reparative effect of nucleoside-nucleotide mixture and their individual components on maintenance of gut integrity and bacterial translocation based on their differential metabolism and utilisation. METHODS: ICR (CD-1) mice were randomised into eight groups of 10 animals each and fed 20% casein diet (control), protein free diet, or protein free diet supplemented with 3 M cytidine, uridine, thymidine, inosine, guanosine monophosphate, or nucleoside-nucleotide mixture for four weeks. On the fourth week, each mouse was injected lipopolysaccharide intraperitoneally (50 micrograms/500 microliters) and the incidence of bacterial translocation, caecal bacterial populations, and the ileal histology, noted 48 hours later. RESULTS: The death rate in the control group was 40% compared with 10% in the nucleoside-nucleotide mixture and 20% each in the individual components groups, respectively. Bacterial translocation to the mesenteric lymph node did occur in 100% of the surviving mice fed the control diet in comparison with 44% (nucleoside-nucleotide), 50% (cytidine), 75% (thymidine), 75% (uridine), 63% (inosine), and 63% (guanosine monophosphate). Histologically, the damage to the gut was more distinct in the protein free diet group. Villous height, crypt depth, and wall thickness in the nucleoside-nucleotide mixture group mean (SEM) (5.01 (0.34); 0.87 (0.14); 0.33 (0.10)), were respectively, higher compared with the protein free diet (3.34 (0.34); 0.61 (0.03); 0.18 (0.04)) group. In the cytidine group, crypt depth (0.86) (0.08)), and wall thickness (0.30 (0.002)) were higher. The same measurements in the components groups tended to be higher than the protein free diet group. Caecal bacterial populations were, however, similar in all groups. CONCLUSIONS: These results suggest that dietary nucleosides and nucleotides are essential nutrients for intestinal repair; nucleotides or cytidine provide a better response.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Protein S is a vitamin K-dependent plasma protein that serves as a cofactor of activated protein C(APC) in its inhibitory action on activated factor V and factor VIII and in its stimulation of fibrinolytic activity. In plasma, part of the protein S is complexed with the C4b-binding protein. Only the free protein S has APC cofactor activity. In our laboratory, 30 patients from 8 nonrelated families were detected that fulfilled the criteria of an isolated protein S deficiency. All patients were heterozygotes for the defect that is inherited as an autosomal-dominant disorder. Patients with a protein S deficiency were found to be at risk for the development of venous thrombotic disease at a relatively young age.
X-linked adrenoleukodystrophy (X-ALD) is characterized by progressive mental and motor deterioration, with demyelination of the central and peripheral nervous system. Its principal biochemical abnormality is the accumulation of very-long-chain fatty acids (VLCFAs) in tissues and body fluids, caused by the impairment of peroxisomal beta-oxidation. The authors have generated a line of mice deficient in ALD protein (ALDP) by gene targeting. ALDP-deficient mice appeared normal clinically, at least up to 12 mo. Western blot analysis showed absence of ALDP in the brain, spinal cord, lung, and kidney. The amounts of C26:0 increased by 240% in the spinal cord. VLCFA beta-oxidation in cultured hepatocytes was reduced to 50% of normal. The authors investigated the roles of ALDP in VLCFA beta-oxidation using the ALDP-deficient mice. Very-long-chain acyl-CoA synthetase (VLACS) is functionally deficient in ALD cells. The impairment of VLCFA beta-oxidation in the ALDP-deficient fibroblasts was not corrected by over-expression of VLACS only, but was done by co-expression of VLACS and ALDP, suggesting that VLACS requires ALDP to function. VLACS was detected in the peroxisomal and microsomal fractions of the liver from both types of mice. Peroxisomal VLACS was clearly decreased in the ALDP-deficient mouse. Thus, ALDP is involved in the peroxisomal localization of VLACS.