Nutrition & Metabolism最新文献

{"title":"Effects of riboflavin deficiency and high dietary fat on hepatic lipid accumulation: a synergetic action in the development of non-alcoholic fatty liver disease","authors":"Yanxian Wang, Xiangyu Bian, Min Wan, Weiyun Dong, Weina Gao, Zhanxin Yao, Changjiang Guo","doi":"10.1186/s12986-023-00775-8","DOIUrl":"https://doi.org/10.1186/s12986-023-00775-8","url":null,"abstract":"Non-alcoholic fatty liver disease (NAFLD) is characterized by excessive lipid accumulation in the liver. Riboflavin, one of water soluble vitamins, plays a role in lipid metabolism and antioxidant function. However, the effects of riboflavin deficiency on NAFLD development have not yet to be fully explored. In the present study, an animal model of NAFLD was induced by high fat diet feeding in mice and a cellular model of NAFLD was developed in HepG2 cells by palmitic acid (PA) exposure. The effects of riboflavin deficiency on lipid metabolism and antioxidant function were investigated both in vivo and in vitro. In addition, the possible role of peroxisome proliferator-activated receptor gamma (PPARγ) was studied in HepG2 cells using gene silencing technique. The results showed that riboflavin deficiency led to hepatic lipid accumulation in mice fed high fat diet. The expressions of fatty acid synthase (FAS) and carnitine palmitoyltransferase 1 (CPT1) were up-regulated, whereas that of adipose triglyceride lipase (ATGL) down-regulated. Similar changes in response to riboflavin deficiency were demonstrated in HepG2 cells treated with PA. Factorial analysis revealed a significant interaction between riboflavin deficiency and high dietary fat or PA load in the development of NAFLD. Hepatic PPARγ expression was significantly upregulated in mice fed riboflavin deficient and high fat diet or in HepG2 cells treated with riboflavin deficiency and PA load. Knockdown of PPARγ gene resulted in a significant reduction of lipid accumulation in HepG2 cells exposed to riboflavin deficiency and PA load. There is a synergetic action between riboflavin deficiency and high dietary fat on the development of NAFLD, in which PPARγ may play an important role.","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"29 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139079986","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":"Deficiency of Trex1 leads to spontaneous development of type 1 diabetes","authors":"Jiang-Man Zhao, Zhi-Hui Su, Qiu-Ying Han, Miao Wang, Xin Liu, Jing Li, Shao-Yi Huang, Jing Chen, Xiao-Wei Li, Xia-Ying Chen, Zeng-Lin Guo, Shuai Jiang, Jie Pan, Tao Li, Wen Xue, Tao Zhou","doi":"10.1186/s12986-023-00777-6","DOIUrl":"https://doi.org/10.1186/s12986-023-00777-6","url":null,"abstract":"Type 1 diabetes is believed to be an autoimmune condition, characterized by destruction of insulin-producing cells, due to the detrimental inflammation in pancreas. Growing evidences have indicated the important role of type I interferon in the development of type 1 diabetes. Trex1-deficient rats were generated by using CRISPR-Cas9. The fasting blood glucose level of rat was measured by a Roche Accuchek blood glucose monitor. The levels of insulin, islet autoantibodies, and interferon-β were measured using enzyme-linked immunosorbent assay. The inflammatory genes were detected by quantitative PCR and RNA-seq. Hematein-eosin staining was used to detect the pathological changes in pancreas, eye and kidney. The pathological features of kidney were also detected by Masson trichrome and periodic acid-Schiff staining. The distribution of islet cells, immune cells or ssDNA in pancreas was analyzed by immunofluorescent staining. In this study, we established a Trex1-deletion Sprague Dawley rat model, and unexpectedly, we found that the Trex1−/− rats spontaneously develop type 1 diabetes. Similar to human diabetes, the hyperglycemia in rats is accompanied by diabetic complications such as diabetic nephropathy and cataract. Mechanistical investigation revealed the accumulation of ssDNA and the excessive production of proinflammatory cytokines, including IFN-β, in Trex1 null pancreas. These are likely contributing to the inflammation in pancreas and eventually leading to the decline of pancreatic β cells. Our study links the DNA-induced chronic inflammation to the pathogenesis of type 1 diabetes, and also provides an animal model for type 1 diabetes studies.","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"172 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139079927","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":"Effect of probiotic supplementation on lipoprotein-associated phospholipase A2 in type 2 diabetic patients: a randomized double blind clinical controlled trial","authors":"Salman Jaff, Mohammed Gubari, Sakineh Shab-Bidar, Kurosh Djafarian","doi":"10.1186/s12986-023-00778-5","DOIUrl":"https://doi.org/10.1186/s12986-023-00778-5","url":null,"abstract":"It has been recently reported that lipoprotein-associated phospholipase A2 (Lp-PLA2) may predict the risk of cardiovascular disease. The effect of multi-strain probiotics on Lp-PLA2 in patients with type 2 diabetes is still not clear. This study aimed to determine the effect of multi-strain probiotic supplementation on lipoprotein-associated phospholipase A2, and glycemic status, lipid profile, and body composition in patients with type 2 diabetes. In this randomized double-blind placebo-controlled clinical trial, 68 participants with type 2 diabetes, in the age group of 50–65 years, were recruited and randomly allocated to take either probiotic (n = 34) or placebo (n = 34) for 12 weeks. The primary outcome was lipoprotein-associated phospholipase A2, and secondary outcomes were glycemic parameters, lipid profile, anthropometric characters, and body composition (fat mass and fat-free mass). There was a significant reduction in serum lipoprotein-associated phospholipase A2, in the probiotic group, it dropped by 6.4 units at the end of the study (p < 0.001) compared to the placebo group. Probiotic supplementation also resulted in a significant improvement in the hemoglobin A1c and high-density lipoprotein cholesterol 1.5% (p < 0.001) and 6 mg/dl (p 0.005), respectively. There were no significant changes in other outcomes. Probiotic supplementation was beneficial for reducing Lp-PLA2 and hemoglobin-A1c and improving high-density lipoprotein cholesterol, which may suggest an improvement in the prognosis in patients with type 2 diabetes.","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"28 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139079928","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":"D-mannose promotes the degradation of IDH2 through upregulation of RNF185 and suppresses breast cancer","authors":"Ruonan Zhang, Ziyin Tian, Yanping Xu, Lei Lv","doi":"10.1186/s12986-023-00774-9","DOIUrl":"https://doi.org/10.1186/s12986-023-00774-9","url":null,"abstract":"D-mannose, an epimer of glucose, which is abundant in some fruits, such as cranberry, has been previously reported to inhibit urinary tract infection. In recent years, the potential function of D-mannose has been broadened into the regulation of other inflammation diseases and cancer. It was reported that D-mannose can increase reactive oxygen species (ROS) production, while IDH2 is important for the generation of NADPH, the crucial reducing factor. These findings prompted us to determine whether D-mannose can regulate IDH2 and IDH2-mediated NADPH production in tumor. The breast cancer cell line MDA-MB-231 was cultured and treated with 100mM D-mannose. IDH2 expression was detected by Western Blot and qRT-PCR. RNA-seq was conducted to identify the differentially expressed genes. BioGRID database was used to find the IDH2 interactors. Tumor cells were collected to measure the NADPH production using the NADP+/NADPH detection Kit. Colony formation assay and CCK-8 assay were conducted to evaluate the proliferation of cells. D-mannose can promote IDH2 protein degradation through ubiquitination-proteasome pathway. Mechanistically, D-mannose treatment upregulated the expression of an E3 ligase - RNF185, which can interact with IDH2 and promotes its proteasomal degradation. Consequently, IDH2-mediated NADPH production was inhibited by D-mannose, the proliferation of breast cancer cells was retarded, and the sensitivity to pro-oxidant of breast cancer cells was elevated. Our study demonstrated that D-mannose can degrade IDH2 and inhibit the production of NADPH to suppress the proliferation of breast cancer cells and render the breast cancer cells more sensitive to pro-oxidant treatment. Furthermore, we illustrated the E3 ligase RNF185 plays an important role in D-mannose-mediated proteasomal degradation of IDH2.","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"99 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139084527","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":"Amelioration of Atherosclerosis by lycopene is linked to the modulation of gut microbiota dysbiosis and related gut-heart axis activation in high-fat diet-fed ApoE^-/- mice.","authors":"Tengcan Tu, Hao Liu, Zhenhao Liu, Yunyi Liang, Chujun Tan, Dan Feng, Jun Zou","doi":"10.1186/s12986-023-00772-x","DOIUrl":"10.1186/s12986-023-00772-x","url":null,"abstract":"<p><strong>Background: </strong>Interplay between gut microbiota and heart, termed \"gut-heart\" axis, has a crucial role in the pathogenesis of atherosclerosis. Our previous study showed that lycopene possesses anti-inflammatory and anti-atherosclerotic effects, but its link to the gut microbiota is poorly understood. Herein, we surmised that lycopene could regulate the gut microbiota, exert anti-atherosclerotic effect by regulating the \"gut-heart\" axis.</p><p><strong>Methods: </strong>Male ApoE^-/- mice were fed a high-fat diet (HFD) with or without lycopene (0.1% w/w) for 19 weeks. Gut microbiota was analyzed by 16 S rRNA sequencing, the protein levels of zonula occludens-1 (ZO-1), occludin, toll-like receptor 4 (TLR4) and phospho-nuclear factor-κB (NF-κB) p65 were measured by Western blotting, the levels of serum inflammatory factors including monocyte chemotactic protein 1 (MCP-1), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 were assayed using ELISA kits. Also, the concentrations of serum lipopolysaccharide (LPS), D-lactic acid (D-LA) and diamine peroxidase (DAO) were measured through ELISA method.</p><p><strong>Results: </strong>The aortic sinus sections revealed that lycopene supplementation significantly reduced the extent of atherosclerotic lesions and inhibited atherosclerosis development caused by HFD. The analysis of gut microbiota showed that lycopene reduced the ratio of Firmicutes/Bacteroides and increased the relative abundance of Verrucomicrobia, Akkermansia and Alloprevotella, which were related to elevated intestinal barrier function and reduced inflammation. Moreover, lycopene up-regulated the expression of intestinal ZO-1 and occludin and decreased serum LPS, D-LA and DAO levels. In addition, lycopene inhibited the expression of TLR4 and phospho-NF-κB p65 in aortic sinus plaque, serum MCP-1, TNF-α, IL-1β, and IL-6 levels were also lowered by lycopene treatment.</p><p><strong>Conclusions: </strong>Our results indicated the protective effect of lycopene against atherosclerosis induced by HFD and further revealed that its mechanism might be its prebiotic effect on maintaining gut microbiota homeostasis and improving intestinal barrier function, consequently reducing serum LPS-triggered inflammatory response in the heart.</p>","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"20 1","pages":"53"},"PeriodicalIF":4.5,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10691047/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138470643","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":"Correction: The association between dietary quality scores with C-reactive protein and novel biomarkers of inflammation platelet-activating factor and lipoprotein-associated phospholipase A2: a cross-sectional study.","authors":"Carolyn J English, Anna E Lohning, Hannah L Mayr, Mark Jones, Helen MacLaughlin, Dianne P Reidlinger","doi":"10.1186/s12986-023-00771-y","DOIUrl":"10.1186/s12986-023-00771-y","url":null,"abstract":"","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"20 1","pages":"52"},"PeriodicalIF":4.5,"publicationDate":"2023-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10683409/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138445594","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":"Exploring the underlying mechanisms of fisetin in the treatment of hepatic insulin resistance via network pharmacology and in vitro validation.","authors":"Tian Li, Junjun Ling, Xingrong Du, Siyu Zhang, Yan Yang, Liang Zhang","doi":"10.1186/s12986-023-00770-z","DOIUrl":"10.1186/s12986-023-00770-z","url":null,"abstract":"<p><strong>Objective: </strong>To characterize potential mechanisms of fisetin on hepatic insulin resistance (IR) using network pharmacology and in vitro validation.</p><p><strong>Methods: </strong>Putative targets of fisetin were retrieved from the Traditional Chinese Medicine Systems Pharmacology database, whereas the potential genes of hepatic IR were obtained from GeneCards database. A protein-protein interaction (PPI) network was constructed according to the intersection targets of fisetin and hepatic IR using the Venn diagram. The biological functions and potential pathways related to genes were determined using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Cell experiments were also conducted to further verify the mechanism of fisetin on hepatic IR.</p><p><strong>Results: </strong>A total of 118 potential targets from fisetin were associated with hepatic IR. The areas of nodes and corresponding degree values of TP53, AKT1, TNF, IL6, CASP3, CTNNB1, JUN, SRC, epidermal growth factor receptor (EGFR), and HSP90AA1 were larger and could be easily found in the PPI network. Furthermore, GO analysis revealed that these key targets were significantly involved in multiple biological processes that participated in oxidative stress and serine/threonine kinase activity. KEGG enrichment analysis showed that the PI3K/AKT signaling pathway was a significant pathway involved in hepatic IR. Our in vitro results demonstrated that fisetin treatment increased the expressions of EGFR and IRS in HepG2 and L02 cells under normal or IR conditions. Western blot results revealed that p-AKT/AKT levels were significantly up-regulated, suggesting that fisetin was involved in the PI3K/AKT signaling pathway to regulate insulin signaling.</p><p><strong>Conclusion: </strong>We explored the pharmacological actions and the potential molecular mechanism of fisetin in treating hepatic IR from a holistic perspective. Our study lays a theoretical foundation for the development of fisetin for type 2 diabetes.</p>","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"20 1","pages":"51"},"PeriodicalIF":4.5,"publicationDate":"2023-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10666360/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138299705","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":"Intrauterine growth restriction alters kidney metabolism at the end of nephrogenesis.","authors":"Sheng-Yuan Ho, Merryl Esther Yuliana, Hsiu-Chu Chou, Chung-Ming Chen","doi":"10.1186/s12986-023-00769-6","DOIUrl":"10.1186/s12986-023-00769-6","url":null,"abstract":"<p><strong>Background: </strong>This study investigated the effect of uteroplacental insufficiency (UPI) on renal development by detecting metabolic alterations in the kidneys of rats with intrauterine growth restriction (IUGR).</p><p><strong>Methods: </strong>On gestational day 17, pregnant Sprague Dawley rats were selected and allocated randomly to either the IUGR group or the control group. The IUGR group received a protocol involving the closure of bilateral uterine vessels, while the control group underwent a sham surgery. The rat pups were delivered on gestational day 22 by natural means. Pups were randomly recruited from both the control and IUGR groups on the seventh day after birth. The kidneys were surgically removed to conduct Western blot and metabolomic analyses.</p><p><strong>Results: </strong>IUGR was produced by UPI, as evidenced by the significantly lower body weights of the pups with IUGR compared to the control pups on postnatal day 7. UPI significantly increased the levels of cleaved caspase-3 (p < 0.05) and BAX/Bcl-2 (p < 0.01) in the pups with IUGR. Ten metabolites exhibited statistically significant differences between the groups (q < 0.05). Metabolic pathway enrichment analysis demonstrated statistically significant variations between the groups in the metabolism related to fructose and mannose, amino and nucleotide sugars, and inositol phosphate.</p><p><strong>Conclusions: </strong>UPI alters kidney metabolism in growth-restricted newborn rats and induces renal apoptosis. The results of our study have the potential to provide new insights into biomarkers and metabolic pathways that are involved in the kidney changes generated by IUGR.</p>","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"20 1","pages":"50"},"PeriodicalIF":4.5,"publicationDate":"2023-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10664663/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138291506","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":"A comparative study on indicators of vitamin A status and risk factors for sensitivity and specificity of the methods to detect vitamin A deficiency.","authors":"Olivier O Sombié, Augustin N Zeba, Jérome W Somé, Adama Kazienga, Michael Grahn, Sherry A Tanumihardjo, Stefaan De Henauw, Souheila Abbeddou","doi":"10.1186/s12986-023-00768-7","DOIUrl":"10.1186/s12986-023-00768-7","url":null,"abstract":"<p><strong>Background: </strong>Serum retinol (SR) and retinol-binding protein (RBP) are commonly used indicators, but they are affected by infections and inflammation. This study aimed to assess the sensitivity and specificity of VA indicators to detect vitamin A deficiency (VAD) in 36-59-month-old children living in a rural area in Burkina Faso.</p><p><strong>Methods: </strong>In a community-based study, two cross-sectional surveys were carried out from November 2016 to September 2017 in the health district of Dandé in Burkina Faso. The surveys included 115 children 36-59 months old. Indicators of VA and inflammation assessed in all children included SR, RBP and total liver VA reserves (TLR) estimated by retinol isotope dilution, and inflammation markers (C-reactive protein (CRP) and alpha 1-acid glycoprotein (AGP)). We calculated the sensitivity, specificity, positive and negative predictive values. In addition, the effects of inflammation, helminth infection, and season on sensitivity and specificity were assessed.</p><p><strong>Results: </strong>The prevalence of VAD assessed by SR (< 0.7 µmol/L), RBP (< 0.7 µmol/L), and TLR (< 0.1 µmol/g liver) were, respectively, 30.9%, 33.3%, and 0%. Compared to TLR, the specificity, positive predictive value, and negative predictive value of SR were 71.1%, 0%, and 100%, and of RBP, were 68.9%, 0%, and 100%, respectively. The sensitivity was indeterminable for SR and RBP. The specificity of SR and RBP was lower during the dry season. Elevated CRP (> 5.0 mg/L) and AGP (> 1.0 g/L) were detected in 1.9% and 28.6% of children, respectively. The adjustment of VA indicators for inflammation improved SR's specificity to 75.9% and decreased RBP's specificity to 67.8%.</p><p><strong>Conclusion: </strong>No cases of VAD were identified by TLR. However, (inflammation-adjusted) SR and RBP had varying accuracy in the estimation of VAD.</p><p><strong>Trial registration: </strong>The study was registered, retrospectively, on 22 March 2018 as a clinical trial with the Pan African Clinical Trials Registry under the number Cochrane South Africa; PACTR201803002999356.</p>","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"20 1","pages":"49"},"PeriodicalIF":4.5,"publicationDate":"2023-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10652566/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136398481","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":"Early adulthood weight change, midlife \"Life's essential 8\" health status and risk of cardiometabolic diseases: a chinese nationwide cohort study.","authors":"Qiuyu Cao,&nbsp;Mian Li,&nbsp;Guijun Qin,&nbsp;Li Yan,&nbsp;Jiang He,&nbsp;Min Xu,&nbsp;Yu Xu,&nbsp;Tiange Wang,&nbsp;Yuhong Chen,&nbsp;Shuangyuan Wang,&nbsp;Hong Lin,&nbsp;Zhiyun Zhao,&nbsp;Zhengnan Gao,&nbsp;Tianshu Zeng,&nbsp;Ruying Hu,&nbsp;Xuefeng Yu,&nbsp;Gang Chen,&nbsp;Qing Su,&nbsp;Yiming Mu,&nbsp;Lulu Chen,&nbsp;Xulei Tang,&nbsp;Qin Wan,&nbsp;Guixia Wang,&nbsp;Feixia Shen,&nbsp;Zuojie Luo,&nbsp;Yingfen Qin,&nbsp;Li Chen,&nbsp;Yanan Huo,&nbsp;Qiang Li,&nbsp;Zhen Ye,&nbsp;Yinfei Zhang,&nbsp;Chao Liu,&nbsp;Youmin Wang,&nbsp;Shengli Wu,&nbsp;Tao Yang,&nbsp;Huacong Deng,&nbsp;Jiajun Zhao,&nbsp;Lixin Shi,&nbsp;Guang Ning,&nbsp;Weiqing Wang,&nbsp;Jieli Lu,&nbsp;Yufang Bi","doi":"10.1186/s12986-023-00765-w","DOIUrl":"10.1186/s12986-023-00765-w","url":null,"abstract":"<p><strong>Background: </strong>The association between weight change during early adulthood and cardiometabolic diseases remains uncertain in Chinese population. Whether the association varies with comprehensive cardiovascular health (CVH) in midlife assessed by \"Life's Essential 8\" has not been characterized. We aim to examine the associations of early adulthood weight change and midlife \"Life's Essential 8\" CVH status with cardiometabolic outcomes in a Chinese cohort.</p><p><strong>Methods: </strong>The study participants were from the China Cardiometabolic Disease and Cancer Cohort (4 C) Study. This analysis included 72,610 middle-aged and older participants followed for a median of 3.6 years. At baseline, the participants recalled body weight at age 20 and 40 years, and we calculated change in weight and BMI between 20 and 40 years of age. Health behaviors information in \"Life's Essential 8\" was collected by questionnaire, and health factors were measured in the study center. During follow-up, we ascertained incident cardiovascular events based on medical records, and diagnosed incident diabetes according to the American Diabetes Association 2010 criteria.</p><p><strong>Results: </strong>72,610 study participants were included with a mean age of 56.0 ± 8.8 years and 29% of them were males. Weight gain of more than 10 kg between 20 and 40 years of age was associated with 22% increased risk of incident cardiovascular events (HR: 1.22; 95%CI: 1.04-1.43) and 38% increased risk of diabetes (HR: 1.38; 95%CI: 1.25-1.53) compared to stable weight. Besides, the association of weight gain more than 10 kg in early adulthood with cardiometabolic risk was even stronger in those with low CVH score in midlife (HR: 2.44; 95%CI: 2.01-2.97 for incident cardiovascular events; HR: 2.20; 95%CI: 1.90-2.55 for incident diabetes) or with few ideal cardiovascular health metrics in midlife.</p><p><strong>Conclusions: </strong>Our study indicated that weight gain in early adulthood was associated with significantly increased risk of cardiometabolic diseases. And the association could be stronger in those with poor CVH profiles in midlife. These findings confirmed the significance of weight management during early adulthood and suggested that individuals who experienced substantial weight gain in early life should be encouraged to maintain good CVH status in Chinese population.</p>","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"20 1","pages":"48"},"PeriodicalIF":4.5,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10621175/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71425467","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}