Journal of Nutritional Biochemistry最新文献

{"title":"Chronically increased osteoclastogenesis in adult celiac disease patients does not hinder improvement in bone health induced by gluten-free diet: Role of vitamin D, OPG and IL-6","authors":"Patrik Skubica ,&nbsp;Iva Hoffmanova ,&nbsp;Pavlina Dankova","doi":"10.1016/j.jnutbio.2025.109871","DOIUrl":"10.1016/j.jnutbio.2025.109871","url":null,"abstract":"<div><div>The etiology of bone loss in celiac disease (CeD) remains a clinical challenge, with uncertainties present such as the extent of involvement of malabsorption and inflammation-induced osteoresorption processes in development of osteopenia/osteoporosis (OPN/OP), or reasons for failure to achieve healthy bone mass (BMD) even after long-term gluten-free diet (GFD) treatment. This observational prospective study explores the <em>in vitro</em> osteoclastogenic potential of peripheral blood precursors originating from adult active (newly diagnosed and untreated) celiac disease patients (aCeD) and describes the longitudinal changes in osteoclastogenesis after long-term adherence to GFD. To find connections between <em>in vitro</em> observations and <em>in vivo</em> bone metabolism changes, serum levels of 25(OH)D3, PTH, bCTX, PINP, CRP, IL-6, RANKL and OPG were measured before and after GFD and levels of these markers were correlated with the rate of osteoclastogenesis <em>in vitro</em>. OPG and IL-6 showed associations with BMD and/or presence of OPN/OP. Patients after GFD (CeD-GFD) exhibited improved BMD and increased serum 25(OH)D3 levels, alongside reduced bCTX and PINP levels. Compared to healthy donors, aCeD osteoclast genesis <em>in vitro</em> was higher and, surprisingly, remained elevated even in CeD-GFD patients. Negative correlation was found between osteoclastogenesis rate and serum OPG in aCeD, while osteoclastogenesis rate positively correlated with PTH in CeD-GFD. These results highlight OPG as marker for risk of OPN/OP in CeD and suggest that improvement of BMD after GFD is a result of uncoupling between bone metabolism and osteoresorptive action of osteoclasts after GFD.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"139 ","pages":"Article 109871"},"PeriodicalIF":4.8,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468523","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":"Low phylloquinone intake deteriorates endothelial function in normolipidemic and dyslipidaemic mice","authors":"Agnieszka Kij ,&nbsp;Anna Kieronska-Rudek ,&nbsp;Anna Bar ,&nbsp;Izabela Czyzynska-Cichon ,&nbsp;Magdalena Strus ,&nbsp;Lucja Kozien ,&nbsp;Grazyna Wiecek ,&nbsp;Natalia Zeber-Lubecka ,&nbsp;Maria Kulecka ,&nbsp;Grzegorz Kwiatkowski ,&nbsp;Kamil Przyborowski ,&nbsp;Tasnim Mohaissen ,&nbsp;Magdalena Sternak ,&nbsp;Elzbieta Buczek ,&nbsp;Agnieszka Zakrzewska ,&nbsp;Bartosz Proniewski ,&nbsp;Kamil Kus ,&nbsp;Magdalena Franczyk-Zarow ,&nbsp;Renata B. Kostogrys ,&nbsp;Elsbeth J. Pieterman ,&nbsp;Stefan Chlopicki","doi":"10.1016/j.jnutbio.2025.109867","DOIUrl":"10.1016/j.jnutbio.2025.109867","url":null,"abstract":"<div><div>While the plasma phylloquinone (PK) concentration is inversely correlated with cardiovascular risk, the involvement of PK in regulating endothelial function has not been directly investigated. Therefore, in this study we assessed the effects of short-term treatment with PK-deficient diets (5–10 weeks) on endothelial function in normolipidemic 14-week-old male C57BL/6JCmd mice and age-matched dyslipidaemic male E3L.CETP mice. Our results show that in normolipidemic mice dietary PK deficiency was associated with a marked reduction of PK levels in the plasma and liver (liquid chromatography-mass spectrometry measurements) and with impaired endothelium-dependent vasodilation assessed <em>in vivo</em> by magnetic resonance imaging (MRI). Dietary PK deficiency-induced endothelial dysfunction was fully reversed by PK supplementation. In dyslipidaemic E3L.CETP mice, dietary PK deficiency exacerbated preexisting endothelial dysfunction. Furthermore, dietary PK deficiency decreased menaquinone-4 (MK-4) levels in the aorta but did not affect blood coagulation (calibrated automated thrombography), microbiota composition (culturing and next-generation sequencing), and gut menaquinone production. In conclusion, our study demonstrated for the first time that sufficient dietary PK intake supports endothelial function in normolipidemic and dyslipidaemic mice indicating nutritional significance of dietary PK in the maintenance of endothelial function in humans.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"140 ","pages":"Article 109867"},"PeriodicalIF":4.8,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468590","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":"Pharmacokinetics of primary atractyligenin metabolites after coffee consumption","authors":"Roman Lang ,&nbsp;Melanie Haas ,&nbsp;Barbara Danzer ,&nbsp;Veronika Somoza ,&nbsp;Thomas Skurk","doi":"10.1016/j.jnutbio.2025.109869","DOIUrl":"10.1016/j.jnutbio.2025.109869","url":null,"abstract":"<div><div>Coffee brew is an integral part of the individual diet worldwide. Roasted coffee contains numerous bioactive substances whose significance for health is investigated in nutritional studies. Food biomarkers are recommended to correlate coffee consumption and health effects in the most unbiased way possible. Metabolites of atractyligenin derivatives from roasted coffee have been suggested as candidate analytes indicating coffee consumption.</div><div>UHPLC-MS/MS analysis revealed that atractyligenin (1), 2-<em>O</em>-<em>β</em>-D-glucosylatractyligenin and 3′-<em>O</em>-<em>β</em>-D-glucosyl-2′-<em>O</em>-isovaleryl-2-<em>O</em>-<em>β</em>-D-glucosylatractyligenin were extracted into coffee brew. Their concentrations in filtered and unfiltered coffee did not differ significantly, suggesting independence from the preparation method.</div><div>In a coffee intervention study (<em>n</em>=12, female/male 6/6), atractyligenin metabolites were not detectable in plasma after three days of coffee abstinence. After coffee, atractyligenin (1) and atractyligenin-19-<em>O</em>-<em>β</em>-D-glucuronide (M1) were the quantitatively dominant atractyligenin metabolites in plasma and showed two peaks each after 0.5 and 10 h, respectively. Half-live of 1 after the first c_max in plasma was ∼0.31 h. 1 and M1 were detectable in plasma, indicating coffee consumption for up to 24 h after one serving.</div><div>Within 10 h, ∼13.7% of the atractyligenin glycosides supplied by coffee brew were excreted in urine as the metabolites 1 and M1. Metabolites 2<em>β</em>‑hydroxy-15-oxoatractylan-4<em>α</em>-carboxy-19-<em>O</em>-<em>β</em>-D-glucuronide (M2) and 2<em>β</em>‑hydroxy-15-oxoatractylan-4<em>α</em>-carboxylic acid-2-<em>O</em>-<em>β</em>-D-glucuronide (M3) were detected in only some samples and appeared unreliable as indicators for coffee consumption. No concentration differences between female and male study participants were observed in plasma and urine.</div><div>In conclusion atractyligenin and its 19-<em>O</em>-<em>β</em>-D-glucuronide are promising markers of <em>Arabica</em> coffee consumption in plasma and urine for both men and women, independent of the brewing method.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"139 ","pages":"Article 109869"},"PeriodicalIF":4.8,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143441140","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":"In vivo metabolic effects of naringin in reducing oxidative stress and protecting the vascular endothelium in dyslipidemic mice","authors":"Runlei Zhang ,&nbsp;Shengxian Wu ,&nbsp;Chao Ye ,&nbsp;Pengyang Li ,&nbsp;Bing Xu ,&nbsp;Yue Wang ,&nbsp;Zheng Yang ,&nbsp;Xinyi Chen ,&nbsp;Jing Chen","doi":"10.1016/j.jnutbio.2025.109866","DOIUrl":"10.1016/j.jnutbio.2025.109866","url":null,"abstract":"<div><div>Naringin, a flavonoid, has high antioxidant activity and hypolipidemic pharmacological effects. In this study, an animal model of dyslipidemia was established by feeding <em>Apoe^-/-</em> mice a high-fat diet for 4 weeks. Subsequently, the mice were administered Naringin via gavage at doses of 50 mg/(kg·d), 100 mg/(kg·d), or 200 mg/(kg·d) for an additional 4 weeks. The research utilized liquid chromatography–mass spectrometry (LC–MS) metabolomics in conjunction with analyses of serum oxidative stress markers, Hematoxylin-eosin staining, Masson's trichome staining, and immunohistochemical staining. Naringin treatment reduced serum total cholesterol, triglycerides, and low-density lipoprotein cholesterol concentrations (<em>P</em>&lt;.05), reversed disorders of vascular structure and morphology, increased serum nicotinamide adenine dinucleotide phosphate hydride and glutathione concentrations (<em>P</em>&lt;.05), reduced serum peroxynitrite concentrations (<em>P</em>&lt;.05), promoted aortic endothelial nitric oxide synthase protein expression and inhibited aortic prolyl isomerase-1 protein expression. Twenty differentiated metabolites were obtained from the serum by LC–MS assay, followed by 16 differential metabolic pathways after enrichment. Among the metabolic pathways, glycolysis/gluconeogenesis, the pentose phosphate pathway, purine metabolism, ascorbate metabolism, and aldarate metabolism are the most relevant metabolic pathways by which naringin reduces oxidative stress. Our findings suggest that naringin can reduce oxidative stress levels associated with dyslipidemia through multiple metabolic pathways, protect vascular endothelial function, and thus providing a novel and promising natural medicine for treating dyslipidemia.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"139 ","pages":"Article 109866"},"PeriodicalIF":4.8,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143425650","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":"Ligusticum cycloprolactam ameliorates hyperuricemic nephropathy through inhibition of TLR4/NF-κB signaling","authors":"Zhe Chen ,&nbsp;Rong Chen ,&nbsp;Jiamin Wang ,&nbsp;Lin Zhu ,&nbsp;Jie Niu ,&nbsp;Minghui Li ,&nbsp;Kaireng Wu ,&nbsp;Juxian Mo ,&nbsp;Siqi Zheng ,&nbsp;Bing Liu ,&nbsp;Ping Zhou ,&nbsp;Tian Lan","doi":"10.1016/j.jnutbio.2025.109864","DOIUrl":"10.1016/j.jnutbio.2025.109864","url":null,"abstract":"<div><div>Hyperuricemia is a metabolic disease attributed to a sustained dysregulation of purine metabolism, manifesting as consistently elevated blood uric acid levels. Hyperuricemic nephropathy (HN) is a renal complication of hyperuricemia. It is characterized by the deposition of urate crystals, inflammatory cell infiltration and tubulointerstitial injury. Ligusticum cycloprolactam (LIGc) is a novel monomeric derivative of the active ingredient ligustilide (LIG) from <em>Angelica sinensis</em> (Oliv.). LIG demonstrates anti-inflammatory and antioxidant properties. Nevertheless, the therapeutic potential of LIGc to ameliorate HN required further investigation. Our study revealed that LIGc effectively reduced serum uric acid and attenuated HN in mice induced by co-administering potassium oxonate and hypoxanthine. Our research demonstrated that LIGc treatment improved renal function in mice with HN by regulating the expression of uric acid transporters. Histopathological analysis showed that LIGc treatment reduced tubular damage, inflammatory infiltration and interstitial collagen deposition. Mechanistically, LIGc alleviated renal injury by inhibiting the TLR4/NF-κB signaling pathway both in <em>vivo</em> and in <em>vitro</em>. Our study revealed that LIGc effectively mitigated HN by attenuating the inflammatory response through the TLR4/NF-κB signaling pathway, providing new perspectives for the treatment of HN.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"139 ","pages":"Article 109864"},"PeriodicalIF":4.8,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143425652","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":"Quinoa protein and its hydrolysate improve the fatigue resistance of mice: a potential mechanism to relieve oxidative stress and inflammation and improve energy metabolism","authors":"Yuanrong Tuo ,&nbsp;Siwang Peng ,&nbsp;Yiju Li ,&nbsp;Jiamin Dang ,&nbsp;Zhi Feng ,&nbsp;Long Ding ,&nbsp;Shuangkui Du ,&nbsp;Xuebo Liu ,&nbsp;Liying Wang","doi":"10.1016/j.jnutbio.2025.109863","DOIUrl":"10.1016/j.jnutbio.2025.109863","url":null,"abstract":"<div><div>Fatigue is commonly marked by reduced endurance and impaired function, often linked to overexertion and chronic conditions. Quinoa (<em>Chenopodium quinoa</em> Willd.), with its rich amino acids and resilience to harsh conditions, offers a novel strategy for combating fatigue. This study explored the antifatigue effects of quinoa protein (QPro) and its hydrolysate (QPH) in weight-loaded swimming mice. After 4 weeks of oral administration, QPro and QPH significantly prolonged swimming duration, reduced serum fatigue biomarkers (lactic acid, urea nitrogen, lactate dehydrogenase, creatine kinase), and elevated glycogen reserves in the liver and muscle. RT-qPCR analysis indicated that QPH activated hepatic gluconeogenesis via G6Pase and PEPCK signaling and enhanced mitochondrial function through PGC-1α/NRF1/TFAM signaling in muscle. Additionally, QPro and QPH boosted antioxidant defenses by improving antioxidant enzyme activity, reducing malondialdehyde through the Nrf2/HO-1 pathway, and suppressing inflammation by reducing TNF-α and IL-6 levels. Network pharmacology identified 31 key targets involved in energy metabolism and inflammation, providing novel insights into the molecular mechanisms underlying the antifatigue properties of quinoa peptides. These findings highlight the potential of QPro and QPH as natural and bioactive ingredients in functional foods for enhancing endurance and mitigating fatigue.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"139 ","pages":"Article 109863"},"PeriodicalIF":4.8,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143425664","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 flavonoid actions on senescence, aging, and applications for health","authors":"Bruce A Watkins ,&nbsp;Alyson E. Mitchell ,&nbsp;Andrew C. Shin ,&nbsp;Fereshteh Dehghani ,&nbsp;Chwan-Li Shen","doi":"10.1016/j.jnutbio.2025.109862","DOIUrl":"10.1016/j.jnutbio.2025.109862","url":null,"abstract":"<div><div>Fruits and vegetables contain biologically active phenolic compounds that show mitigating effects against free radical damage and inflammation. The unique properties of phenolic compounds are protection against oxidative stress, and inception and potentiating of inflammation in the body. Aging is manifest with changes in epigenetic modifications and as with living systems undergo entropy. The gradual decline of body functions and in many cases with aging the cellular processes of senescence are contributors to age-related diseases. Herein the focus is on phenolic compounds as a diet approach to delay the negative consequences of aging. The actions of phenolic compounds on the biology of aging and senescence are presented. The phenolic compounds called flavonoids which are found in many fruits are potential antisenescence factors that benefit health by reducing damage to DNA and the senescence-associated phenotypic cell changes in healthy cells during aging. Flavonoids are proposed to delay and palliate aging where senescence is involved. The dietary sources of natural phenolic compounds afford protection in the aging process and include as some examples naringenin, hesperidin, quercetin, kaempferol, luteolin, genistein, epigallocatechin gallate, and resveratrol. Many of these compounds possess antisenescence effects. The purpose of the review is to discuss where food flavonoids interact with the targets of senescence and how these compounds can attenuate aging-related events. The goal is to provide greater insight into dietary flavonoids and how they improve health and lower the consequences of aging. A novel aspect of this review is the application of flavonoids to neuroprotective effects in brain to reduce pain and improve health with aging.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"139 ","pages":"Article 109862"},"PeriodicalIF":4.8,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143391136","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":"L-theanine prevents ulcerative colitis by regulating the CD4+ T cell immune response through the gut microbiota and its metabolites","authors":"Wei Xu ,&nbsp;Aoxiang Liu ,&nbsp;Zhihua Gong ,&nbsp;Wenjun Xiao","doi":"10.1016/j.jnutbio.2025.109845","DOIUrl":"10.1016/j.jnutbio.2025.109845","url":null,"abstract":"<div><div>The disturbance of gut microbiota and its metabolites are considered to be the causes of ulcerative colitis (UC), which leads to immune abnormalities. Diet is the most important regulator of gut microbiota; therefore, it has a beneficial impact on UC. A novel food ingredient, <span>l</span>-theanine, alters the gut microbiota, thereby regulating gut immunity. However, whether <span>l</span>-theanine prevents UC by altering the gut microbiota, as well as the underlying mechanisms, remains unknown. Here, <span>l</span>-theanine was used to optimize the gut microbiota and its metabolites. Furthermore, to explore the mechanism by which <span>l</span>-theanine prevents UC, an <span>l</span>-theanine fecal microbiota solution was used to prevent dextran sulfate sodium-induced UC via fecal microbiota transplantation. Improvements in the colonic structure, colon histology scores, immune factors (IL-10), and inflammatory factors (IL-1β) demonstrated the preventive effect of <span>l</span>-theanine on UC. The <em>16S</em> rDNA and metabolomic results showed that tryptophan-, short chain fatty acid-, and bile acid-related microbiota, such as Muribaculaceae, Lachnospiraceae, Alloprevotella, and Prevotellaceae were the dominant. Flow cytometry results showed that <span>l</span>-theanine decreased helper T (Th)1 and Th17 immune responses, and increased Th2 and T-regulatory immune responses via regulation of antigen-presenting cell responses, such as dendritic cells and macrophages. Therefore, <span>l</span>-theanine regulated the immune response of colon CD4 + <em>T</em> cells to dendritic cell and macrophage antigen presentation via tryptophan-, short chain fatty acid-, and bile acid-related microbiota, thereby preventing dextran sulfate sodium-induced UC.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"139 ","pages":"Article 109845"},"PeriodicalIF":4.8,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143374372","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":"Lactucin and lactucopicrin ameliorate obesity in high-fat diet fed mice by promoting white adipose tissue browning through the activation of the AMPK/SIRT1/PGC-1α pathway","authors":"Yewei Zhong,&nbsp;Junlin Yan,&nbsp;Yi Lei,&nbsp;Rui Zhang,&nbsp;Adalaiti Abudurexiti,&nbsp;Shuwen Qi,&nbsp;Wenhui Hou,&nbsp;Xiaoli Ma","doi":"10.1016/j.jnutbio.2025.109851","DOIUrl":"10.1016/j.jnutbio.2025.109851","url":null,"abstract":"<div><div>Lactucin and lactucopicrin are the characteristic lipid-lowering active components found in <em>Cichorium glandulosum</em>. However, their effects and underlying mechanisms in obesity remain unclear. In the present study, C57BL/6J mice were simultaneously subjected to a high-fat diet (HFD) and treated with drugs to investigate the impacts of lactucin and lactucopicrin on HFD-induced obese mice. The results demonstrated that in HFD obese mice, lactucin and lactucopicrin significantly decreased body weight and the weights of adipose tissues, improved serum metabolic parameters, and increased the content of irisin. Regarding the intermediate metabolites of intestinal flora, which are closely associated with white adipose tissue (WAT) browning, lactucin and lactucopicrin treatment led to a reduction in the levels of 12-α-OH/non-12-α-OH bile acids (BAs) and also tended to enhance the levels of short-chain fatty acids (SCFAs). qRT-PCR results indicated that lactucin and lactucopicrin treatment elevated the expression levels of genes related to beige fat markers, thermogenesis, mitochondrial biogenesis, and lipolysis in WAT, as well as those of thermogenesis and lipolysis genes in brown adipose tissue (BAT). Western blot analysis revealed that lactucin and lactucopicrin up-regulated the expression of uncoupling protein 1 (UCP1), the core protein in thermogenesis, in both WAT and BAT. Moreover, they also up-regulated the expression levels of AMP-activated kinase (AMPK), sirtuin 1 (SIRT1), and PPARγ coactivator 1-alpha (PGC-1α), which are key pathway proteins involved in WAT browning. Furthermore, 16S rRNA sequencing results showed that in HFD obese mice, lactucin and lactucopicrin improved the composition and function of the intestinal microbiota. In conclusion, lactucin and lactucopicrin may promote WAT browning by activating the AMPK/SIRT1/PGC-1α pathway, thereby ameliorating obesity in HFD mice.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"139 ","pages":"Article 109851"},"PeriodicalIF":4.8,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143255954","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 “Pomegranate (Punica granatum L.) phytochemicals target the components of metabolic syndrome” [Journal of Nutritional Biochemistry 131 (2024) 109670]","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.2024.109793","DOIUrl":"10.1016/j.jnutbio.2024.109793","url":null,"abstract":"","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"136 ","pages":"Article 109793"},"PeriodicalIF":4.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142801166","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}