We conducted a retrospective case-control study to assess the efficacy of personalized health guidance interventions on individuals with type 2 diabetes mellitus and obesity. A selection was made of individuals in regular visits to the Takagi Hospital for medical checkups between January 2017, and October 2021. Totally, 108 subjects (cases) with health guidance were divided into 2 groups: one group without pharmacotherapy for diabetes mellitus in medical institutions (n = 92) and another group with pharmacotherapy (n = 116). Cases were provided with personalized health guidance interventions by public health nurses for 30 min, in accordance with the Japanese clinical guidelines for the prevention of lifestyle-related diseases. Sex- and age-matched controls were chosen from individuals with diabetes mellitus without health guidance. The intervention without pharmacotherapy resulted in improvements in health indicators, including body weight, waist circumference, diastolic blood pressure, triglyceride levels, and γ-glutamyl trans-peptidase. These positive effects were not observed in the control group without health guidance. The therapeutic effects of health guidance were observed in cases where pharmacotherapy was administered. In conclusion, the implementation of individual health guidance interventions may prove to be effective for individuals with type 2 diabetes mellitus and obesity who regularly attend medical checkups.
{"title":"Improvement trend for individual health guidance intervention according to Japan clinical guidelines by public health nurses for type 2 diabetes mellitus who visited for medical checkups regularly: a case-control preliminary report.","authors":"Rina Matsuo, Tomohiro Imamura, Ayako Takamori, Takuya Kishi, Miwako Minami, Junko Miyakawa, Natsuki Yoshitake, Ai Hayashi, Yuki Nakayama, Natsumi Egashira, Minako Teramoto, Hiroko Ishinari, Itsuka Kajiyama, Satomi Fujisaki, Hitomi Kakiyama, Kanako Satou, Rei Nakafusa, Chika Tanaka, Megumi Tanaka, Yuki Isomura, Kenichi Izumi, Shoichiro Ohta, Nobuya Souta, Norihito Matsuo, Kyosuke Yamamoto, Sadatoshi Tsuji, Tsukuru Umemura, Kuniyasu Takagi, Kazuma Fujimoto","doi":"10.3164/jcbn.23-52","DOIUrl":"10.3164/jcbn.23-52","url":null,"abstract":"<p><p>We conducted a retrospective case-control study to assess the efficacy of personalized health guidance interventions on individuals with type 2 diabetes mellitus and obesity. A selection was made of individuals in regular visits to the Takagi Hospital for medical checkups between January 2017, and October 2021. Totally, 108 subjects (cases) with health guidance were divided into 2 groups: one group without pharmacotherapy for diabetes mellitus in medical institutions (<i>n</i> = 92) and another group with pharmacotherapy (<i>n</i> = 116). Cases were provided with personalized health guidance interventions by public health nurses for 30 min, in accordance with the Japanese clinical guidelines for the prevention of lifestyle-related diseases. Sex- and age-matched controls were chosen from individuals with diabetes mellitus without health guidance. The intervention without pharmacotherapy resulted in improvements in health indicators, including body weight, waist circumference, diastolic blood pressure, triglyceride levels, and γ-glutamyl trans-peptidase. These positive effects were not observed in the control group without health guidance. The therapeutic effects of health guidance were observed in cases where pharmacotherapy was administered. In conclusion, the implementation of individual health guidance interventions may prove to be effective for individuals with type 2 diabetes mellitus and obesity who regularly attend medical checkups.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"1 1","pages":"141-145"},"PeriodicalIF":2.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10948351/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69361709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01Epub Date: 2023-11-03DOI: 10.3164/jcbn.22-105_Erratum
[This corrects the article DOI: 10.3164/jcbn.22-105.].
[此处更正了文章 DOI:10.3164/jcbn.22-105.]。
{"title":"Erratum.","authors":"","doi":"10.3164/jcbn.22-105_Erratum","DOIUrl":"https://doi.org/10.3164/jcbn.22-105_Erratum","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3164/jcbn.22-105.].</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"74 1","pages":"90"},"PeriodicalIF":2.4,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10822761/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139642236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Reactive oxygen species (ROS) and highly reactive oxygen species (hROS) secreted by leukocytes are crucial to innate immunity; however, they pose a risk of oxidative stress. To monitor their balance in daily health check-ups, optical technologies for the simultaneous measurement of ROS (superoxide radicals) and hROS (hypochlorite ions) that utilize only a few microliters of whole blood have been developed. The aim of this study was to clarify whether this system could assess the effects of fat ingestion on postprandial oxidative status. Eight healthy young Japanese women ingested a beverage containing oral fat tolerance test cream. Blood samples were collected before and 0.5, 1, 2, 4, and 6 h after fat ingestion. Blood ROS and hROS levels, oxidative stress markers, and biochemical markers were monitored. Consistent with previous studies, triglyceride levels significantly increased at 4 h (p<0.01) and returned to near-baseline levels 6 h after ingestion. ROS levels peaked significantly at 2 h (p<0.05), and hROS levels peaked significantly at 1 (p<0.05) and 2 h (p<0.01) after ingestion. This study offers an insight into the acute effects of fat ingestion on leukocyte activity and provides a methodology for monitoring postprandial oxidative status.
{"title":"Effect of fat ingestion on postprandial oxidative status in healthy young women: a pilot study.","authors":"Kozo Takeuchi, Kimiko Kazumura, Kaori Kuzawa, Yukiko Hatano, Masashi Nagai, Michitaka Naito","doi":"10.3164/jcbn.23-50","DOIUrl":"10.3164/jcbn.23-50","url":null,"abstract":"<p><p>Reactive oxygen species (ROS) and highly reactive oxygen species (hROS) secreted by leukocytes are crucial to innate immunity; however, they pose a risk of oxidative stress. To monitor their balance in daily health check-ups, optical technologies for the simultaneous measurement of ROS (superoxide radicals) and hROS (hypochlorite ions) that utilize only a few microliters of whole blood have been developed. The aim of this study was to clarify whether this system could assess the effects of fat ingestion on postprandial oxidative status. Eight healthy young Japanese women ingested a beverage containing oral fat tolerance test cream. Blood samples were collected before and 0.5, 1, 2, 4, and 6 h after fat ingestion. Blood ROS and hROS levels, oxidative stress markers, and biochemical markers were monitored. Consistent with previous studies, triglyceride levels significantly increased at 4 h (<i>p</i><0.01) and returned to near-baseline levels 6 h after ingestion. ROS levels peaked significantly at 2 h (<i>p</i><0.05), and hROS levels peaked significantly at 1 (<i>p</i><0.05) and 2 h (<i>p</i><0.01) after ingestion. This study offers an insight into the acute effects of fat ingestion on leukocyte activity and provides a methodology for monitoring postprandial oxidative status.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"1 1","pages":"30-36"},"PeriodicalIF":2.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10822754/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69361270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vitamin D insufficiency, milder than deficiency, is common, and a risk of various diseases. Since vitamin D exert diverse actions, both skeletal and non-skeletal, its insufficiency is a risk of various diseases including osteoporosis, sarcopenia, cardiovascular disease, cancer, and even mortality. Regarding the association of vitamin D status and disease risk, a marked discrepancy exists between the results from the observational studies and intervention studies, mostly yielding the positive and negative results in the former and latter, respectively. Such inconsistency probably arises from methodological problems, of which the baseline vitamin D status would be the most important. Vitamin D intervention would be effective in the deficient/insufficient subjects, but not in sufficient subjects. Since the elderly subjects, especially the institutionalized people, are mostly vitamin D deficient/insufficient, they are likely to benefit from improvement of vitamin D status. Vitamin insufficiency is a risk of various diseases, and correcting the vitamin status alone would reduce the risk of many diseases, and favorable to avoid the undesirable consequences of polypharmacy in the elderly. Additionally, disease prevention by nutritional improvement is cheap and free from side effects, and suited for the primary prevention of diseases.
维生素 D 不足比缺乏更为常见,也是各种疾病的风险因素之一。由于维生素 D 在骨骼和非骨骼方面具有多种作用,因此维生素 D 不足有可能导致各种疾病,包括骨质疏松症、肌肉疏松症、心血管疾病、癌症,甚至死亡。关于维生素 D 状态与疾病风险的关系,观察性研究和干预性研究的结果存在明显差异,前者和后者的结果大多分别为阳性和阴性。这种不一致可能是由于方法问题造成的,其中最重要的是维生素 D 的基线状况。维生素 D 干预对缺乏/不足的受试者有效,但对充足的受试者无效。由于老年人,尤其是住在养老院的人,大多缺乏维生素 D,因此他们很可能从改善维生素 D 状态中受益。维生素缺乏是多种疾病的风险因素,仅纠正维生素状况就能降低多种疾病的风险,并有利于避免老年人服用多种药物的不良后果。此外,通过改善营养来预防疾病既便宜又无副作用,适用于疾病的初级预防。
{"title":"Vitamin D insufficiency and disease risk in the elderly.","authors":"Kiyoshi Tanaka, Misora Ao, Junko Tamaru, Akiko Kuwabara","doi":"10.3164/jcbn.23-59","DOIUrl":"10.3164/jcbn.23-59","url":null,"abstract":"<p><p>Vitamin D insufficiency, milder than deficiency, is common, and a risk of various diseases. Since vitamin D exert diverse actions, both skeletal and non-skeletal, its insufficiency is a risk of various diseases including osteoporosis, sarcopenia, cardiovascular disease, cancer, and even mortality. Regarding the association of vitamin D status and disease risk, a marked discrepancy exists between the results from the observational studies and intervention studies, mostly yielding the positive and negative results in the former and latter, respectively. Such inconsistency probably arises from methodological problems, of which the baseline vitamin D status would be the most important. Vitamin D intervention would be effective in the deficient/insufficient subjects, but not in sufficient subjects. Since the elderly subjects, especially the institutionalized people, are mostly vitamin D deficient/insufficient, they are likely to benefit from improvement of vitamin D status. Vitamin insufficiency is a risk of various diseases, and correcting the vitamin status alone would reduce the risk of many diseases, and favorable to avoid the undesirable consequences of polypharmacy in the elderly. Additionally, disease prevention by nutritional improvement is cheap and free from side effects, and suited for the primary prevention of diseases.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"1 1","pages":"9-16"},"PeriodicalIF":2.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10822750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69361803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Quercetin is a natural flavonol and has various health beneficial functions. Our pervious study demonstrated that long-term feeding (13 weeks) of quercetin and its glycosides, isoquercitrin, rutin, and enzymatically modified isoquercitrin, which is a mixture of quercetin monoglycoside and its oligoglycosides, prevented hyperglycemia and adiposity in mice fed a high-fat diet but not standard diet. It is, however, unclear whether a single administration of these compounds prevent postprandial hyperglycemia or not. In the present study, we estimated their prevention effect on acute hyperglycemia by an oral glucose tolerance test in ICR mice and investigated its mechanism. It was found that quercetin glycosides, but not the aglycone, suppressed acute hyperglycemia and isoquercitrin showed the strongest effect among the glycosides. As the underlying mechanism, quercetin glycosides promoted translocation of glucose transporter 4 to the plasma membrane of skeletal muscle of mice through phosphorylation of adenosine monophosphate-activated protein kinase and its upstream Ca2+/calmodulin-dependent protein kinase kinase β without activating the insulin- and JAK/STAT-signal pathways. In conclusion, single oral administration of quercetin glycosides prevented a blood sugar spike by promoting glucose transporter 4 translocation through activating the CAMKKβ/AMPK signaling pathway.
{"title":"Single oral administration of quercetin glycosides prevented acute hyperglycemia by promoting GLUT4 translocation in skeletal muscles through the activation of AMPK in mice.","authors":"Yoko Yamashita, Hao Jiang, Fukiko Okada, Tomoya Kitakaze, Yasukiyo Yoshioka, Hitoshi Ashida","doi":"10.3164/jcbn.23-30","DOIUrl":"10.3164/jcbn.23-30","url":null,"abstract":"<p><p>Quercetin is a natural flavonol and has various health beneficial functions. Our pervious study demonstrated that long-term feeding (13 weeks) of quercetin and its glycosides, isoquercitrin, rutin, and enzymatically modified isoquercitrin, which is a mixture of quercetin monoglycoside and its oligoglycosides, prevented hyperglycemia and adiposity in mice fed a high-fat diet but not standard diet. It is, however, unclear whether a single administration of these compounds prevent postprandial hyperglycemia or not. In the present study, we estimated their prevention effect on acute hyperglycemia by an oral glucose tolerance test in ICR mice and investigated its mechanism. It was found that quercetin glycosides, but not the aglycone, suppressed acute hyperglycemia and isoquercitrin showed the strongest effect among the glycosides. As the underlying mechanism, quercetin glycosides promoted translocation of glucose transporter 4 to the plasma membrane of skeletal muscle of mice through phosphorylation of adenosine monophosphate-activated protein kinase and its upstream Ca<sup>2+</sup>/calmodulin-dependent protein kinase kinase β without activating the insulin- and JAK/STAT-signal pathways. In conclusion, single oral administration of quercetin glycosides prevented a blood sugar spike by promoting glucose transporter 4 translocation through activating the CAMKKβ/AMPK signaling pathway.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"1 1","pages":"37-46"},"PeriodicalIF":2.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10822753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69361553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The impact of nutrition therapy in the acute phase on post-intensive care syndrome (PICS) remains unclear. We conducted a multicenter prospective study on adult patients with COVID-19 who required mechanical ventilation for more than three days. The questionnaire was mailed after discharge. Physical PICS, defined as less than 90 points on the Barthel index (BI), was assigned as the primary outcome. We examined the types of nutrition therapy in the first week that affected PICS components. 269 eligible patients were evaluated 10 months after discharge. Supplemental parenteral nutrition (SPN) >400 kcal/day correlated with a lower occurrence of physical PICS (10% vs 21.92%, p = 0.042), whereas the amounts of energy and protein provided, early enteral nutrition, and a gradual increase in nutrition delivery did not, and none correlated with cognitive or mental PICS. A multivariable regression analysis revealed that SPN had an independent impact on physical PICS (odds ratio 0.33, 95% CI 0.12-0.92, p = 0.034), even after adjustments for age, sex, body mass index and severity. Protein provision ≥1.2 g/kg/day was associated with a lower occurrence of physical PICS (odds ratio 0.42, 95% CI 0.16-1.08, p = 0.071). In conclusion, SPN in the acute phase had a positive impact on physical PICS for ventilated patients with COVID-19.
{"title":"Relationship between critical care nutrition and post-intensive care syndrome in surviving ventilated patients with COVID-19: a multicenter prospective observational study.","authors":"Kensuke Nakamura, Junji Hatakeyama, Keibun Liu, Kazuma Yamakawa, Takeshi Nishida, Shinichiro Ohshimo, Shigeaki Inoue, Satoru Hashimoto, Shuhei Maruyama, Daisuke Kawakami, Yoshitaka Ogata, Katsura Hayakawa, Hiroaki Shimizu, Taku Oshima, Tatsuya Fuchigami, Osamu Nishida","doi":"10.3164/jcbn.23-66","DOIUrl":"10.3164/jcbn.23-66","url":null,"abstract":"<p><p>The impact of nutrition therapy in the acute phase on post-intensive care syndrome (PICS) remains unclear. We conducted a multicenter prospective study on adult patients with COVID-19 who required mechanical ventilation for more than three days. The questionnaire was mailed after discharge. Physical PICS, defined as less than 90 points on the Barthel index (BI), was assigned as the primary outcome. We examined the types of nutrition therapy in the first week that affected PICS components. 269 eligible patients were evaluated 10 months after discharge. Supplemental parenteral nutrition (SPN) >400 kcal/day correlated with a lower occurrence of physical PICS (10% vs 21.92%, <i>p</i> = 0.042), whereas the amounts of energy and protein provided, early enteral nutrition, and a gradual increase in nutrition delivery did not, and none correlated with cognitive or mental PICS. A multivariable regression analysis revealed that SPN had an independent impact on physical PICS (odds ratio 0.33, 95% CI 0.12-0.92, <i>p</i> = 0.034), even after adjustments for age, sex, body mass index and severity. Protein provision ≥1.2 g/kg/day was associated with a lower occurrence of physical PICS (odds ratio 0.42, 95% CI 0.16-1.08, <i>p</i> = 0.071). In conclusion, SPN in the acute phase had a positive impact on physical PICS for ventilated patients with COVID-19.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"1 1","pages":"74-81"},"PeriodicalIF":2.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10822758/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69361807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Simplifying the diagnostic criteria for sarcopenia is key to establishing effective interventions. Herein, we aimed to clarify novel diagnostic factors. We calculated novel fat indices [total fat index (TFI) and limb fat index (LFI)] and clarified factors leading to pre-sarcopenia and sarcopenia in 594 enrolled older adults. Physical measurements [height, weight, body mass index (BMI), gait speed, grip strength, and skeletal muscle mass] were performed. Sarcopenia was determined using established diagnostic criteria (pre-sarcopenia, n = 102; sarcopenia, n = 42). Age was associated with sarcopenia status. BMI, TFI, and LFI were lower in patients with pre-sarcopenia and sarcopenia. Logistic regression analysis showed the following odds ratios (ORs) for pre-sarcopenia: BMI [OR: 0.787, 95% confidence interval (CI): 0.7-0.885], LFI (OR: 0.589, 95% CI: 0.402-0.863), and age (OR: 1.06, 95% CI: 1.02-1.1). ORs for sarcopenia (vs pre-sarcopenia) were as follows: LFI (OR: 50.6, 95% CI: 10.2-250.0), age (OR: 1.1, 95% CI: 1.0-1.2), and BMI (OR: 0.418, 95% CI: 0.28-0.608). Our findings contribute to informing medical guidelines.
{"title":"The role of fat indices as factors leading to sarcopenia in older adults residing in underpopulated areas.","authors":"Yasutaka Mizukami, Hidenori Onishi, Yuta Mifuku, Masafumi Kubota, Ryouko Ikeda, Hiroyuki Hayashi, Osamu Yamamura","doi":"10.3164/jcbn.23-33","DOIUrl":"10.3164/jcbn.23-33","url":null,"abstract":"<p><p>Simplifying the diagnostic criteria for sarcopenia is key to establishing effective interventions. Herein, we aimed to clarify novel diagnostic factors. We calculated novel fat indices [total fat index (TFI) and limb fat index (LFI)] and clarified factors leading to pre-sarcopenia and sarcopenia in 594 enrolled older adults. Physical measurements [height, weight, body mass index (BMI), gait speed, grip strength, and skeletal muscle mass] were performed. Sarcopenia was determined using established diagnostic criteria (pre-sarcopenia, <i>n</i> = 102; sarcopenia, <i>n</i> = 42). Age was associated with sarcopenia status. BMI, TFI, and LFI were lower in patients with pre-sarcopenia and sarcopenia. Logistic regression analysis showed the following odds ratios (ORs) for pre-sarcopenia: BMI [OR: 0.787, 95% confidence interval (CI): 0.7-0.885], LFI (OR: 0.589, 95% CI: 0.402-0.863), and age (OR: 1.06, 95% CI: 1.02-1.1). ORs for sarcopenia (vs pre-sarcopenia) were as follows: LFI (OR: 50.6, 95% CI: 10.2-250.0), age (OR: 1.1, 95% CI: 1.0-1.2), and BMI (OR: 0.418, 95% CI: 0.28-0.608). Our findings contribute to informing medical guidelines.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"1 1","pages":"70-73"},"PeriodicalIF":2.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10822752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69361178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This study investigated the effects of miso, a traditional fermented soybean food in Japan, on muscle mass atrophy. Eight week old male C57BL/6J mice were fed high fat/high sucrose diet with or without miso for 12 weeks. A miso diet increased soleus muscle weights (p<0.05) and reduced intraperitoneal glucose tolerance and insulin tolerance (p<0.05). The miso diet downregulated the Tnfα and Ccl2 expression, related to inflammation, and Trim63 and Fbxo32 expression, related to muscle atrophy, in the soleus muscle (p<0.05). The miso diet increased short-chain fatty acids levels, including acetic, propanoic, and butanoic acids, in the feces, serum, and soleus muscle (p<0.05). According to the LEfSe analysis, the miso diet increased family Prevotellaceae, family Christensenellaceae, family Dehalobacterium, family Desulfitibacter; family Deferribacteraceae, order Deferribacterales, class Deferribacteres; and family Gemmatimonadaceae, order Gemmatimonadetes, and class Gemmatimonadales, whereas the miso diet decreased family Microbacteriaceae, order Micrococcales, class Actinobacteria, and family Lactobacillaceae. Miso suppressed high fat/high sucrose diet induced impaired glucose tolerance, low muscle strength, and muscle atrophy by improving dysbiosis and increasing short-chain fatty acids production and provides new insights into the preventive effects of fermented foods on sarcopenia.
{"title":"Miso, fermented soybean paste, suppresses high-fat/high-sucrose diet-induced muscle atrophy in mice.","authors":"Yoshitaka Hashimoto, Takuro Okamura, Ryo Bamba, Yuta Yoshimura, Chihiro Munekawa, Ayumi Kaji, Akane Miki, Saori Majima, Takafumi Senmaru, Emi Ushigome, Hiroshi Takakuwa, Ryoichi Sasano, Naoko Nakanishi, Masahide Hamaguchi, Michiaki Fukui","doi":"10.3164/jcbn.23-36","DOIUrl":"10.3164/jcbn.23-36","url":null,"abstract":"<p><p>This study investigated the effects of miso, a traditional fermented soybean food in Japan, on muscle mass atrophy. Eight week old male C57BL/6J mice were fed high fat/high sucrose diet with or without miso for 12 weeks. A miso diet increased soleus muscle weights (<i>p</i><0.05) and reduced intraperitoneal glucose tolerance and insulin tolerance (<i>p</i><0.05). The miso diet downregulated the Tnfα and Ccl2 expression, related to inflammation, and Trim63 and Fbxo32 expression, related to muscle atrophy, in the soleus muscle (<i>p</i><0.05). The miso diet increased short-chain fatty acids levels, including acetic, propanoic, and butanoic acids, in the feces, serum, and soleus muscle (<i>p</i><0.05). According to the LEfSe analysis, the miso diet increased family Prevotellaceae, family Christensenellaceae, family Dehalobacterium, family Desulfitibacter; family Deferribacteraceae, order Deferribacterales, class Deferribacteres; and family Gemmatimonadaceae, order Gemmatimonadetes, and class Gemmatimonadales, whereas the miso diet decreased family Microbacteriaceae, order Micrococcales, class Actinobacteria, and family Lactobacillaceae. Miso suppressed high fat/high sucrose diet induced impaired glucose tolerance, low muscle strength, and muscle atrophy by improving dysbiosis and increasing short-chain fatty acids production and provides new insights into the preventive effects of fermented foods on sarcopenia.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"1 1","pages":"63-69"},"PeriodicalIF":2.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10822755/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69361194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-11-01Epub Date: 2023-08-18DOI: 10.3164/jcbn.22-122
Junfang Wu, Shumei Yang, Hua Wu, Yongcheng Huang, Yi Miao
Leucine-rich repeat kinase 2 (LRRK2) plays an important role in a variety of inflammatory diseases, as well as peripheral and central immune responses. At present, there are few reports about the role of LRRK2 in lung cancer, and need to be further explored. The main purpose of this study is to explore the role and mechanism of LRRK2 in lung cancer. The results revealed that the expression of LRRK2 was increased in the tissues of lung cancer patient and lung cancer cells. Further studies found that interference with LRRK2 expression significantly induced the apoptosis, and promoted the expression of caspase-3, caspase-9, and Bax. More importantly, si-LRRK2 inhibited the expression of VEGF and P-gp, indicating inhibition of cell proliferation and drug resistance. What's more, LRRK2 regulated TLR4/NF-κB signaling pathways and NLRP3 inflammasome, and TLR4/NF-κB pathways was involved in the molecular mechanism of LRRK2 on lung cancer cells. In conclusion, this study suggested that the mechanism of si-LRRK2 inhibiting the progression of lung cancer is to regulate the TLR4/NF-κB signaling pathways and NLRP3 inflammasome.
{"title":"Knockdown of LRRK2 inhibits the progression of lung cancer by regulating TLR4/NF-κB pathways and NLRP3 inflammasome.","authors":"Junfang Wu, Shumei Yang, Hua Wu, Yongcheng Huang, Yi Miao","doi":"10.3164/jcbn.22-122","DOIUrl":"10.3164/jcbn.22-122","url":null,"abstract":"<p><p>Leucine-rich repeat kinase 2 (LRRK2) plays an important role in a variety of inflammatory diseases, as well as peripheral and central immune responses. At present, there are few reports about the role of LRRK2 in lung cancer, and need to be further explored. The main purpose of this study is to explore the role and mechanism of LRRK2 in lung cancer. The results revealed that the expression of LRRK2 was increased in the tissues of lung cancer patient and lung cancer cells. Further studies found that interference with LRRK2 expression significantly induced the apoptosis, and promoted the expression of caspase-3, caspase-9, and Bax. More importantly, si-LRRK2 inhibited the expression of VEGF and P-gp, indicating inhibition of cell proliferation and drug resistance. What's more, LRRK2 regulated TLR4/NF-κB signaling pathways and NLRP3 inflammasome, and TLR4/NF-κB pathways was involved in the molecular mechanism of LRRK2 on lung cancer cells. In conclusion, this study suggested that the mechanism of si-LRRK2 inhibiting the progression of lung cancer is to regulate the TLR4/NF-κB signaling pathways and NLRP3 inflammasome.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"1 1","pages":"178-184"},"PeriodicalIF":2.4,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10636582/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69360703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-11-01Epub Date: 2023-08-09DOI: 10.3164/jcbn.23-2
David Julian Arias-Chávez, Patrick Mailloux-Salinas, Jessica Ledesma Aparicio, Guadalupe Bravo, Norma Leticia Gómez-Viquez
Obesity increases the risk of arterial hypertension in young adults and favors an early-onset cardiomyopathy by generating oxidative stress. In this sense, indiscriminate consumption of sucrose and fructose sweetened beverages from early ages causes obesity, however its consequences on the heart when there is a genetic predisposition to develop hypertension are not clear. We compared the effects of sucrose, fructose, and their combination in weanling male spontaneously hypertensive rats to determine the relationship between genetic hypertension, obesity, and consumption of these sugars on the degree of cardiac hypertrophy, oxidative stress and Ca2+/calmodulin dependent protein kinase II delta oxidation. Histological, biochemical, and Western blot studies were performed 12 weeks after treatment initiation. We found that chronic consumption of sucrose or fructose leads to obesity, exacerbates genetic arterial hypertension-induced metabolic alterations, and increases cardiac oxidative stress, Ca2+/calmodulin dependent protein kinase II delta oxidation and cardiac hypertrophy. Nonetheless, when sucrose and fructose are consumed together, metabolic alterations worsen and are accompanied by dilated cardiomyopathy. These data suggest that sucrose and fructose combined consumption starting from maternal weaning in rats with genetic predisposition to arterial hypertension accelerates the progression of cardiomyopathy resulting in an early dilated cardiomyopathy.
{"title":"Combined fructose and sucrose consumption from an early age aggravates cardiac oxidative damage and causes a dilated cardiomyopathy in SHR rats.","authors":"David Julian Arias-Chávez, Patrick Mailloux-Salinas, Jessica Ledesma Aparicio, Guadalupe Bravo, Norma Leticia Gómez-Viquez","doi":"10.3164/jcbn.23-2","DOIUrl":"10.3164/jcbn.23-2","url":null,"abstract":"<p><p>Obesity increases the risk of arterial hypertension in young adults and favors an early-onset cardiomyopathy by generating oxidative stress. In this sense, indiscriminate consumption of sucrose and fructose sweetened beverages from early ages causes obesity, however its consequences on the heart when there is a genetic predisposition to develop hypertension are not clear. We compared the effects of sucrose, fructose, and their combination in weanling male spontaneously hypertensive rats to determine the relationship between genetic hypertension, obesity, and consumption of these sugars on the degree of cardiac hypertrophy, oxidative stress and Ca<sup>2+</sup>/calmodulin dependent protein kinase II delta oxidation. Histological, biochemical, and Western blot studies were performed 12 weeks after treatment initiation. We found that chronic consumption of sucrose or fructose leads to obesity, exacerbates genetic arterial hypertension-induced metabolic alterations, and increases cardiac oxidative stress, Ca<sup>2+</sup>/calmodulin dependent protein kinase II delta oxidation and cardiac hypertrophy. Nonetheless, when sucrose and fructose are consumed together, metabolic alterations worsen and are accompanied by dilated cardiomyopathy. These data suggest that sucrose and fructose combined consumption starting from maternal weaning in rats with genetic predisposition to arterial hypertension accelerates the progression of cardiomyopathy resulting in an early dilated cardiomyopathy.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"1 1","pages":"205-213"},"PeriodicalIF":2.4,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10636576/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69361455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}