Hinata Okamoto, Yuka Kawakami, Mayu Kaneko, Eri Ishida, Megumi Sato, Haruka Matsukawa, Toshio Hosaka, Hidekazu Arai
With the western influence in our diets, food consumption has changed, and our magnesium (Mg) intake is no longer optimal. Serum Mg (S-Mg) level is currently used as an indicator of Mg deficiency and is strictly regulated via compensatory mechanisms. It is believed that a 24-h urine collection can be used to evaluate potential Mg deficiency. This study aimed to assess whether Mg deficiency state as found in urine Mg (U-Mg) excretion and improving such deficiency with a diet that meets the Recommended Dietary Allowances (RDAs) of Mg for 15 d. Healthy Japanese women were recruited for Study 1 (n=22) and Study 2 (n=10). Study 1 was 1-d balance test, where fasting blood and 24-h urine samples were collected. Study 2 was 15-d diet load test, where fasting blood (days 1, 7, and 15) and 24-h urine (odd days) were collected. All test meals were made certain to have met the RDA for Mg for women in their 20s. In Studies 1 and 2, S-Mg was within the normal range. In Study 1, U-Mg excretion was 67.7±17.0 mg/d, with a large dispersion. In Study 2, U-Mg excretion on days 7 and 15 was significantly higher than on day 1, but have no significant differences in U-Mg excretion between days 7-15. U-Mg excretion can be a valuable indicator to evaluate Mg state. In young women, improvements in Mg deficient state were observed after 7-15 d of taking meals that met the RDAs of Mg.
{"title":"The Urinary Excretion of Magnesium as an Effective Magnesium Deficiency State Indicator: A Controlled Intervention Trial.","authors":"Hinata Okamoto, Yuka Kawakami, Mayu Kaneko, Eri Ishida, Megumi Sato, Haruka Matsukawa, Toshio Hosaka, Hidekazu Arai","doi":"10.3177/jnsv.69.21","DOIUrl":"https://doi.org/10.3177/jnsv.69.21","url":null,"abstract":"<p><p>With the western influence in our diets, food consumption has changed, and our magnesium (Mg) intake is no longer optimal. Serum Mg (S-Mg) level is currently used as an indicator of Mg deficiency and is strictly regulated via compensatory mechanisms. It is believed that a 24-h urine collection can be used to evaluate potential Mg deficiency. This study aimed to assess whether Mg deficiency state as found in urine Mg (U-Mg) excretion and improving such deficiency with a diet that meets the Recommended Dietary Allowances (RDAs) of Mg for 15 d. Healthy Japanese women were recruited for Study 1 (n=22) and Study 2 (n=10). Study 1 was 1-d balance test, where fasting blood and 24-h urine samples were collected. Study 2 was 15-d diet load test, where fasting blood (days 1, 7, and 15) and 24-h urine (odd days) were collected. All test meals were made certain to have met the RDA for Mg for women in their 20s. In Studies 1 and 2, S-Mg was within the normal range. In Study 1, U-Mg excretion was 67.7±17.0 mg/d, with a large dispersion. In Study 2, U-Mg excretion on days 7 and 15 was significantly higher than on day 1, but have no significant differences in U-Mg excretion between days 7-15. U-Mg excretion can be a valuable indicator to evaluate Mg state. In young women, improvements in Mg deficient state were observed after 7-15 d of taking meals that met the RDAs of Mg.</p>","PeriodicalId":16624,"journal":{"name":"Journal of nutritional science and vitaminology","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10823778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jun Luo, Xiaohong Chen, Yuwei Yang, Yunbing Liu, Yue Feng, Gang Chen
Senile cataract has become the leading cause of visual impairment and even blindness in the world, but there are few reports on its relationship with methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms. This study is aimed to investigate the correlation between MTHFR gene polymorphisms or its enzyme metabolites and senile cataract. From January 2019 to June 2020, 663 patients with senile cataract at the Mianyang Central Hospital were enrolled as the observation group, and 646 healthy subjects were randomly selected as the control group. MTHFR gene polymorphisms (i.e., CC, CT, or TT genotypes) and serum homocysteine (HCY), folic acid (FOL), vitamin B12 (VitB12), and vitamin B6 (VitB6) levels were detected. The mutation rate of MTHFR C677T and HCY levels in the observation group were significantly higher than those in the control group, whereas FOL, VitB12, and VitB6 were significantly lower. With an increase in the MTHFR C677T mutation, HCY showed an upward trend, whereas FOL and VitB12 showed a decreasing trend in both the observation and control groups. Multiple logistic regression analysis showed that HCY and FOL were associated with senile cataract and MTHFR mutations; VitB12 was only associated with senile cataract. Compared to that with the CC genotype, CT and TT genotypes were associated with an increased senile cataract risk. Monitoring MTHFR gene polymorphisms and changes in serum HCY, FOL, and VitB12 levels could provide references in predicting senile cataract.
{"title":"Association of MTHFR C667T Polymorphism, Homocysteine, and B Vitamins with Senile Cataract.","authors":"Jun Luo, Xiaohong Chen, Yuwei Yang, Yunbing Liu, Yue Feng, Gang Chen","doi":"10.3177/jnsv.69.136","DOIUrl":"https://doi.org/10.3177/jnsv.69.136","url":null,"abstract":"<p><p>Senile cataract has become the leading cause of visual impairment and even blindness in the world, but there are few reports on its relationship with methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms. This study is aimed to investigate the correlation between MTHFR gene polymorphisms or its enzyme metabolites and senile cataract. From January 2019 to June 2020, 663 patients with senile cataract at the Mianyang Central Hospital were enrolled as the observation group, and 646 healthy subjects were randomly selected as the control group. MTHFR gene polymorphisms (i.e., CC, CT, or TT genotypes) and serum homocysteine (HCY), folic acid (FOL), vitamin B<sub>12</sub> (VitB<sub>12</sub>), and vitamin B<sub>6</sub> (VitB<sub>6</sub>) levels were detected. The mutation rate of MTHFR C677T and HCY levels in the observation group were significantly higher than those in the control group, whereas FOL, VitB<sub>12</sub>, and VitB<sub>6</sub> were significantly lower. With an increase in the MTHFR C677T mutation, HCY showed an upward trend, whereas FOL and VitB<sub>12</sub> showed a decreasing trend in both the observation and control groups. Multiple logistic regression analysis showed that HCY and FOL were associated with senile cataract and MTHFR mutations; VitB<sub>12</sub> was only associated with senile cataract. Compared to that with the CC genotype, CT and TT genotypes were associated with an increased senile cataract risk. Monitoring MTHFR gene polymorphisms and changes in serum HCY, FOL, and VitB<sub>12</sub> levels could provide references in predicting senile cataract.</p>","PeriodicalId":16624,"journal":{"name":"Journal of nutritional science and vitaminology","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10053637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Luteolin (LU), a natural compound, has diverse bioactivities; it alleviates lipid accumulation by enhancing the oxidation of fatty acids in nonalcoholic fatty liver disease (NAFLD). Mitochondrial dysfunction promotes the development of steatosis in NAFLD. However, few studies have focused on the mechanism by which LU affects mitochondrial function in NAFLD. In the present study, we investigated whether LU could ameliorate hepatic steatosis and affect mitochondrial function in Western diet-fed mice. After LU treatment, the indicators of hepatic function and markers of mitochondrial biogenesis were evaluated. The results showed that LU intervention 1) decreased the levels of serum triglyceride, total cholesterol, alanine aminotransferase, and low-density lipoprotein cholesterol; 2) increased the succinate dehydrogenase activity of mitochondrial enzyme; and 3) increased mitochondrial biogenesis by upregulating the AMPK/PGC-1α pathway. Therefore, LU might have the potential to prevent NAFLD.
{"title":"Luteolin Ameliorates Hepatic Steatosis and Enhances Mitochondrial Biogenesis via AMPK/PGC-1α Pathway in Western Diet-Fed Mice.","authors":"Tingting Wang, Qin Xu, Yang Cao, Cheng Zhang, Shiyin Chen, Yun Zhang, Tingbo Liang","doi":"10.3177/jnsv.69.259","DOIUrl":"https://doi.org/10.3177/jnsv.69.259","url":null,"abstract":"<p><p>Luteolin (LU), a natural compound, has diverse bioactivities; it alleviates lipid accumulation by enhancing the oxidation of fatty acids in nonalcoholic fatty liver disease (NAFLD). Mitochondrial dysfunction promotes the development of steatosis in NAFLD. However, few studies have focused on the mechanism by which LU affects mitochondrial function in NAFLD. In the present study, we investigated whether LU could ameliorate hepatic steatosis and affect mitochondrial function in Western diet-fed mice. After LU treatment, the indicators of hepatic function and markers of mitochondrial biogenesis were evaluated. The results showed that LU intervention 1) decreased the levels of serum triglyceride, total cholesterol, alanine aminotransferase, and low-density lipoprotein cholesterol; 2) increased the succinate dehydrogenase activity of mitochondrial enzyme; and 3) increased mitochondrial biogenesis by upregulating the AMPK/PGC-1α pathway. Therefore, LU might have the potential to prevent NAFLD.</p>","PeriodicalId":16624,"journal":{"name":"Journal of nutritional science and vitaminology","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10500895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Thanks to Reviewers.","authors":"","doi":"10.3177/jnsv.69.155","DOIUrl":"https://doi.org/10.3177/jnsv.69.155","url":null,"abstract":"","PeriodicalId":16624,"journal":{"name":"Journal of nutritional science and vitaminology","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9379363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ferulic acid (FA) is the most abundant phenolic acid in wheat grains. Recent studies have reported that FA intake significantly suppresses body weight gain and accumulation of fat deposits in mice. However, the mechanism by which FA intake affects body fat accumulation remains unclear. We hypothesized that dietary FA induces the formation of beige adipocytes and contributes to the suppression of body fat accumulation. In this study, we investigated whether dietary FA significantly induces beige adipocyte formation and thermogenesis in mice. We found that intake of dietary FA (control diet supplemented with 10 g of FA/kg diet) for 4 wk significantly decreased white adipose tissue (WAT) deposits and body weight gain and significantly induced beige adipocyte formation in inguinal WAT (iWAT) in mice. Furthermore, dietary FA specifically induced thermogenesis in iWAT, dependent upon the significant induction of uncoupling protein 1 expression. These findings suggest that the dietary FA-mediated reduction of WAT accumulation and body weight gain is associated with the induction of beige adipocyte formation and thermogenesis in iWAT, which increases energy expenditure. Our study presents a novel example of dietary FA intake-mediated bioactivity as a functional food-derived factor.
{"title":"Dietary Ferulic Acid-Mediated Suppression of Fat Deposits Is Associated with Induction of Beige Adipocyte Formation and Thermogenesis in Inguinal White Adipose Tissue in Mice.","authors":"Junpei Tanaka, Takanori Tsuda","doi":"10.3177/jnsv.69.377","DOIUrl":"10.3177/jnsv.69.377","url":null,"abstract":"<p><p>Ferulic acid (FA) is the most abundant phenolic acid in wheat grains. Recent studies have reported that FA intake significantly suppresses body weight gain and accumulation of fat deposits in mice. However, the mechanism by which FA intake affects body fat accumulation remains unclear. We hypothesized that dietary FA induces the formation of beige adipocytes and contributes to the suppression of body fat accumulation. In this study, we investigated whether dietary FA significantly induces beige adipocyte formation and thermogenesis in mice. We found that intake of dietary FA (control diet supplemented with 10 g of FA/kg diet) for 4 wk significantly decreased white adipose tissue (WAT) deposits and body weight gain and significantly induced beige adipocyte formation in inguinal WAT (iWAT) in mice. Furthermore, dietary FA specifically induced thermogenesis in iWAT, dependent upon the significant induction of uncoupling protein 1 expression. These findings suggest that the dietary FA-mediated reduction of WAT accumulation and body weight gain is associated with the induction of beige adipocyte formation and thermogenesis in iWAT, which increases energy expenditure. Our study presents a novel example of dietary FA intake-mediated bioactivity as a functional food-derived factor.</p>","PeriodicalId":16624,"journal":{"name":"Journal of nutritional science and vitaminology","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71521767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Human serum albumin is categorized into human mercaptalbumin (HMA) and human non-mercaptalbumin (HNA), according to the redox state of the cysteine residue at position 34. The ratio of HMA to total albumin (%HMA) is a novel biomarker of oxidative stress as well as protein nutritional status, but measuring %HMA normally requires an expensive analyzer such as HPLC and LC-MS, and can hardly be conducted in many clinical sites. To address this issue, we aimed to develop a methodological basis for estimating %HMA without these analyzers. An analytical method was investigated consisting of three steps, i.e., 1) removal of HMA from serum or plasma by using a thiol-binding resin (i.e., thereby obtaining a HNA fraction), 2) determination of both total albumin and HNA concentrations by a colorimetric assay or ELISA, and 3) calculation of %HMA. Proof-of-concept experiments, using serum and plasma samples of 4 adult volunteers, showed that the estimated value of %HMA obtained by this analytical method was significantly correlated with the theoretical value of %HMA determined by HPLC. The subsequent validation experiment, using 86 serum samples of pregnant women in the Japanese participants of SMILE Iwamizawa, also confirmed the significant association between the estimated and theoretical values of %HMA. This analytical method can be a basis to determine %HMA without using HPLC or LC-MS, contributing to the universalization of %HMA measurement as a clinical test.
{"title":"A Methodological Basis for Estimating Human Mercaptalbumin in Serum and Plasma Using a Thiol-Binding Resin.","authors":"Fuka Tabata, Yasuaki Wada, Satomi Kawakami, Akiko Tamakoshi, Kazuhiro Miyaji","doi":"10.3177/jnsv.69.340","DOIUrl":"10.3177/jnsv.69.340","url":null,"abstract":"<p><p>Human serum albumin is categorized into human mercaptalbumin (HMA) and human non-mercaptalbumin (HNA), according to the redox state of the cysteine residue at position 34. The ratio of HMA to total albumin (%HMA) is a novel biomarker of oxidative stress as well as protein nutritional status, but measuring %HMA normally requires an expensive analyzer such as HPLC and LC-MS, and can hardly be conducted in many clinical sites. To address this issue, we aimed to develop a methodological basis for estimating %HMA without these analyzers. An analytical method was investigated consisting of three steps, i.e., 1) removal of HMA from serum or plasma by using a thiol-binding resin (i.e., thereby obtaining a HNA fraction), 2) determination of both total albumin and HNA concentrations by a colorimetric assay or ELISA, and 3) calculation of %HMA. Proof-of-concept experiments, using serum and plasma samples of 4 adult volunteers, showed that the estimated value of %HMA obtained by this analytical method was significantly correlated with the theoretical value of %HMA determined by HPLC. The subsequent validation experiment, using 86 serum samples of pregnant women in the Japanese participants of SMILE Iwamizawa, also confirmed the significant association between the estimated and theoretical values of %HMA. This analytical method can be a basis to determine %HMA without using HPLC or LC-MS, contributing to the universalization of %HMA measurement as a clinical test.</p>","PeriodicalId":16624,"journal":{"name":"Journal of nutritional science and vitaminology","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71521853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Niacin is involved in many biological reactions relating energy metabolism, redox reactions, DNA repair and longevity, and low NAD levels with aging and feeding high fat diets develop and progress age-related diseases. Although recent findings suggest the requirement of niacin insufficient animal model to further study, appropriate animal models have not been established yet because niacin is biosynthesized from tryptophan via tryptophan-nicotinamide pathway. To establish model mice to evaluate niacin nutritional status, we used kynurenine 3-monooxygenase knock out (KMO-/-) mice which lack NAD biosynthesis pathway from tryptophan. To determine the niacin requirement and assess niacin nutritional markers, 4 wk old KMO-/- mice were fed 2-30 mg/kg nicotinic acid containing diets for 28 d. More than 4 mg/kg but not less than 3 mg/kg nicotinic acid containing diets induced maximum growth, and niacin nutritional markers in the blood, liver and urine increased with increase of dietary nicotinic acid. These results showed that several niacin nutritional markers reflect niacin nutritional status, niacin nutritional status can be controlled by dietary nicotinic acid, and niacin requirement for maximum growth is 4 mg/kg nicotinic acid diets in the KMO-/- mice. This animal model useful to investigate pathophysiology and mechanism of niacin deficiency, clarify the relationships between niacin nutritional status and age-related and lifestyle diseases, and evaluate factors affecting niacin nutritional status.
{"title":"Establishment of Model Mice to Evaluate Low Niacin Nutritional Status.","authors":"Amane Mizutani, Miu Sato, Hidetsugu Fujigaki, Yasuko Yamamoto, Kuniaki Saito, Sho Hatayama, Tsutomu Fukuwatari","doi":"10.3177/jnsv.69.305","DOIUrl":"10.3177/jnsv.69.305","url":null,"abstract":"<p><p>Niacin is involved in many biological reactions relating energy metabolism, redox reactions, DNA repair and longevity, and low NAD levels with aging and feeding high fat diets develop and progress age-related diseases. Although recent findings suggest the requirement of niacin insufficient animal model to further study, appropriate animal models have not been established yet because niacin is biosynthesized from tryptophan via tryptophan-nicotinamide pathway. To establish model mice to evaluate niacin nutritional status, we used kynurenine 3-monooxygenase knock out (KMO<sup>-/-</sup>) mice which lack NAD biosynthesis pathway from tryptophan. To determine the niacin requirement and assess niacin nutritional markers, 4 wk old KMO<sup>-/-</sup> mice were fed 2-30 mg/kg nicotinic acid containing diets for 28 d. More than 4 mg/kg but not less than 3 mg/kg nicotinic acid containing diets induced maximum growth, and niacin nutritional markers in the blood, liver and urine increased with increase of dietary nicotinic acid. These results showed that several niacin nutritional markers reflect niacin nutritional status, niacin nutritional status can be controlled by dietary nicotinic acid, and niacin requirement for maximum growth is 4 mg/kg nicotinic acid diets in the KMO<sup>-/-</sup> mice. This animal model useful to investigate pathophysiology and mechanism of niacin deficiency, clarify the relationships between niacin nutritional status and age-related and lifestyle diseases, and evaluate factors affecting niacin nutritional status.</p>","PeriodicalId":16624,"journal":{"name":"Journal of nutritional science and vitaminology","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71521770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Contents of Volume 69.","authors":"","doi":"10.3177/jnsv.69.493","DOIUrl":"10.3177/jnsv.69.493","url":null,"abstract":"","PeriodicalId":16624,"journal":{"name":"Journal of nutritional science and vitaminology","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139087284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kana Tadokoro, Masanori Ohta, Yukiko Kakuno, Ayaka Iid, Tsuyoshi Nakamura
Zinc (Zn) deficiency is one of the most common nutritional deficiencies worldwide. It is associated with reduced nutritional status and has been reported in cases of growth retardation, alopecia, and decreased serum alkaline phosphatase (ALP). It has also been reported to occur during total parenteral nutrition (TPN) administration and is associated with various diseases, such as liver diseases, diabetes, and kidney disease. We used Zn-deficient mice of ICR and C57BL/6J strains to investigate the various effects of Zn deficiency on the body, assuming that a healthy person may also become deficient in Zn either due to an unbalanced diet or malabsorption. The results showed that a Zn-deficient diet suppressed body weight gain and increased the tissue weight of the kidneys and cecum in both strains of mice. Biochemical data showed no decrease in serum ALP activity in either strain. Furthermore, in C57BL/6J mice, a Zn-deficient diet caused alopecia, loss of villi in the small intestine, and eventually affected the intestinal mucosa, which could be a risk factor for poor nutritional status. Although previous reports have shown that serum ALP activity is decreased during Zn deficiency, this is the first study that used 4-wk-old mice of ICR and C57BL/6J strains to show that serum ALP activity, which is a Zn deficiency marker, did not decrease in the two strains of Zn-deficient mice; furthermore, a Zn-deficient diet causes various symptoms.
锌(Zn)缺乏症是全球最常见的营养缺乏症之一。锌缺乏与营养状况下降有关,有报道称锌缺乏会导致生长迟缓、脱发和血清碱性磷酸酶(ALP)降低。也有报道称,在全肠外营养(TPN)给药过程中会出现锌缺乏,并与肝脏疾病、糖尿病和肾脏疾病等多种疾病相关。假定健康人也可能因饮食不均衡或吸收不良而导致锌缺乏,我们使用ICR和C57BL/6J品系的锌缺乏小鼠来研究锌缺乏对机体的各种影响。结果显示,缺锌饮食抑制了两种品系小鼠体重的增加,并增加了肾脏和盲肠的组织重量。生化数据显示,两种品系小鼠的血清 ALP 活性都没有降低。此外,在 C57BL/6J 小鼠中,缺锌饮食会导致脱发、小肠绒毛脱落,并最终影响肠粘膜,这可能是营养不良的一个危险因素。虽然以前的报告显示缺锌时血清ALP活性会降低,但这是首次使用4周龄的ICR和C57BL/6J品系小鼠进行的研究,结果表明作为缺锌标志物的血清ALP活性在两种品系的缺锌小鼠中都没有降低;此外,缺锌饮食还会引起各种症状。
{"title":"Effect of Zinc-Deficient Diet on Two Strains of Mice.","authors":"Kana Tadokoro, Masanori Ohta, Yukiko Kakuno, Ayaka Iid, Tsuyoshi Nakamura","doi":"10.3177/jnsv.69.444","DOIUrl":"10.3177/jnsv.69.444","url":null,"abstract":"<p><p>Zinc (Zn) deficiency is one of the most common nutritional deficiencies worldwide. It is associated with reduced nutritional status and has been reported in cases of growth retardation, alopecia, and decreased serum alkaline phosphatase (ALP). It has also been reported to occur during total parenteral nutrition (TPN) administration and is associated with various diseases, such as liver diseases, diabetes, and kidney disease. We used Zn-deficient mice of ICR and C57BL/6J strains to investigate the various effects of Zn deficiency on the body, assuming that a healthy person may also become deficient in Zn either due to an unbalanced diet or malabsorption. The results showed that a Zn-deficient diet suppressed body weight gain and increased the tissue weight of the kidneys and cecum in both strains of mice. Biochemical data showed no decrease in serum ALP activity in either strain. Furthermore, in C57BL/6J mice, a Zn-deficient diet caused alopecia, loss of villi in the small intestine, and eventually affected the intestinal mucosa, which could be a risk factor for poor nutritional status. Although previous reports have shown that serum ALP activity is decreased during Zn deficiency, this is the first study that used 4-wk-old mice of ICR and C57BL/6J strains to show that serum ALP activity, which is a Zn deficiency marker, did not decrease in the two strains of Zn-deficient mice; furthermore, a Zn-deficient diet causes various symptoms.</p>","PeriodicalId":16624,"journal":{"name":"Journal of nutritional science and vitaminology","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139087288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Rat Cyp27b1 was successfully expressed in HepG2 cells using an adenovirus vector. High vitamin D 1α-hydroxylation activity was detected in them, whereas no activity was observed in non-infected cells. Similarly, vitamin D 1α-hydroxylation activity was also observed in HepG2 cells expressing Cyp27b1-Flag, which is tagged with a Flag at the C-terminus of Cyp27b1. Western blot analysis using an anti-Flag antibody showed a clear band of Cyp27b1-Flag. Next, we screened three types of anti-Cyp27b1 antibodies, which consist of two commercially available antibodies and our self-made antibody using Cyp27b1- or Cyp27b1-Flag expressing HepG2 cell lysate as a positive control. Surprisingly, Western blot analysis revealed that two commercially available antibodies did not detect Cyp27b1 but specifically detect other proteins. In contrast, our self-made antisera specifically detected Cyp27b1 and Cyp27b1-Flag in the HepG2 cells expressing Cyp27b1 or Cyp27b1-Flag. These commercially available antibodies have been used for the detection of Cyp27b1 by Western blotting and immunohistochemistry. Our results suggest that those data should be reanalyzed.
{"title":"Expression of Rat Cyp27b1 in HepG2 Cells Using Adenovirus Vector and Its Application to Evaluation of Self-Made and Commercially Available Anti-Cyp27b1 Antibodies.","authors":"Chika Nagao, Satoko Kise, Ayano Iijima, Tadashi Okada, Tomoko Nakanishi, Shigeto Sato, Miyu Nishikawa, Shinchi Ikushiro, Kaori Yasuda, Toshiyuki Sakaki","doi":"10.3177/jnsv.69.90","DOIUrl":"https://doi.org/10.3177/jnsv.69.90","url":null,"abstract":"<p><p>Rat Cyp27b1 was successfully expressed in HepG2 cells using an adenovirus vector. High vitamin D 1α-hydroxylation activity was detected in them, whereas no activity was observed in non-infected cells. Similarly, vitamin D 1α-hydroxylation activity was also observed in HepG2 cells expressing Cyp27b1-Flag, which is tagged with a Flag at the C-terminus of Cyp27b1. Western blot analysis using an anti-Flag antibody showed a clear band of Cyp27b1-Flag. Next, we screened three types of anti-Cyp27b1 antibodies, which consist of two commercially available antibodies and our self-made antibody using Cyp27b1- or Cyp27b1-Flag expressing HepG2 cell lysate as a positive control. Surprisingly, Western blot analysis revealed that two commercially available antibodies did not detect Cyp27b1 but specifically detect other proteins. In contrast, our self-made antisera specifically detected Cyp27b1 and Cyp27b1-Flag in the HepG2 cells expressing Cyp27b1 or Cyp27b1-Flag. These commercially available antibodies have been used for the detection of Cyp27b1 by Western blotting and immunohistochemistry. Our results suggest that those data should be reanalyzed.</p>","PeriodicalId":16624,"journal":{"name":"Journal of nutritional science and vitaminology","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9396780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}