• Nutrition Research and Practice
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• v.1 no.4
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• pp.247-253
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• 2007

Alpha-tocopherol transfer protein (${\alpha}$-TTP) is a liver cytosolic transport protein that faciliates ${\alpha}$-tocopherol (${\alpha}$-T) transfer into liver secreted plasma lipoproteins. Genetic defects in ${\alpha}$-TTP, like dietary vitamin E deficiency, are associated with infertility, muscular weakness and neurological disorders. Both human and ${\alpha}$-TTP deficient (${\alpha}-TTP^{-/-}$) mice exhibit severe plasma and tissue vitamin E deficiency that can be attenuated by sufficient dietary ${\alpha}$-T supplementations. In this review, we summarize the literature concerning studies utilizing the ${\alpha}-TTP^{-/-}$ mice. Levels of vitamin E in the ${\alpha}-TTP^{-/-}$ mice do not appear to be directly related to the amounts of dietary ${\alpha}$-T or to the levels of ${\alpha}$-TTP protein in tissues. The ${\alpha}-TTP^{-/-}$ mice appear to present a good model for investigating the specific role of ${\alpha}$-T in tissue vitamin E metabolism. Furthermore, ${\alpha}-TTP^{-/-}$ mice appear to be useful to elucidate functions of ${\alpha}$-TTP beyond its well recognized functions of transferring ${\alpha}$-T from liver to plasma lipoprotein fractions.

• Journal of Nutrition and Health
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• v.40 no.2
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• pp.130-137
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• 2007

Myelin basic protein (MBP), a major structural protein of the myelin, is thought to be important for the maintenance of myelin in the central nervous system (CNS). We investigated the effect of maternal folic acid nutritional status on the folate level and the synthesis of MBP in the offspring. In order to test this hypothesis, female Sprague-Dawley rats were fed either folic acid sufficient (8 mg/kg diet) or deficient (0 mg/kg diet) diet from 2 wks prior to the mating throughout the entire pregnancy, lactation and weaning period. We examined plasma folate level by the radioimmunoassay and homocysteine level by HPLC, respectively. The MBP expression was measured by the western blot analysis. The maternal folic acid deficiency decreased plasma folate level with a concomitant increase in plasma homocysteine level in their offspring. The maternal folic acid deficiency decreased hepatic levels of SAM and SAM/SAH ratio with a concomitant increase in hepatic levels of SAH and the MBP expression of spinal cord in their offspring at 7 wks of age. These results suggest that maternal folic acid nutritional status affect plasma folate and homocysteine level in their offspring. Moreover, the maternal folic acid deficiency mi호t inhibit the MBP expression of the spinal cord and disrupt many other vital CNS reactions in their offspring.

• Journal of Nutrition and Health
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• v.2 no.4
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• pp.113-125
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• 1969

These experiments were designed to study the influence of early protein undernutrition on growth, behaviors toward food, general attitude toward a new environment, brain size and body composition of the experimental rats. The following experimental groups were studied. Lactation period (3 weeks) (Diets of mother rats) 25% Casein diet 12% Casein diet 25% Casein diet 25% Casein diet 12% Casein diet 12% Casein diet After-weaning protein deprivation period None deprivation (25% Casein diet) None deprivation (25% Casein diet) 5% Casein diet (4 weeks) 5% Casein diet (8 weeks) 5% Casein diet (4 weeks) 5% Casein diet (8 weeks) After a long period of rehabilitation with 25% casein diet the following results were obtained. 1. Growth rate during lactation period is closely related with the protein levels of the diet for mother rats. The average body weight of offsprings of the mother rat fed 25% casein diet is 46.0 grams at 21 days old. However, that of the mother rat fed 12% casein diet is only 25.0 grams. 2. The group of protein undernutrition during lactation (S weeks) (offsprings of mother rat fed low protein diet, 12% casein diet) could never catch up with the normal group in its growth even after twenty-four (24) weeks of rehabilitation. 3. However, the groups of protein undernutrition during either four (4) or even eight (8) weeks after weaning could catch up with the normal group in their growth after long period of rehabilitation. 4. The absolute amounts of carcass protein and fat of the normal group are larger than those of the protein deficient groups. In terms of percent carcass, however, the normal group showed higher body fat and lower body protein than the early deficient groups. However, there is no difference between preweaning (3 weeks) and postweaning (8 weeks) deficient groups. It is assumed, from these differences in body composition, that there might be any differences in physiological and metabolic functions among these various groups, and also that the basic formation of various metabolic regulators (protein-nature) might be fixed mostly during lactation and postweaning period. 5. The groups of protein undernutrition during either three (3) weeks lactation or four (4) weeks after weaning are not so remarkably different from the normal group in their amounts of food intake and spillage. However, the groups of undernutrition during either eight (8) weeks postweaning or eleven (11) weeks (3 weeks lactation period plus 8 weeks postweaning period) showed higher amounts of food intake and spillage. In these respects, it seems that desire for food is closely related with the degree of early hunger in protein and also seems that the longer be deficient in early life the more food spillage is found. 6. Both preweaning and postweaning deficient groups showed generally nervous and restless. The normal group is staid and showed less mobilities. 7. The average size of the brains of the group subjected to protein deficiency during three (3) weeks lactation period is smaller than that of the group of the eight (8) weeks postweaning deficiency. This means that the development of the brain is made mostly during lactation period. The group of the eleven (11) weeks postnatal deficiency is significantly different from the normal group in its brain development. It is assumed, in connection with the results of various maze tests reported, that the brain size is closely related with the intellectual ability.

• Asian-Australasian Journal of Animal Sciences
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• v.20 no.7
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• pp.1120-1126
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• 2007

An iron-fortified whey protein concentrate (Fe-WPC) was prepared by addition of ferric chloride to concentrated whey. A large part of the iron in the Fe-WPC existed as complexes with proteins such as ${\beta}$-lactoglobulin. The bioavailability of iron from Fe-WPC was evaluated using iron-deficient rats, in comparison with heme iron. Rats were separated into a control group and an iron-deficiency group. Rats in the control group were given the standard diet containing ferrous sulfate as the source of iron throughout the experimental feeding period. Rats in the iron-deficiency group were made anemic by feeding on an Fe-deficient diet without any added iron for 3 wk. After the iron-deficiency period, the iron-deficiency group was separated into an Fe-WPC group and a heme iron group fed Fe-WPC and hemin as the sole source of iron, respectively. The hemoglobin content, iron content in liver, hemoglobin regeneration efficiency (HRE) and apparent iron absorption rate were examined when iron-deficient rats were fed either Fe-WPC or hemin as the sole source of iron for 20 d. Hemoglobin content was significantly higher in the rats fed the Fe-WPC diet than in rats fed the hemin diet. HRE in rats fed the Fe-WPC diet was significantly higher than in rats fed the hemin diet. The apparent iron absorption rate in rats fed the Fe-WPC diet tended to be higher than in rats fed the hemin diet (p = 0.054). The solubility of iron in the small intestine of rats at 2.5 h after ingestion of the Fe-WPC diet was approximately twice that of rats fed the hemin diet. These results indicated that the iron bioavailability of Fe-WPC was higher than that of hemin, which seemed due, in part, to the different iron solubility in the intestine.

• Asian-Australasian Journal of Animal Sciences
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• v.16 no.6
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• pp.903-909
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• 2003

For the last two decades, energy utilization of growing chicks has been studied more and more. This paper focuses on the energy utilization estimated by the metabolizable energy (ME) values and the efficiency at which ME is used for growth of chicks under various nutritional environment. Degree of saturation of dietary fats is responsible for nitrogen-corrected apparent metabolizable energy (AMEn) of fats. The effect of dietary fat sources on heat production depends on the kind of unsaturated fatty acids as well as the degree of saturation. Medium chain triglyceride shows lower AME and net energy than long chain triglyceride. Phytase as feed additives increases the AME values of the diet along with improvement of the phosphorous utilization. Ostriches have higher ability to metabolize the energy of fiber-rich foodstuffs than fowls. Their higher ability seems to be associated with fermentation of fiber in the hindgut. Proportions of macronutrients in the diets have influenced not only the gain of body protein and energy but also the oxidative phosphorylation of the chicken liver. Essential amino acids deficiency reduces ME/GE (energy metabolizability) little, if any. Growing chicks respond to a deficiency of single essential amino acids with the reduction of energy retained as protein and increased energy retained as fat. Thus, energy retention is proportional to ME intake despite deficiency, and efficiency of ME utilization is not affected by deficiency of amino acids. Effect of oral administration of clenbuterol, a beta-adrenergic agonist, on the utilization of ME varies with the dose of the agents. Although the heat production related to eating behavior has been estimated less than 5% of ME, tube-feeding diets decreases HI by about 30%.

• Journal of Nutrition and Health
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• v.9 no.1
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• pp.1-6
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• 1976

• Proceedings of the PSK Conference
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• 2001.10a
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• pp.101-101
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• 2001

• Asian-Australasian Journal of Animal Sciences
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• v.31 no.11
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• pp.1795-1806
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• 2018

Objective: The study was designed to establish choline deficiency model (CDM) in broilers for evaluating efficacy of polyherbal formulation (PHF) in comparison with synthetic choline chloride (SCC). Methods: A total of 2,550 one-day-old Cobb 430 broiler chicks were randomly assigned to different groups in three experiments. In experiment 1, G1 and G2 served as normal controls and were fed a basal diet with 100% soybean meal (SBM) as a major protein source supplemented with and without SCC, respectively. In G3, G4, G5, and G6 groups, SBM was replaced at 25%, 50%, 75%, and 100% by soy protein isolate (SPI) to induce a graded level of choline deficiency. In experiment 2, PHF (500 and 1,000 g/ton) in comparison with SCC (1,000 g/ton) were evaluated. In experiment 3, dose-response of PHF (200, 400, and 500 g/ton) with SCC (400 g/ton) was determined. Results: Replacement of SBM by SPI produced a linear decrease in body weight gain (BWG) with a poor feed conversion ratio (FCR). 25% SBM replacement by SPI yielded an optimum negative impact on BWG and FCR; hence, it is considered for further studies. In experiment 2, PHF (500 and 1,000 g/ton) and SCC (1,000 g/ton) showed a similar performance in BWG, FCR and relative liver weight. In experiment 3, PHF produced an optimum efficacy at 400 g/ton and was comparable to SCC in the restoration of serum aspartate aminotransferase activity, abdominal fat, breast muscle lipid content and liver histopathological abnormalities. Conclusion: Replacement of SBM by SPI caused choline deficiency characterised by worsening of BWG, FCR, elevation in liver enzymes and histopathological changes indicating fatty liver. CDM was found valid for evaluating SCC and PHF. It is concluded that PHF has the potential to mimic biological activities of SCC through the restoration of negative effects caused by CDM.

• Nutritional Sciences
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• v.7 no.4
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• pp.218-222
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• 2004

Iron deficiency anemia (IDA) is the world's most common nutritional problem. It is characterized by a low hemoglobin (Hb) level and low iron status. A study was conducted to investigate the incidence of iron deficiency anemia in day scholar girls belonging to different socioeconomic strata at Punjab University, Lahore. Iron status of the subjects was estimated by measuring Hb, hematocrit (Hct), red blood cell (RBC) count, mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCR), serum iron, serum ferritin, total protein and albumin. Results indicated that females belonging to low socioeconomic strata had lower values for Hb, Hct, RBC count, total protein and albumin. Serum iron, serum ferritin, MCV and MCH values fell within the normal range for all of the socioeconomic groups. However, serum iron and ferritin varied with socioeconomic status and higher-income groups had significantly higher serum iron and ferritin. It was concluded that anemia may develop due to poor intake and absorption of iron and that those in the low-income bracket are the most affected group.

• BMB Reports
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• v.48 no.7
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• pp.371-372
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• 2015

MicroRNAs (miRNAs) can regulate the expression of genes that are involved in multiple cellular pathways. However, their targets and mechanism of action associated with the autophagy pathway are not fully investigated yet. EWSR1 (EWS RNA-Binding Protein 1/Ewing Sarcoma Break Point Region 1) gene encodes a RNA/DNA binding protein that is ubiquitously expressed and plays roles in numerous cellular processes. Recently, our group has shown that EWSR1 deficiency leads to developmental failure and accelerated senescence via processing of miRNAs, but its role in the regulation of autophagy remains elusive. In this context, we further investigated and found that EWSR1 deficiency triggers the activation of the DROSHA-mediated microprocessor complex and increases the levels of miR125a and miR351, which directly target Uvrag. Interestingly, the miR125a- and miR351-targeted reduction of Uvrag led to the inhibition of autophagy in both ewsr1 knockout (KO) MEFs and ewsr1 KO mice. In summary, our study demonstrates that EWSR1 is associated with the posttranscriptional regulation of Uvrag via miRNA processing. The regulation of autophagy pathway in miRNAs-Uvrag-dependent manner provides a novel mechanism of EWSR1 deficiency-related cellular dysfunction. [BMB Reports 2015; 48(7): 371-372]