Journal of Nutritional Biochemistry最新文献

{"title":"Blackcurrants shape gut microbiota profile and reduce risk of postmenopausal osteoporosis via the gut-bone axis: Evidence from a pilot randomized controlled trial","authors":"Briana M. Nosal ,&nbsp;Staci N. Thornton ,&nbsp;Manije Darooghegi Mofrad ,&nbsp;Junichi R. Sakaki ,&nbsp;Kyle J. Mahoney ,&nbsp;Zachary Macdonald ,&nbsp;Lauren Daddi ,&nbsp;Thi Dong Binh Tran ,&nbsp;George Weinstock ,&nbsp;Yanjiao Zhou ,&nbsp;Elaine Choung-Hee Lee ,&nbsp;Ock K. Chun","doi":"10.1016/j.jnutbio.2024.109701","DOIUrl":"10.1016/j.jnutbio.2024.109701","url":null,"abstract":"<div><p>This study aimed to investigate the effects of blackcurrant (BC) on gut microbiota abundance and composition, inflammatory and immune responses, and their relationship with bone mass changes. The effects of BC on bone mineral density (BMD), gut microbiota, and blood inflammatory and immune biomarkers were evaluated using DXA, stool and fasting blood collected from a pilot three-arm, randomized, double-blind, placebo-controlled clinical trial. Fifty-one peri- and early postmenopausal women aged 45–60 years were randomly assigned into one of three treatment groups for 6 months: control, low BC (392 mg/day) and high BC (784 mg/day); and 40 women completed the trial. BC supplementation for 6 months effectively mitigated the loss of whole-body BMD (<em>P</em>&lt;.05). Six-month changes (%) in peripheral IL-1β (<em>P</em>=.056) and RANKL (<em>P</em>=.052) for the high BC group were marginally significantly lower than the control group. Six-month changes in whole-body BMD were inversely correlated with changes in RANKL (<em>P</em>&lt;.01). In proteome analysis, four plasma proteins showed increased expression in the high BC group: IGFBP4, tetranectin, fetuin-B, and vitamin K-dependent protein S. BC dose-dependently increased the relative abundance of <em>Ruminococcus 2</em> (<em>P</em>&lt;.05), one of six bacteria correlated with BMD changes in the high BC group (<em>P</em>&lt;.05), suggesting it might be the key bacteria that drove bone protective effects. Daily BC consumption for 6 months mitigated bone loss in this population potentially through modulating the gut microbiota composition and suppressing osteoclastogenic cytokines. Larger-scale clinical trials on the potential benefits of BC and connection of <em>Ruminococcus 2</em> with BMD maintenance in postmenopausal women are warranted.</p><p>Trial Registration: NCT04431960, <span><span>https://classic.clinicaltrials.gov/ct2/show/NCT04431960</span><svg><path></path></svg></span>.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"133 ","pages":"Article 109701"},"PeriodicalIF":4.8,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141633729","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 pectin and inulin: A promising adjuvant supplement for collagen-induced arthritis through gut microbiome restoration and CD4+ T cell reconstitution","authors":"","doi":"10.1016/j.jnutbio.2024.109699","DOIUrl":"10.1016/j.jnutbio.2024.109699","url":null,"abstract":"<div><p>Dietary strategies rich in fiber have been demonstrated to offer benefits to individuals afflicted with rheumatoid arthritis (RA). However, the specific mechanisms through which a high-fiber diet (HFD) mitigates RA's autoimmunity remain elusive. Herein, we investigate the influence of pectin- and inulin-rich HFD on collagen-induced arthritis (CIA). We establish that HFD significantly alleviates arthritis in CIA mice by regulating the Th17/Treg balance. The rectification of aberrant T cell differentiation by the HFD is linked to the modulation of gut microbiota, augmenting the abundance of butyrate in feces. Concurrently, adding butyrate to the drinking water mirrors the HFD's impact on ameliorating CIA, encompassing arthritis mitigation, regulating intestinal barrier integrity, and restoring the Th17/Treg equilibrium. Butyrate reshapes the metabolic profile of CD4⁺ T cells in an AMPK-dependent manner. Our research underscores the importance of dietary interventions in rectifying gut microbiota for RA management and offers an explanation of how diet-derived microbial metabolites influence RA's immune-inflammatory-reaction.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"133 ","pages":"Article 109699"},"PeriodicalIF":4.8,"publicationDate":"2024-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141554937","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":"Bioaccessibility and Caco-2 cell uptake of iron chlorophyllin using a biologically relevant digestion model","authors":"","doi":"10.1016/j.jnutbio.2024.109698","DOIUrl":"10.1016/j.jnutbio.2024.109698","url":null,"abstract":"<div><p>Iron deficiency remains a top nutrient deficiency worldwide. Iron chlorophyllin (IC), a compound structurally analogous to heme, utilizes the protoporphyrin ring of chlorophyll to bind iron. IC has previously been shown to deliver more iron to Caco-2 cells than FeSO₄, the most common form prescribed for supplementation. However, previous test conditions used digestive conditions outside of those observed in humans. This study sought to assess IC bioaccessibility and Caco-2 cell uptake using physiologically relevant digestive solutions, pH, and incubation time, as compared to other iron sources (i.e., FeSO₄, and hemoglobin (Hb)). Co-digestion with ascorbic acid (AA) and albumin was also investigated.</p><p>Following gastric, duodenal, and jejunal digestion, IC-bound iron was less bioaccessible than iron delivered as FeSO₄, and IC-bound iron was less bioaccessible than Hb-bound iron. IC-bound iron bioaccessibility was not affected by AA and was enhanced 2x when co-digested with a low dose of albumin. However, Caco-2 cell incubation with IC-containing digesta increased cell ferritin 2.5x more than FeSO₄ alone, and less than Hb. IC with AA or with 400 mg albumin also increased cell ferritin more than IC alone, with the greatest increases observed following incubation of digesta containing IC + AA + 400 mg albumin.</p><p>These results suggest IC can serve as an improved source of iron for supplementation as compared to FeSO_4. These results also support further <em>in vivo</em> investigations of IC-based iron delivery in populations at risk of iron deficiency.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"132 ","pages":"Article 109698"},"PeriodicalIF":4.8,"publicationDate":"2024-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0955286324001311/pdfft?md5=7b5b50c0eebe026709b68e3b38ff7a42&pid=1-s2.0-S0955286324001311-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141538015","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":"Zinc-glutathione mitigates alcohol-induced intestinal and hepatic injury by modulating intestinal zinc-transporters in mice","authors":"","doi":"10.1016/j.jnutbio.2024.109697","DOIUrl":"10.1016/j.jnutbio.2024.109697","url":null,"abstract":"<div><p>Long-term alcohol overconsumption impairs intestinal and hepatic structure and function, along with dysregulation of zinc homeostasis. We previously found that zinc-glutathione (Zn-GSH) complex effectively suppressed alcohol-induced liver injury in mice. This study was undertaken to test the hypothesis that Zn-GSH suppresses alcohol-induced liver injury by modulating intestinal zinc transporters. Mice were subjected to long-term ethanol feeding, as per the NIAAA model, with groups receiving either an ethanol diet alone or an ethanol diet supplemented with Zn-GSH. Treatment groups were carefully monitored for alcohol consumption and subjected to a final binge drinking exposure. The results showed that Zn-GSH increased the survival rate and decreased the recovery time from binge drinking-induced drunkenness. Histopathological analyses demonstrated a reduction in liver steatosis and the preservation of intestinal integrity by Zn-GSH. It was observed that Zn-GSH prevented the reduction of Zn and GSH levels while increasing alcohol dehydrogenase and aldehyde dehydrogenase in both liver and intestine. Importantly, the expression and protein abundance of zinc transporters ZnT-1, ZIP-1, ZIP-4, ZIP-6, and ZIP-14, all of which are critically involved in intestinal zinc transport and homeostasis, were significantly increased or preserved by Zn-GSH in response to alcohol exposure. This study thus highlights the critical role of Zn-GSH in maintaining intestinal zinc homeostasis by modulating zinc transporters, thereby preventing alcohol-induced intestinal and hepatic injury.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"132 ","pages":"Article 109697"},"PeriodicalIF":4.8,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141534616","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":"Sex-dependent susceptibility to brain metabolic dysfunction and memory impairment in response to pre and postnatal high-fat diet","authors":"","doi":"10.1016/j.jnutbio.2024.109675","DOIUrl":"10.1016/j.jnutbio.2024.109675","url":null,"abstract":"<div><p>The developing brain is sensitive to the impacts of early-life nutritional intake. This study investigates whether maternal high fat diet (HFD) causes glucose metabolism impairment, neuroinflammation, and memory impairment in immature and adult offspring, and whether it may be affected by postweaning diets in a sex-dependent manner in adult offspring. After weaning, female rats were fed HFD (55.9% fat) or normal chow diet (NCD; 10% fat) for 8 weeks before mating, during pregnancy, and lactation. On postnatal day 21 (PND21), the male and female offspring of both groups were split into two new groups, and NCD or HFD feeding was maintained until PND180. On PND21 and PND180, brain glucose metabolism, inflammation, and Alzheimer's pathology-related markers were by qPCR. In adult offspring, peripheral insulin resistance parameters, spatial memory performance, and brain glucose metabolism (18F-FDG-PET scan and protein levels of IDE and GLUT3) were assessed. Histological analysis was also performed on PND21 and adult offspring. On PND21, we found that maternal HFD affected transcript levels of glucose metabolism markers in both sexes. In adult offspring, more profoundly in males, postweaning HFD in combination with maternal HFD induced peripheral and brain metabolic disturbances, impaired memory performance and elevated inflammation, dementia risk markers, and neuronal loss. Our results suggest that maternal HFD affects brain glucose metabolism in the early ages of both sexes. Postweaning HFD sex-dependently causes brain metabolic dysfunction and memory impairment in later-life offspring; effects that can be worsened in combination with maternal HFD.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"132 ","pages":"Article 109675"},"PeriodicalIF":4.8,"publicationDate":"2024-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141468802","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":"1,25-(OH)2D3 promotes hair growth by inhibiting NLRP3/IL-1β and HIF-1α/IL-1β signaling pathways","authors":"","doi":"10.1016/j.jnutbio.2024.109695","DOIUrl":"10.1016/j.jnutbio.2024.109695","url":null,"abstract":"<div><p>Vitamin D is a crucial vitamin that participates in various biological processes through the Vitamin D Receptor (VDR). While there are studies suggesting that VDR might regulate hair growth through ligand-independent mechanisms, the efficacy of Vitamin D in treating hair loss disorders has also been reported. Here, through <em>in vivo</em> experiments in mice, <em>in vitro</em> organ culture of hair follicles, and cellular-level investigations, we demonstrate that 1,25-(OH)₂D₃ promotes mouse hair regeneration, prolongs the hair follicle anagen, and enhances the proliferation and migration capabilities of dermal papilla cells and outer root sheath keratinocytes in a VDR-dependent manner. Transcriptome analysis of VDR-knockout mouse skin reveals the involvement of HIF-1α, NLRP3, and IL-1β in these processes. Finally, we confirm that 1,25-(OH)₂D₃ can counteract the inhibitory effects of DHT on hair growth. These findings suggest that 1,25-(OH)₂D₃ has a positive impact on hair growth and may serve as a potential therapeutic agent for androgenetic alopecia (AGA).</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"132 ","pages":"Article 109695"},"PeriodicalIF":4.8,"publicationDate":"2024-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141468801","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":"CTRP9 alleviates diet induced obesity through increasing lipolysis mediated by enhancing autophagy-initiation complex formation.","authors":"Shengyun Lei ,&nbsp;Xuehui Li ,&nbsp;Anju Zuo ,&nbsp;Shiyan Ruan ,&nbsp;Yuan Guo","doi":"10.1016/j.jnutbio.2024.109694","DOIUrl":"10.1016/j.jnutbio.2024.109694","url":null,"abstract":"<div><p>Recently, emerging evidence has suggested that obesity become a prevalent health threat worldwide. Reportedly, CTRP9 can ameliorate HFD induced obesity. However, the molecular mechanism underlying the role of CTRP9 in obesity remains elusive. In this study, we reported its major function in the regulation of lipolysis. First, we found that the expression of CTRP9 was decreased in mature adipocytes and white adipose tissue of obese mice. Then, we showed that overexpression adipose tissue CTRP9 alleviated diet-induced obesity and adipocytes hypertrophy, improved glucose intolerance and raised energy expenditure. Moreover, CTRP9 increased the lipolysis in vitro and vivo. Additionally, we determined that CTRP9 enhanced autophagy flux in adipocytes. Intriguingly, knock down Beclin1 by SiRNA abolished the effect of CTRP9 on lipolysis. Mechanically, CTRP9 enhanced the expression of SNX26. We demonstrated that SNX26 was a component of the ATG14L-Beclin1-VPS34 complex and enhanced the assembly of the autophagy-initiation complex. Collectively, our results suggested that CTRP9 alleviated diet induced obesity through enhancing lipolysis mediated by autophagy-initiation complex formation.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"131 ","pages":"Article 109694"},"PeriodicalIF":4.8,"publicationDate":"2024-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141437044","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":"Therapeutic potential of the ketogenic diet: A metabolic switch with implications for neurological disorders, the gut-brain axis, and cardiovascular diseases","authors":"Sheyda Shahpasand ,&nbsp;Seyyed Hossein Khatami ,&nbsp;Sajad Ehtiati ,&nbsp;Parsa Alehossein ,&nbsp;Farzaneh Salmani ,&nbsp;Alireza Haghbin Toutounchi ,&nbsp;Tayebe Zarei ,&nbsp;Mohammad Reza Shahmohammadi ,&nbsp;Reza Khodarahmi ,&nbsp;Vajiheh Aghamollaii ,&nbsp;Abbas Tafakhori ,&nbsp;Saeed Karima","doi":"10.1016/j.jnutbio.2024.109693","DOIUrl":"10.1016/j.jnutbio.2024.109693","url":null,"abstract":"<div><p>The Ketogenic Diet (KD) is a dietary regimen that is low in carbohydrates, high in fats, and contains adequate protein. It is designed to mimic the metabolic state of fasting. This diet triggers the production of ketone bodies through a process known as ketosis. The primary objective of KD is to induce and sustain ketosis, which has been associated with numerous health benefits. Recent research has uncovered promising therapeutic potential for KD in the treatment of various diseases. This includes evidence of its effectiveness as a dietary strategy for managing intractable epilepsy, a form of epilepsy that is resistant to medication. We are currently assessing the efficacy and safety of KD through laboratory and clinical studies. This review focuses on the anti-inflammatory properties of the KD and its potential benefits for neurological disorders and the gut-brain axis. We also explore the existing literature on the potential effects of KD on cardiac health. Our aim is to provide a comprehensive overview of the current knowledge in these areas. Given the encouraging preliminary evidence of its therapeutic effects and the growing understanding of its mechanisms of action, randomized controlled trials are warranted to further explore the rationale behind the clinical use of KD. These trials will ultimately enhance our understanding of how KD functions and its potential benefits for various health conditions. We hope that our research will contribute to the body of knowledge in this field and provide valuable insights for future studies.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"132 ","pages":"Article 109693"},"PeriodicalIF":4.8,"publicationDate":"2024-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141331206","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-gene network analysis reveals the effects of early maternal nutrition on mineral homeostasis and energy metabolism in the fetal liver transcriptome of beef heifers","authors":"","doi":"10.1016/j.jnutbio.2024.109691","DOIUrl":"10.1016/j.jnutbio.2024.109691","url":null,"abstract":"<div><p>Maternal nutrition during pregnancy influences fetal development; however, the regulatory markers of fetal programming across different gestational phases remain underexplored in livestock models. Herein, we investigated the regulatory role of long non-coding RNAs (lncRNAs) on fetal liver gene expression, the impacts of maternal vitamin and mineral supplementation, and the rate of maternal body weight gain during the periconceptual period. To this end, crossbred Angus heifers (n=31) were randomly assigned to a 2×2 factorial design to evaluate the main effects of the rate of weight gain (low gain [LG, avg. daily gain of 0.28 kg/day] vs. moderate gain [MG, avg. daily gain of 0.79 kg/day]) and vitamins and minerals supplementation (VTM vs. NoVTM). On day 83±0.27 of gestation, fetuses were collected for morphometric measurements, and fetal liver was collected for transcriptomic and mineral analyses. The maternal diet significantly affected fetal liver development and mineral reserves. Using an RNA-Seq approach, we identified 320 unique differentially expressed genes (DEGs) across all six comparisons (FDR &lt;0.05). Furthermore, lncRNAs were predicted through the FEELnc pipeline, revealing 99 unique differentially expressed lncRNAs (DELs). The over-represented pathways and biological processes (BPs) were associated with energy metabolism, Wnt signaling, CoA carboxylase activity, and fatty acid metabolism. The DEL-regulated BPs were associated with metal ion transport, pyrimidine metabolism, and classical energy metabolism-related glycolytic, gluconeogenic, and TCA cycle pathways. Our findings suggest that lncRNAs regulate mineral homeostasis- and energy metabolism-related gene networks in the fetal liver in response to early maternal nutrition.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"132 ","pages":"Article 109691"},"PeriodicalIF":4.8,"publicationDate":"2024-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141327603","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":"A high-fat diet induces changes in mesenteric adipose tissue accelerating early-stage pancreatic carcinogenesis in mice","authors":"Aya S. Ead ,&nbsp;Joanna Wirkus ,&nbsp;Karen Matsukuma ,&nbsp;Gerardo G. Mackenzie","doi":"10.1016/j.jnutbio.2024.109690","DOIUrl":"10.1016/j.jnutbio.2024.109690","url":null,"abstract":"<div><p>Increased adiposity is a significant risk factor for pancreatic cancer development. Multiple preclinical studies have documented that high-fat, high calorie diets, rich in omega-6 fatty acids (FA) accelerate pancreatic cancer development. However, the effect of a high-fat, low sucrose diet (HFD), on pancreatic carcinogenesis remains unclear. We evaluated the impact of a HFD on early-stage pancreatic carcinogenesis in the clinically relevant <em>Kras^LSL-G12D/+; Ptf1a^Cre/+</em> (KC) genetically engineered mouse model, and characterized the role of the mesenteric adipose tissue (MAT). Cohorts of male and female KC mice were randomly assigned to a control diet (CD) or a HFD, matched for FA composition (9:1 of omega-6 FA: omega-3 FA), and fed their diets for 8 weeks. After 8 weeks on a HFD, KC mice had significantly higher body weight, fat mass, and serum leptin compared to CD-fed KC mice. Furthermore, a HFD accelerated pancreatic acinar-to-ductal metaplasia (ADM) and proliferation, associated with increased activation of ERK and STAT3, and macrophage infiltration in the pancreas, compared to CD-fed KC mice. Metabolomics analysis of the MAT revealed sex differences between diet groups. In females, a HFD altered metabolites related to FA (α-linolenic acid and linoleic acid) and amino acid metabolism (alanine, aspartate, glutamate). In males, a HFD significantly affected pathways related to alanine, aspartate, glutamate, linoleic acid, and the citric acid cycle. A HFD accelerates early pancreatic ADM through multifaceted mechanisms, including effects at the tumor and surrounding MAT. The sex-dependent changes in MAT metabolites could explain some of the sex differences in HFD-induced pancreatic ADM.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"131 ","pages":"Article 109690"},"PeriodicalIF":4.8,"publicationDate":"2024-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0955286324001232/pdfft?md5=0b68bf724c45591bc1a95e126d64bc3b&pid=1-s2.0-S0955286324001232-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141321043","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}