Journal of Nutritional Biochemistry最新文献

{"title":"Dietary modulation of microRNAs in insulin resistance and type 2 diabetes","authors":"Vinícius Cooper Capetini ,&nbsp;Bruna Jardim Quintanilha ,&nbsp;Bruna Ruschel Ewald Vega Garcia ,&nbsp;Marcelo Macedo Rogero","doi":"10.1016/j.jnutbio.2024.109714","DOIUrl":"10.1016/j.jnutbio.2024.109714","url":null,"abstract":"<div><p>The prevalence of type 2 diabetes is increasing worldwide. Various molecular mechanisms have been proposed to interfere with the insulin signaling pathway. Recent advances in proteomics and genomics indicate that one such mechanism involves the post-transcriptional regulation of insulin signaling by microRNA (miRNA). These noncoding RNAs typically induce messenger RNA (mRNA) degradation or translational repression by interacting with the 3′ untranslated region (3′UTR) of target mRNA. Dietary components and patterns, which can either enhance or impair the insulin signaling pathway, have been found to regulate miRNA expression in both <em>in vitro</em> and <em>in vivo</em> studies. This review provides an overview of the current knowledge of how dietary components influence the expression of miRNAs related to the control of the insulin signaling pathway and discusses the potential application of these findings in precision nutrition.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"133 ","pages":"Article 109714"},"PeriodicalIF":4.8,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141889528","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":"Nobiletin promotes lipolysis of white adipose tissue in a circadian clock-dependent manner","authors":"Xudong Li ,&nbsp;Runxuan Zhuang ,&nbsp;Zhitian Lu ,&nbsp;Fan Wu ,&nbsp;Xiaoli Wu ,&nbsp;Ke Zhang ,&nbsp;Min Wang ,&nbsp;Wenxue Li ,&nbsp;Huijie Zhang ,&nbsp;Wei Zhu ,&nbsp;Bo Zhang","doi":"10.1016/j.jnutbio.2024.109696","DOIUrl":"10.1016/j.jnutbio.2024.109696","url":null,"abstract":"<div><p>Nobiletin has been reported to protect against obesity-related metabolic disorders by enhancing the circadian rhythm; however its effects on lipid metabolism in adipose tissue are unclear. In this study, mice were fed with high-fat diet (HFD) for four weeks firstly and gavaged with 50 or 200 mg/kg bodyweight/day nobiletin at Zeitgeber time (ZT) 4 for another four weeks while still receiving HFD. At the end of the 8-week experimental period, the mice were sacrificed at ZT4 or ZT8 on the same day. Mature 3T3-L1 adipocytes were treated with nobiletin in the presence or absence of si<em>Bmal1</em>, si<em>Rora</em>, si<em>Rorc</em>, SR8278 or SR9009. Nobiletin reduced the weight of white adipose tissue (WAT) and the size of adipocytes in WAT. At ZT4, nobiletin decreased the TG, TC and LDL-c levels and increased serum FFA level and glucose tolerance. Nobiletin triggered the lipolysis of mesenteric and epididymal WAT at both ZT4 and ZT16. Nobiletin increased the level of RORγ at ZT16, that of BMAL1 and PPARγ at ZT4, and that of ATGL at both ZT4 and ZT16. Nobiletin increased lipolysis and ATGL levels in 3T3-L1 adipocytes in <em>Bmal1-</em> or <em>Rora/c-</em> dependent manner. Dual luciferase assay indicated that nobiletin enhanced the transcriptional activation of RORα/γ on <em>Atgl</em> promoter and decreased the repression of RORα/γ on PPARγ-binding <em>PPRE</em>. Promoter deletion analysis indicated that nobiletin inhibited the suppression of PPARγ-mediated <em>Atgl</em> transcription by RORα/γ. Taken together, nobiletin elevated lipolysis in WAT by increasing ATGL levels through activating the transcriptional activity of RORα/γ and decreasing the repression of RORα/γ on PPARγ-binding <em>PPRE</em>.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"132 ","pages":"Article 109696"},"PeriodicalIF":4.8,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141878845","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":"Corrigendum to “Genistein attenuates memory impairment in Alzheimer's disease via ERS-mediated apoptotic pathway in vivo and in vitro” [The Journal of Nutritional Biochemistry Volume 109 (2022) 109118]","authors":"Huawu Gao ,&nbsp;Xin Lei ,&nbsp;Shu Ye ,&nbsp;Ting Ye ,&nbsp;Rupeng Hua ,&nbsp;Guoquan Wang ,&nbsp;Hang Song ,&nbsp;Peng Zhou ,&nbsp;Yan Wang ,&nbsp;Biao Cai","doi":"10.1016/j.jnutbio.2024.109710","DOIUrl":"10.1016/j.jnutbio.2024.109710","url":null,"abstract":"","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"131 ","pages":"Article 109710"},"PeriodicalIF":4.8,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0955286324001438/pdfft?md5=0980d1fc46a69061a69ea5e2a58930c4&pid=1-s2.0-S0955286324001438-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141878844","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":"Dietary protein affects tissue accumulation of mercury and induces hepatic Phase I and Phase II enzyme expression after co-exposure with methylmercury in mice","authors":"Ragnhild Marie Mellingen ,&nbsp;Josef Daniel Rasinger ,&nbsp;Ole Jakob Nøstbakken ,&nbsp;Lene Secher Myrmel ,&nbsp;Annette Bernhard","doi":"10.1016/j.jnutbio.2024.109712","DOIUrl":"10.1016/j.jnutbio.2024.109712","url":null,"abstract":"<div><p>Methylmercury (MeHg) is a ubiquitous environmental contaminant, well known for its neurotoxic effects. MeHg can interact with several nutrients in the diet and affect nutrient metabolism, however the interaction between MeHg and dietary proteins has not been thoroughly investigated. Male BALB/c mice were fed diets based on either casein, cod or chicken as protein sources, which were or were not spiked with MeHg (3.5 mg Hg kg⁻¹). Following 13 weeks of dietary exposure to MeHg, the animals accumulated mercury in a varying degree depending on the diet, where the levels of mercury were highest in the mice fed casein and MeHg, lower in mice fed cod and MeHg, and lowest in mice fed chicken and MeHg in all tissues assessed. Assessment of gut microbiota revealed differences in microbiota composition based on the different protein sources. However, the introduction of MeHg eliminated this difference. Proteomic profiling of liver tissue uncovered the influence of the dietary protein sources on a range of enzymes related to Phase I and Phase II detoxification mechanisms, suggesting an impact of the diet on MeHg metabolism and excretion. Also, enzymes linked to pathways including methionine and glycine betaine cycling, which in turn impact the production of glutathione, an important MeHg conjugation molecule, were up-regulated in mice fed chicken as dietary protein. Our findings indicate that dietary proteins can affect expression of hepatic enzymes that potentially influence MeHg metabolism and excretion, highlighting the relevance of considering the dietary composition in risk assessment of MeHg through dietary exposure.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"133 ","pages":"Article 109712"},"PeriodicalIF":4.8,"publicationDate":"2024-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0955286324001451/pdfft?md5=7cbbbb9116bb210273943973ae04c1e7&pid=1-s2.0-S0955286324001451-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141878843","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":"The attenuation of gut microbiota-derived short-chain fatty acids elevates lipid transportation through suppression of the intestinal HDAC3-H3K27ac-PPAR-γ axis in gestational diabetes mellitus","authors":"Hao Chen ,&nbsp;Shi-Han Wang ,&nbsp;Hong-Li Li ,&nbsp;Xiao-Bo Zhou ,&nbsp;Lin-Wei Zhou ,&nbsp;Chang Chen ,&nbsp;Toby Mansell ,&nbsp;Boris Novakovic ,&nbsp;Richard Saffery ,&nbsp;Philip N. Baker ,&nbsp;Ting-Li Han ,&nbsp;Hua Zhang","doi":"10.1016/j.jnutbio.2024.109708","DOIUrl":"10.1016/j.jnutbio.2024.109708","url":null,"abstract":"<div><p>Gut flora is considered to modulate lipid transport from the intestine into the bloodstream, and thus may potentially participate in the development of GDM. Although previous studies have shown that the intestinal microbiota influences lipid transport and metabolism in GDM, the precise mechanisms remain elusive. To address this, we used a high-fat diet (HFD)-induced GDM mouse model and conducted 16s rRNA sequencing and fecal metabolomics to assess gut microbial community shifts and associated metabolite changes. Western blot, ELISA, and chromatin immunoprecipitation (ChIP) were utilized to elucidate how gut microbiota affect intestinal lipid transport and the insulin sensitivity of hepatic, adipose, and skeletal muscle tissues. We found that HFD impaired the oral glucose tolerance test (OGTT) and insulin tolerance test (ITT) in pregnant mice. 16s rRNA sequencing demonstrated profound compositional changes, especially in the relative abundances of <em>Firmicutes</em> and <em>Bacteroidetes</em>. Metabolomics analysis presented a decline in the concentration of short-chain fatty acids (SCFAs) in the GDM group. Western blot analyses showed an upregulation of HDAC3 and a concurrent reduction in H3K27 acetylation in the intestine. ChIP-qPCR showed that PPAR-γ was inhibited, which in turn activated lipid-transporter CD36. ELISA and insulin signaling pathway detection in insulin-target organs showed high concentrations of circulating fatty acids and triglycerides and insulin resistance in insulin-target organs. Our results suggest that gut microbiota is closely associated with the development of GDM, partly because decreased gut flora-associated SCFAs activate CD36 by suppressing the HDAC3-H3K27ac-PPAR-γ axis to transport excessive fatty acids and triglycerides into blood circulation, thereby dysregulating the insulin sensitivity of insulin target organs.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"133 ","pages":"Article 109708"},"PeriodicalIF":4.8,"publicationDate":"2024-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0955286324001414/pdfft?md5=7173d1a691aa25f8ee6ed880a79238c2&pid=1-s2.0-S0955286324001414-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141766375","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":"Sestrin2 in POMC neurons modulates energy balance and obesity related metabolic disorders via mTOR signaling","authors":"Huiling Hu ,&nbsp;Xiaoxia Lu ,&nbsp;Yuqing He ,&nbsp;Jing Li ,&nbsp;Shoujie Wang ,&nbsp;Zhijun Luo ,&nbsp;Ying Wang ,&nbsp;Jie Wei ,&nbsp;Hao Huang ,&nbsp;Chaohui Duan ,&nbsp;Nannan Sun","doi":"10.1016/j.jnutbio.2024.109703","DOIUrl":"10.1016/j.jnutbio.2024.109703","url":null,"abstract":"<div><p>Sestrin2 is a highly conserved protein that can be induced under various stress conditions. Researches have revealed that the signaling pathway of the mammalian target of rapamycin (mTOR) is essential in modulating both glucose and lipid metabolism. However, the precise involvement of Sestrin2 in the hypothalamus, particularly in pro-opiomelanocortin (POMC) neurons, in control of energy homeostasis remains uncertain. In this study, we aimed to investigate the functional role of Sestrin2 in hypothalamic POMC neurons in regulation of energy balance, as well as revealing the underlying mechanisms. Therefore, cre-dependent AAV virus encoding or silencing Sestrin2 was injected into the hypothalamic ARC of pomc-cre transgenic mice. The results demonstrated that Sestrin2 overexpression in POMC neurons ameliorated high-fat diet (HFD)-induced obesity and increased energy expenditure. Conversely, Sestrin2 deficiency in POMC neurons predisposed mice to HFD induced obesity. Additionally, the thermogenesis of brown adipose tissue and lipolysis of inguinal white adipose tissue were both enhanced by the increased sympathetic nerve innervation in Sestrin2 overexpressed mice. Further exploration revealed that Sestrin2 overexpression inhibited the mTOR signaling pathway in hypothalamic POMC neurons, which may account for the alleviation of systematic metabolic disturbance induced by HFD in these mice. Collectively, our findings demonstrate that Sestrin2 in POMC neurons plays a pivotal role in maintaining energy balance in a context of HFD-induced obesity by inhibiting the mTOR pathway, providing new insights into how hypothalamic neurons respond to nutritional signals to protect against obesity-associated metabolic dysfunction.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"133 ","pages":"Article 109703"},"PeriodicalIF":4.8,"publicationDate":"2024-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141723788","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":"Gymnemic acid alleviates gut barrier disruption and lipid dysmetabolism via regulating gut microbiota in HFD hamsters","authors":"Yumeng Li ,&nbsp;Mingzhe Sun ,&nbsp;Xutong Tian ,&nbsp;Tongtong Bao ,&nbsp;Qian Yu ,&nbsp;Nyuk Ling Ma ,&nbsp;Renyou Gan ,&nbsp;Wai San Cheang ,&nbsp;Xin Wu","doi":"10.1016/j.jnutbio.2024.109709","DOIUrl":"10.1016/j.jnutbio.2024.109709","url":null,"abstract":"<div><p>Gut microbiota dysbiosis and gut barrier disruption are key events associated with high-fat diet (HFD)-induced systemic metabolic disorders. Gymnemic acid (GA) has been reported to have an important role in alleviating HFD-induced disorders of glycolipid metabolism, but its regulatory role in HFD-induced disorders of the gut microbiota and gut barrier function has not been elucidated. Here we showed that GA intervention in HFD-induced hamsters increased the relative abundance of short-chain fatty acid (SCFA)-producing microbes including <em>Lactobacillus</em> (<em>P</em>&lt;.05) and <em>Lachnoclostridium</em> (<em>P</em>&lt;.01) in the gut, and reduced the relative abundance of lipopolysaccharide (LPS)-producing microbes including <em>Enterococcus</em> (<em>P</em>&lt;.05) and <em>Bacteroides</em> (<em>P</em>&lt;.05), subsequently improving HFD-induced intestinal barrier dysfunction and systemic inflammation. Specifically, GA intervention reduced mRNA expression of inflammatory cytokines, including <em>IL-1β, IL-6</em>, and <em>TNF-α</em> (<em>P</em>&lt;.01), increased mRNA expression of antioxidant-related genes, including <em>Nfe2l2, Ho-1</em>, and <em>Nqo1</em> (<em>P</em>&lt;.01), and increased mRNA expression of intestinal tight junction proteins, including <em>Occludin</em> and <em>Claudin-1</em> (<em>P</em>&lt;.01), thereby improving gut barrier function of HFD hamsters. This ameliorative effect of GA on the gut of HFD hamsters may further promote lipid metabolic balance in liver and adipose tissue by regulating the Toll-like receptor 4 (TLR4)-nuclear factor-κB (NF-κB) signaling pathway. Taken together, these results systematically revealed the important role of GA in regulating HFD-induced gut microbiota disturbance and gut barrier function impairment, providing a potential clinical theoretical basis for targeted treatment of HFD-induced microbiota dysbiosis.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"133 ","pages":"Article 109709"},"PeriodicalIF":4.8,"publicationDate":"2024-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141759326","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":"Dietary restriction and fasting alleviate radiation-induced intestinal injury by inhibiting cGAS/STING activation","authors":"Li-Li Zhang ,&nbsp;Jia-Ying Xu ,&nbsp;Wei Wei ,&nbsp;Zhi-Qiang Hu ,&nbsp;Yan Zhou ,&nbsp;Jia-Yang Zheng ,&nbsp;Yu Sha ,&nbsp;Lin Zhao ,&nbsp;Jing Yang ,&nbsp;Qi Sun ,&nbsp;Li-Qiang Qin","doi":"10.1016/j.jnutbio.2024.109707","DOIUrl":"10.1016/j.jnutbio.2024.109707","url":null,"abstract":"<div><p>Radiation injury to the intestine is one of the most common complications in patients undergoing abdominal or pelvic cavity radiotherapy, limiting the clinical application of this treatment. Evidence shows the potential benefits of dietary restriction in improving metabolic profiles and age-related diseases. The present study investigated the effects and mechanisms of dietary restriction in radiation-induced intestinal injury. The mice were randomly divided into the control group, 10 Gy total abdominal irradiation (TAI) group, and groups pretreated with 30% caloric restriction (CR) for 7 days or 24 h fasting before TAI. After radiation, the mice were returned to ad libitum. The mice were sacrificed 3.5 days after radiation, and tissue samples were collected. CR and fasting reduced radiation-induced intestinal damage and promoted intestinal recovery by restoring the shortened colon length, improving the impaired intestinal structure and permeability, and remodeling gut microbial structure. CR and fasting also significantly reduced mitochondrial damage and DNA damage, which in turn reduced activation of the cyclic GMP-AMP synthase/stimulator of interferon gene (cGAS/STING) pathway and the production of type I interferon and other chemokines in the jejunum. Since the cGAS/STING pathway is linked with innate immunity, we further showed that CR and fasting induced polarization to immunosuppressive M2 macrophage, decreased CD8⁺ cytotoxic T lymphocytes, and downregulated proinflammatory factors in the jejunum. Our findings indicated that CR and fasting alleviate radiation-induced intestinal damage by reducing cGAS/STING-mediated harmful immune responses.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"133 ","pages":"Article 109707"},"PeriodicalIF":4.8,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141759325","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":"Protective role of cells and spores of Shouchella clausii SF174 against fructose-induced gut dysfunctions in small and large intestine","authors":"Anella Saggese ,&nbsp;Valentina Barrella ,&nbsp;Angela Di Porzio ,&nbsp;Antonio Dario Troise ,&nbsp;Andrea Scaloni ,&nbsp;Luisa Cigliano ,&nbsp;Giovanni Scala ,&nbsp;Loredana Baccigalupi ,&nbsp;Susanna Iossa ,&nbsp;Ezio Ricca ,&nbsp;Arianna Mazzoli","doi":"10.1016/j.jnutbio.2024.109706","DOIUrl":"10.1016/j.jnutbio.2024.109706","url":null,"abstract":"<div><p>The oral administration of probiotics is nowadays recognized as a strategy to treat or prevent the consequences of unhealthy dietary habits. Here we analyze and compare the effects of the oral administration of vegetative cells or spores of <em>Shouchella clausii</em> SF174 in counteracting gut dysfunctions induced by 6 weeks of high fructose intake in a rat model. Gut microbiota composition, tight junction proteins, markers of inflammation and redox homeostasis were evaluated in ileum and colon in rats fed fructose rich diet and supplemented with cells or spores of <em>Shouchella clausii</em> SF174. Our results show that both spores and cells of SF174 were effective in preventing the fructose-induced metabolic damage to the gut, namely establishment of “leaky gut”, inflammation and oxidative damage, thus preserving gut function. Our results also suggest that vegetative cells and germination-derived cells metabolize part of the ingested fructose at the ileum level.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"133 ","pages":"Article 109706"},"PeriodicalIF":4.8,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0955286324001396/pdfft?md5=3ee29d7b7f515c53e14bd3679ebf1fca&pid=1-s2.0-S0955286324001396-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141759327","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":"Gut microbes, diet, and genetics as drivers of metabolic liver disease: a narrative review outlining implications for precision medicine","authors":"Jake B. Hermanson ,&nbsp;Samar A. Tolba ,&nbsp;Evan A. Chrisler ,&nbsp;Vanessa A. Leone","doi":"10.1016/j.jnutbio.2024.109704","DOIUrl":"10.1016/j.jnutbio.2024.109704","url":null,"abstract":"<div><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is rapidly increasing in prevalence, impacting over a third of the global population. The advanced form of MASLD, Metabolic dysfunction-associated steatohepatitis (MASH), is on track to become the number one indication for liver transplant. FDA-approved pharmacological agents are limited for MASH, despite over 400 ongoing clinical trials, with only a single drug (resmetirom) currently on the market. This is likely due to the heterogeneous nature of disease pathophysiology, which involves interactions between highly individualized genetic and environmental factors. To apply precision medicine approaches that overcome interpersonal variability, in-depth insights into interactions between genetics, nutrition, and the gut microbiome are needed, given that each have emerged as dynamic contributors to MASLD and MASH pathogenesis. Here, we discuss the associations and molecular underpinnings of several of these factors individually and outline their interactions in the context of both patient-based studies and preclinical animal model systems. Finally, we highlight gaps in knowledge that will require further investigation to aid in successfully implementing precision medicine to prevent and alleviate MASLD and MASH.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"133 ","pages":"Article 109704"},"PeriodicalIF":4.8,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141727344","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}