Journal of Nutritional Biochemistry最新文献

{"title":"Association between flavonoid intake and rheumatoid arthritis among US adults","authors":"Yan Chen ,&nbsp;Haoxian Tang ,&nbsp;Nan Luo ,&nbsp;Xiaoqing Liang ,&nbsp;Penchao Yang ,&nbsp;Xuan Zhang ,&nbsp;Jingtao Huang ,&nbsp;Qinglong Yang ,&nbsp;Shuxin Huang ,&nbsp;Ling Lin","doi":"10.1016/j.jnutbio.2024.109673","DOIUrl":"10.1016/j.jnutbio.2024.109673","url":null,"abstract":"<div><p>Basic research shows that flavonoids have anti-inflammatory effects that influence rheumatoid arthritis (RA) in rats. Investigating potential dietary interventions for RA helps prevent the onset and progression of the disease. Clinical evidence on the association of flavonoid and subclass intake with RA is lacking. Using three survey cycles of 2007–2008, 2009–2010, and 2017–2018 from the National Health and Nutrition Survey and the United States Department of Agriculture's Food and Nutrient Database for Dietary Studies (FNDDS), we analyzed 7,419 American adults (≥20 years old). The values of flavonoid and subclass intake were calculated using FNDDS. The status questions for self-reported RA were from the NHANES codebook. Weighted analyses, revealed that among the 7,419 participants included in this study (mean age of 44.69 years [standard error, 0.40] and 3,584 [48.31%] were female), 408 met the classification criteria for RA. According to the multivariable logistic regression model, compared with the risk of RA in the first quartile (Q1), the risks of RA in the second quartile (Q2), the third quartile (Q3) and the fourth quartile (Q4) were lower (Q2: OR=0.55, 95% CI: 0.38–0.80; Q3: OR=0.66, 95% CI: 0.44–0.97; Q4: OR=0.64, 95% CI: 0.46–0.89; trend: <em>P</em>=.03). The association between total flavonoids and RA remained significant after full consideration of confounding factors. With regard to the subclasses of flavonoids, high flavanones intake was associated with low RA prevalence in Model 3 (Q3: OR= 0.60, 95% CI:0.39–0.92; Q4: OR = 0.56, 95% CI: 0.32–0.99, trend: <em>P</em>=.02), but no such association was found in the other subclasses. Total flavonoids intake protected against RA, and the risk of developing RA decreased significantly with increasing intake of total flavonoids. Total flavonoids and flavanones were significantly associated with reduced RA risk for the American adult population. We highlighted the importance of employing diverse methodologies to assess the health effects of flavonoids.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141310883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects and mechanisms of sciadonic acid on colonic transit function through regulating 5-HT4/cAMP/PKA/AQP4 signaling pathway in STC model mice","authors":"Zhuoli Yu ,&nbsp;Lalai Zikela ,&nbsp;Dingli Wang ,&nbsp;Xuezhu Wang ,&nbsp;Huilin Zhu ,&nbsp;Songtao Li ,&nbsp;Qiang Han","doi":"10.1016/j.jnutbio.2024.109676","DOIUrl":"10.1016/j.jnutbio.2024.109676","url":null,"abstract":"<div><p><em>Torreya grandis</em> (<em>T. grandis</em>) oil has been reported to alleviate symptoms of slow transit constipation (STC). However, the impact of sciadonic acid (SA), a distinctive fatty acid found in <em>T. grandis</em> oil, on the pathological progression of STC remains unclear. This study aimed to evaluate the effect of SA on STC and uncover the underlying mechanisms. The STC model was established by feeding Balb/c mice with loperamide. After 2 weeks of intervention, SA significantly improved weight loss and intestinal motility decline induced by STC, along with enhancing plasma indices and reducing colon pathological damage. SA effectively reversed the STC-induced decrease in the 5-HT4/cAMP/PKA/AQP4 signaling pathway genes and expression. Furthermore, 16S rRNA analysis demonstrated that SA mitigated the imbalance of the intestinal microbiota induced by STC, by reducing the ratio of <em>Firmicutes</em> to <em>Bacteroidetes</em> (F/B) and increasing the abundance of beneficial bacteria such as <em>Akkermansia</em>. In conclusion, SA intervention alleviated colonic dysfunction in STC mice. The activation of the SA-mediated 5-HT4/cAMP/PKA/AQP4 signaling pathway may serve as a potential target for STC treatment. These findings suggest that SA holds promise as a treatment option for STC and could potentially be extended to other related gut diseases for further investigation.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141293495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibiting mitochondrial citrate shuttling induces hepatic triglyceride deposition in Nile tilapia (Oreochromis niloticus) through lipid anabolic remodeling","authors":"Jun-Xian Wang ,&nbsp;Yuan Luo ,&nbsp;Samwel Mchele Limbu ,&nbsp;Yu-Cheng Qian ,&nbsp;Yan-Yu Zhang ,&nbsp;Rui-Xin Li ,&nbsp;Wen-Hao Zhou ,&nbsp;Fang Qiao ,&nbsp;Li-Qiao Chen ,&nbsp;Mei-Ling Zhang ,&nbsp;Zhen-Yu Du","doi":"10.1016/j.jnutbio.2024.109678","DOIUrl":"10.1016/j.jnutbio.2024.109678","url":null,"abstract":"<div><p>The solute carrier family 25 member 1 (Slc25a1)-dependent mitochondrial citrate shuttle is responsible for exporting citrate from the mitochondria to the cytoplasm for supporting lipid biosynthesis and protein acetylation. Previous studies on Slc25a1 concentrated on pathological models. However, the importance of Slc25a1 in maintaining metabolic homeostasis under normal nutritional conditions remains poorly understood. Here, we investigated the mechanism of mitochondrial citrate shuttle in maintaining lipid metabolism homeostasis in male Nile tilapia (<em>Oreochromis niloticus</em>). To achieve the objective, we blocked the mitochondrial citrate shuttle by inhibiting Slc25a1 under normal nutritional conditions. Slc25a1 inhibition was established by feeding Nile tilapia with 250 mg/kg 1,2,3-benzenetricarboxylic acid hydrate for 6 weeks or intraperitoneal injecting them with dsRNA to knockdown <em>slc25a1b</em> for 7 days. The Nile tilapia with Slc25a1 inhibition exhibited an obesity-like phenotype accompanied by fat deposition, liver damage and hyperglycemia. Moreover, Slc25a1 inhibition decreased hepatic citrate-derived acetyl-CoA, but increased hepatic triglyceride levels. Furthermore, Slc25a1 inhibition replenished cytoplasmic acetyl-CoA through enhanced acetate pathway, which led to hepatic triglycerides accumulation. However, acetate-derived acetyl-CoA caused by hepatic Slc25a1 inhibition did not activate <em>de novo</em> lipogenesis, but rather modified protein acetylation. In addition, hepatic Slc25a1 inhibition enhanced fatty acids esterification through acetate-derived acetyl-CoA, which increased Lipin1 acetylation and its protein stability. Collectively, our results illustrate that inhibiting mitochondrial citrate shuttle triggers lipid anabolic remodeling and results in lipid accumulation, indicating the importance of mitochondrial citrate shuttle in maintaining lipid metabolism homeostasis.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141283964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gallic acid attenuates murine ulcerative colitis by promoting group 3 innate lymphocytes, affecting gut microbiota, and bile acid metabolism","authors":"Yun Leng ,&nbsp;Xiao Zhang ,&nbsp;Qian Zhang,&nbsp;Jiaxuan Xia,&nbsp;Yuefeng Zhang,&nbsp;Chong Ma,&nbsp;Kun Liu,&nbsp;Hao Li,&nbsp;Yanjun Hong,&nbsp;Zhiyong Xie","doi":"10.1016/j.jnutbio.2024.109677","DOIUrl":"10.1016/j.jnutbio.2024.109677","url":null,"abstract":"<div><p>Gallic acid (GA), a plant phenol that is widely distributed in fruits and vegetables, and exhibits a protective role against ulcerative colitis (UC). UC is an inflammatory disease characterized by immune response disorders. However, the role and mechanism of action of GA in gut immunity remain unknown. Here, we observed that GA treatment improved enteritis symptoms, decreased the concentrations of cytokines TNF-α, IFN-γ, IL-6, IL-17A, and IL-23, increased the concentrations of cytokines IL-10, TGF-β and IL-22, and increased the proportion of group 3 innate lymphoid cells (ILC3) in mesenteric lymph nodes and lamina propria. However, GA did not upregulate ILC3 or impair UC in antibody-treated sterile mice. Notably, transplantation of fecal bacteria derived from GA-treated UC mice, instead of UC mice, increased ILC3 levels. Therefore, we analyzed the gut microbiota and related metabolites to elucidate the mechanism promoting ILC3. We determined that GA treatment altered the diversity of the gut microbiota and activated the bile acid (BA) metabolic pathway. We evaluated three BAs, namely, UDCA, isoalloLCA, and 3-oxoLCA that were significantly upregulated after GA treatment, improved UC symptoms, and elevated the proportion of ILC3 <em>in vivo</em> and <em>in vitro</em>. Collectively, these data indicate that GA attenuates UC by elevating ILC3 proportion, regulating the gut microbiota, and impacting BA metabolism. Additionally, we highlight the modulatory effects of BAs on ILC3 for the first time. Our findings provide novel insights into the multiple roles of GA in alleviating UC and provide a mechanistic explanation that supports the dietary nutrition in UC therapy.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141283901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA MALAT1-miR-339-5p-NIS axis is involved in the increased level of thyroid stimulating hormone (TSH) induced by combined exposure of high iodine and hyperlipidemia","authors":"Jinyin Yao ,&nbsp;Chunpeng Lv ,&nbsp;Peng Liu ,&nbsp;Lijun Fan ,&nbsp;Zhiwei Zhang ,&nbsp;Yi Chen ,&nbsp;Xianglan Chen ,&nbsp;Xiaodan Zhang ,&nbsp;Chunyu Zhang ,&nbsp;Jinyu Li ,&nbsp;Xuesong Wang ,&nbsp;Wen Jiang ,&nbsp;Jianxin Niu ,&nbsp;Feng Song ,&nbsp;Wei Zhang ,&nbsp;Dianjun Sun","doi":"10.1016/j.jnutbio.2024.109672","DOIUrl":"10.1016/j.jnutbio.2024.109672","url":null,"abstract":"<div><p>Hypothyroidism and subclinical hypothyroidism were both characterized by elevated levels of thyroid stimulating hormone (TSH). Previous studies had found that high iodine or hyperlipidemia alone was associated with increased TSH level. However, their combined effects on TSH have not been elucidated. In this study, combination of high iodine and hyperlipidemia was established through the combined exposure of high-water iodine and high fat diet in Wistar rats. The results showed that combined exposure of high iodine and high fat can induce higher TSH level. The mRNA and protein levels of sodium iodide transporters (NIS) and type 1 deiodinase (D1) in thyroid tissues, which were crucial genes in the synthesis of thyroid hormones, decreased remarkably in combined exposure group. Mechanistically, down-regulated long non-coding RNA (lncRNA) metastasis associated in lung denocarcinoma transcript 1 (MALAT1) may regulate the expression of NIS by increasing miR-339-5p, and regulating D1 by increasing miR-224-5p. Then, the above findings were explored in subjects exposed to high water iodine and hyperlipidemia. The results indicated that in population combined with high iodine and hyperlipidemia, TSH level increased to higher level and lncRNA MALAT1-miR-339-5p-NIS axis was obviously activated. Collectively, this study found that combined exposure of high iodine and hyperlipidemia induced a higher level of TSH, and lncRNA MALAT1-miR-339-5p-NIS axis may play important role.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141186552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Citrulline supplementation exacerbates sepsis severity in infected preterm piglets via early induced immunosuppression","authors":"Jingren Zhong ,&nbsp;Sebastian Høj Johansen ,&nbsp;Ole Bæk ,&nbsp;Duc Ninh Nguyen","doi":"10.1016/j.jnutbio.2024.109674","DOIUrl":"10.1016/j.jnutbio.2024.109674","url":null,"abstract":"<div><p>Arginine (ARG)/Citrulline (CIT) deficiency is associated with increased sepsis severity after infection. Supplementation of CIT to susceptible patients with ARG/CIT deficiency such as preterm newborns with suspected infection might prevent sepsis, via maintaining immune and vascular function. Caesarean-delivered, parenterally nourished preterm pigs were treated with CIT (1g/kg bodyweight) via oral or continuous intravenous supplementation, then inoculated with live <em>Staphylococcus epidermidis</em> and clinically monitored for 14 h. Blood, liver, and spleen samples were collected for analysis. <em>In vitro</em> cord blood stimulation was performed to explore how CIT and ARG affect premature blood cell responses. After infection, oral CIT supplementation led to higher mortality, increased blood bacterial load, and systemic and hepatic inflammation. Intravenous CIT administration showed increased inflammation and bacterial burdens without significantly affecting mortality. Liver transcriptomics and data from <em>in vitro</em> blood stimulation indicated that CIT induces systemic immunosuppression in preterm newborns, which may impair resistance response to bacteria at the early stage of infection, subsequently causing later uncontrollable inflammation and tissue damage. The early stage of CIT supplementation exacerbates sepsis severity in infected preterm pigs, likely via inducing systemic immunosuppression.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0955286324001074/pdfft?md5=621ed60d5683bfa85e879fe7ff215c28&pid=1-s2.0-S0955286324001074-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141200188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pomegranate (Punica granatum L.) phytochemicals target the components of metabolic syndrome","authors":"Lucas Fornari Laurindo ,&nbsp;Victória Dogani Rodrigues ,&nbsp;Giulia Minniti ,&nbsp;Antonelly Cassio Alves de Carvalho ,&nbsp;Tereza Laís Menegucci Zutin ,&nbsp;Lindsay K. DeLiberto ,&nbsp;Anupam Bishayee ,&nbsp;Sandra Maria Barbalho","doi":"10.1016/j.jnutbio.2024.109670","DOIUrl":"10.1016/j.jnutbio.2024.109670","url":null,"abstract":"<div><p>Pomegranate <em>(Punica granatum</em> L.) is a multipurpose dietary and medicinal plant known for its ability to promote various health benefits. Metabolic syndrome (MetS) is a complex metabolic disorder driving health and socioeconomic challenges worldwide. It may be characterized by insulin resistance, abdominal obesity, hypertension, and dyslipidemia. This study aims to conduct a review of pomegranate's effects on MetS parameters using a mechanistic approach relying on pre-clinical studies. The peel, juice, roots, bark, seeds, flowers, and leaves of the fruit present several bioactive compounds that are related mainly to anti-inflammatory and antioxidant activities as well as cardioprotective, antidiabetic, and antiobesity effects. The use of the juice extract can work as a potent inhibitor of angiotensin-converting enzyme activities, consequently regulating blood pressure. The major bioactive compounds found within the fruit are phenolic compounds (hydrolysable tannins and flavonoids) and fatty acids. Alkaloids, punicalagin, ellagitannins, ellagic acid, anthocyanins, tannins, flavonoids, luteolin, and punicic acid are also present. The antihyperglycemia, antihyperlipidemia, and weight loss promoting effects are likely related to the anti-inflammatory and antioxidant effects. When considering clinical application, pomegranate extracts are found to be frequently well-tolerated, further supporting its efficacy as a treatment modality. We suggest that pomegranate fruit, extract, or processed products can be used to counteract MetS-related risk factors. This review represents an important step towards exploring potential avenues for further research in this area.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141070929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Approaches to nutritional research using organoids; fructose treatment induces epigenetic changes in liver organoids","authors":"Mirai Yamazaki ,&nbsp;Hiroya Yamada ,&nbsp;Eiji Munetsuna ,&nbsp;Yoshitaka Ando ,&nbsp;Genki Mizuno ,&nbsp;Atsushi Teshigawara ,&nbsp;Hayato Ichikawa ,&nbsp;Yuki Nouchi ,&nbsp;Itsuki Kageyama ,&nbsp;Takuya Wakasugi ,&nbsp;Hiroaki Ishikawa ,&nbsp;Nobutaka Ohgami ,&nbsp;Koji Suzuki ,&nbsp;Koji Ohashi","doi":"10.1016/j.jnutbio.2024.109671","DOIUrl":"10.1016/j.jnutbio.2024.109671","url":null,"abstract":"<div><p>Nutritional researches have successfully used animal models to gain new insights into nutrient action. However, comprehensive descriptions of their molecular mechanisms of action remain elusive as appropriate <em>in vitro</em> evaluation systems are lacking. Organoid models can mimic physiological structures and reproduce <em>in vivo</em> functions, making them increasingly utilized in biomedical research for a better understand physiological and pathological phenomena. Therefore, organoid modeling can be a powerful approach for to understand the molecular mechanisms of nutrient action. The present study aims to demonstrate the utility of organoids in nutritional research by further investigating the molecular mechanisms responsible for the negative effects of fructose intake using liver organoids. Here, we treated liver organoids with fructose and analyzed their gene expression profiles and DNA methylation levels. Microarray analysis demonstrated that fructose-treated organoids exhibited increased selenoprotein p (<em>Sepp1</em>) gene expression, whereas pyrosequencing assays revealed reduced DNA methylation levels in the <em>Sepp1</em> region. These results were consistent with observations using hepatic tissues from fructose-fed rats. Conversely, no differences in <em>Sepp1</em> mRNA and DNA methylation levels were observed in two-dimensional cells. These results suggest that organoids serve as an ideal <em>in vitro</em> model to recapitulate <em>in vivo</em> tissue responses and help to validate the molecular mechanisms of nutrient action compared to conventional cellular models.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141070959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transgenerational impact of maternal zinc deficiency on offspring metabolic outcomes in Drosophila melanogaster","authors":"Kamaldeen Olalekan Sanusi ,&nbsp;Murtala Bello Abubakar ,&nbsp;Kasimu Ghandi Ibrahim ,&nbsp;Mustapha Umar Imam","doi":"10.1016/j.jnutbio.2024.109669","DOIUrl":"10.1016/j.jnutbio.2024.109669","url":null,"abstract":"<div><p>Maternal zinc deficiency significantly influences fetal development and long-term health outcomes, yet its transgenerational effects remain poorly understood. This study aims to investigate the transgenerational effects of maternal zinc deficiency on metabolic outcomes in <em>Drosophila melanogaster</em>. Zinc deficiency was induced in Drosophila by incorporating TPEN (N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine) into their diet. Offspring (F1 to F3) were maintained on a standard diet for subsequent analyses. Various metabolic markers, including glucose, trehalose, glycogen, and triglyceride levels, were assessed, and gene expression analyses were conducted to examine the molecular responses across generations. Significant reductions in locomotor performance in female F1 flies and increased body weight in the F2 generation were observed. Maternal zinc deficiency exhibited gender- and generation-specific impacts on metabolic markers. Notably, an adaptive response in the F3 generation included increased catalase activity and total antioxidant capacity, along with decreased malondialdehyde levels. Gene expression analyses revealed upregulation of <em>DILP2</em> mRNA across generations and significant variations in <em>PEPCK, SOD1, CAT, EGR</em>, and <em>UPD2</em> mRNA levels, demonstrating intricate responses to maternal zinc deficiency. This study provides a holistic understanding of the consequences of maternal zinc deficiency, emphasizing the complex interplay between zinc status and metabolic outcomes across generations in Drosophila. These findings lay the foundation for future research elucidating the underlying molecular mechanisms, with potential implications for humans. The insights gained contribute to informing targeted interventions aimed at optimizing offspring health in the context of maternal zinc deficiency.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140957415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vitamin D3 improves glucose metabolism and attenuates inflammation in prediabetic human and mice","authors":"Yujing Zhang ,&nbsp;Peng Ni ,&nbsp;Yufan Miao ,&nbsp;Hao Chen ,&nbsp;Lulu Tang ,&nbsp;Hanlu Song ,&nbsp;Wenjie Li ,&nbsp;Xing Li","doi":"10.1016/j.jnutbio.2024.109659","DOIUrl":"10.1016/j.jnutbio.2024.109659","url":null,"abstract":"<div><p>Prediabetes is a crucial stage for prevention and treatment of diabetes, and vitamin D (VD) has been found to be linked to the development of prediabetes and diabetes. Thus, we aimed to identify the effect of VD supplementation on glucose metabolism in prediabetic participants and mice. A 1:1 paired design of randomized, placebo-controlled trial with 1600 IU/day VD₃ or placebo was administered to individuals with prediabetes, two-way repeated-measures ANCOVA was used to analyze glycolipid and inflammatory factors. A high-fat diet induced prediabetic KKay mice were utilized to evaluate the effects of VD₃ with 16 weeks supplementation. Generalized estimation equation, one way ANOVA were used to analyze continuous monitoring indexes and terminal indexes, respectively. Exercise capacity, skeletal muscle pathological features and relevant proteins were examined. The clinical results showed that VD₃ could improve insulin secretion and decrease inflammation. Results of KKay mice exhibited that VD₃ not only ameliorate glycolipid metabolism and inflammatory indicators, but also regulated pathological changes of skeletal muscle and exercise capacity. Mechanistically, our results demonstrated that VD₃ could inhibit the TLR4/NFκB and activate PI3K/AKT signaling pathway. Collectively, the study indicated that VD₃ exerts its beneficial effects by inhibiting TLR4/NFκB to decrease inflammatory response, and activating PI3K/AKT signaling pathway to regulate glucose homeostasis.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140855190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}