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Article ; Online: Dietary Niacin Intake and Mortality Among Individuals With Nonalcoholic Fatty Liver Disease.

Pan, Jie / Zhou, Yujia / Pang, Nengzhi / Yang, Lili

JAMA network open

2024 Volume 7, Issue 2, Page(s) e2354277

Abstract: Importance: Evidence regarding the effect of dietary niacin intake on the risk of mortality among patients with nonalcoholic fatty liver disease (NAFLD) is scarce.: Objective: To examine the association of dietary niacin intake with all-cause ... ...

Abstract	Importance: Evidence regarding the effect of dietary niacin intake on the risk of mortality among patients with nonalcoholic fatty liver disease (NAFLD) is scarce. Objective: To examine the association of dietary niacin intake with all-cause mortality and cardiovascular disease (CVD) mortality among individuals with NAFLD. Design, setting, and participants: This cohort study used data from the National Health and Nutrition Examination Survey (2003-2018). In total, 4315 adults aged 20 years or older with NAFLD were included, with NAFLD defined using the United States Fatty Liver Index. Exposure: Dietary niacin intake levels. Main outcomes and measures: Weighted Cox proportional hazards models and restricted cubic splines were used to estimate hazard ratios and 95% CIs for all-cause and CVD mortality. Data were analyzed March 1 to September 1, 2023. Results: This cohort study included data from 4315 participants in the analysis (mean [SD] age, 52.5 [16.2] years; 1670 participants ≥60 years [weighted, 30.9%]; 2351 men [weighted, 55.0%]). During a median (IQR) follow-up of 8.8 (4.6-11.8) years, 566 deaths were recorded, of which 197 were attributed to CVD. Compared with participants with a niacin intake of 18.4 mg or lower (the lowest tertile), the multivariable-adjusted hazard ratios for participants with a niacin intake of 26.7 mg or higher (the highest tertile) were 0.70 (95% CI, 0.50-0.96) for all-cause mortality (P = .03 for trend) and 0.65 (95% CI, 0.35-1.20) for CVD mortality (P = .16 for trend). Conclusions and relevance: Findings from this cohort study suggest that higher dietary niacin intake may be associated with lower risk of all-cause mortality among individuals with NAFLD. There was no evident inverse association between dietary niacin intake and the risk of CVD mortality.
MeSH term(s)	Adult ; Male ; Humans ; Middle Aged ; Non-alcoholic Fatty Liver Disease ; Niacin ; Cohort Studies ; Nutrition Surveys ; Cardiovascular Diseases
Chemical Substances	Niacin (2679MF687A)
Language	English
Publishing date	2024-02-05
Publishing country	United States
Document type	Journal Article
ISSN	2574-3805
ISSN (online)	2574-3805
DOI	10.1001/jamanetworkopen.2023.54277
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Article ; Online: Association between Dietary Niacin Intake and Nonalcoholic Fatty Liver Disease: NHANES 2003-2018.

Pan, Jie / Hu, Yuhua / Pang, Nengzhi / Yang, Lili

Nutrients

2023 Volume 15, Issue 19

Abstract: Evidence regarding the association between dietary niacin intake and nonalcoholic fatty liver disease (NAFLD) is limited. The objective of this study was to examine the association of dietary niacin intake with NAFLD. Subjects aged 20 years and older who ...

Abstract	Evidence regarding the association between dietary niacin intake and nonalcoholic fatty liver disease (NAFLD) is limited. The objective of this study was to examine the association of dietary niacin intake with NAFLD. Subjects aged 20 years and older who participated in the National Health and Nutrition Examination Survey (NHANES) 2003-2018 were included in this study. Dietary niacin intake was assessed by two 24-h dietary recalls. NAFLD was defined using the United States fatty liver index (US-FLI). Weighted logistic regression models and restricted cubic splines were used to examine the association between dietary niacin and NAFLD. Of the 12,355 participants in this study, 4378 had NAFLD. There is no evident nonlinear relationship between dietary niacin intake and the presence of NAFLD in the restricted cubic spline regression (
MeSH term(s)	Humans ; United States/epidemiology ; Non-alcoholic Fatty Liver Disease/epidemiology ; Non-alcoholic Fatty Liver Disease/etiology ; Nutrition Surveys ; Niacin ; Diet ; Nutritional Status
Chemical Substances	Niacin (2679MF687A)
Language	English
Publishing date	2023-09-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu15194128
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Article: Increased Serum Adipsin Correlates with MAFLD and Metabolic Risk Abnormalities.

Pan, Jie / Li, Qiuyan / Sun, Yan / Gu, Yingying / Ding, Yijie / Pang, Nengzhi / Zhou, Yujia / Pei, Lei / Gao, Mengqi / Ma, Sixi / Xiao, Ying / Wu, Feilong / Hu, De / Chen, Yu-Ming / Yang, Lili

Diabetes, metabolic syndrome and obesity : targets and therapy

2023 Volume 16, Page(s) 187–200

Abstract: Purpose: A panel of international experts proposed a new definition of fatty liver in 2020, namely metabolic dysfunction-associated fatty liver disease (MAFLD). As an adipokine, adipsin is closely related to metabolic-related diseases. In this study, we ...

Abstract	Purpose: A panel of international experts proposed a new definition of fatty liver in 2020, namely metabolic dysfunction-associated fatty liver disease (MAFLD). As an adipokine, adipsin is closely related to metabolic-related diseases. In this study, we aimed to evaluate the relationship among MAFLD, serum adipsin, and metabolic risk abnormalities. Methods: Our study was a cross-sectional study based on the first follow-up of the Guangzhou Nutrition and Health Study (GNHS). A total of 908 patients with hepatic steatosis were involved in our study. Detailed data of patients were collected based upon questionnaire information, physical examination, and blood biochemical test. Results: Among the 908 patients, 789 patients were diagnosed with MAFLD. The levels of serum adipsin in the MAFLD group and non-MAFLD group were (3543.00 (3187.94-3972.50) ng/mL) and (3095.33 (2778.71-3354.77) ng/mL) ( Conclusion: Increased serum adipsin correlates with MAFLD. Both adipsin levels as well as fatty liver severity increase with higher numbers of metabolic risk abnormalities.
Language	English
Publishing date	2023-01-23
Publishing country	New Zealand
Document type	Journal Article
ZDB-ID	2494854-8
ISSN	1178-7007
ISSN	1178-7007
DOI	10.2147/DMSO.S396335
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Article: Associations between Adipokines and Metabolic Dysfunction-Associated Fatty Liver Disease Using Three Different Diagnostic Criteria.

Pan, Jie / Ding, Yijie / Sun, Yan / Li, Qiuyan / Wei, Tianyi / Gu, Yingying / Zhou, Yujia / Pang, Nengzhi / Pei, Lei / Ma, Sixi / Gao, Mengqi / Xiao, Ying / Hu, De / Wu, Feilong / Yang, Lili

Journal of clinical medicine

2023 Volume 12, Issue 6

Abstract: Background: A panel of experts proposed a new definition of metabolic dysfunction-associated fatty liver disease (MAFLD) in 2020. To date, the associations between adipokines, such as adiponectin, adipsin, and visfatin and MAFLD remain unclear. ... ...

Abstract	Background: A panel of experts proposed a new definition of metabolic dysfunction-associated fatty liver disease (MAFLD) in 2020. To date, the associations between adipokines, such as adiponectin, adipsin, and visfatin and MAFLD remain unclear. Therefore, we aimed to evaluate the associations between each of these three adipokines and MAFLD using different diagnostic criteria. Methods: In total, 221 participants were included in our study based on medical examination. Detailed questionnaire information, physical examination, abdominal ultrasound, and blood-biochemical-test indexes were collected. The levels of adipokines were tested by using an enzyme immunoassay. Logistic regression models were used to assess the associations of the adipokines with MAFLD. Results: In total, 122 of the participants were diagnosed with MAFLD. Higher levels of adipsin and lower levels of adiponectin were found in the MAFLD group than in the non-MAFLD group (all Conclusion: Adipsin levels were positively associated with MAFLD and adiponectin levels were inversely associated with MAFLD. The strength of these associations varied according to the different diagnostic criteria for MAFLD.
Language	English
Publishing date	2023-03-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662592-1
ISSN	2077-0383
ISSN	2077-0383
DOI	10.3390/jcm12062126
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Article ; Online: Improving Mitochondrial Function in Skeletal Muscle Contributes to the Amelioration of Insulin Resistance by Nicotinamide Riboside.

Li, Qiuyan / Jiang, Xuye / Zhou, Yujia / Gu, Yingying / Ding, Yijie / Luo, Jing / Pang, Nengzhi / Sun, Yan / Pei, Lei / Pan, Jie / Gao, Mengqi / Ma, Sixi / Xiao, Ying / Hu, De / Wu, Feilong / Yang, Lili

International journal of molecular sciences

2023 Volume 24, Issue 12

Abstract: High-fat diet (HFD)-induced insulin resistance (IR) in skeletal muscle is often accompanied by mitochondrial dysfunction and oxidative stress. Boosting nicotinamide adenine dinucleotide (NAD) using nicotinamide riboside (NR) can effectively decrease ... ...

Abstract	High-fat diet (HFD)-induced insulin resistance (IR) in skeletal muscle is often accompanied by mitochondrial dysfunction and oxidative stress. Boosting nicotinamide adenine dinucleotide (NAD) using nicotinamide riboside (NR) can effectively decrease oxidative stress and increase mitochondrial function. However, whether NR can ameliorate IR in skeletal muscle is still inconclusive. We fed male C57BL/6J mice with an HFD (60% fat) ± 400 mg/kg·bw NR for 24 weeks. C2C12 myotube cells were treated with 0.25 mM palmitic acid (PA) ± 0.5 mM NR for 24 h. Indicators for IR and mitochondrial dysfunction were analyzed. NR treatment alleviated IR in HFD-fed mice with regard to improved glucose tolerance and a remarkable decrease in the levels of fasting blood glucose, fasting insulin and HOMA-IR index. NR-treated HFD-fed mice also showed improved metabolic status regarding a significant reduction in body weight and lipid contents in serum and the liver. NR activated AMPK in the skeletal muscle of HFD-fed mice and PA-treated C2C12 myotube cells and upregulated the expression of mitochondria-related transcriptional factors and coactivators, thereby improving mitochondrial function and alleviating oxidative stress. Upon inhibiting AMPK using Compound C, NR lost its ability in enhancing mitochondrial function and protection against IR induced by PA. In summary, improving mitochondrial function through the activation of AMPK pathway in skeletal muscle may play an important role in the amelioration of IR using NR.
MeSH term(s)	Male ; Mice ; Animals ; Insulin Resistance/physiology ; AMP-Activated Protein Kinases/metabolism ; Mice, Inbred C57BL ; Mitochondria ; Muscle, Skeletal/metabolism ; Insulin/metabolism ; Palmitic Acid/pharmacology ; Palmitic Acid/metabolism ; Diet, High-Fat/adverse effects
Chemical Substances	nicotinamide-beta-riboside (0I8H2M0L7N) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Insulin ; Palmitic Acid (2V16EO95H1)
Language	English
Publishing date	2023-06-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241210015
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Article: CBD Alleviates Liver Injuries in Alcoholics With High-Fat High-Cholesterol Diet Through Regulating NLRP3 Inflammasome-Pyroptosis Pathway.

Jiang, Xuye / Gu, Yingying / Huang, Yuanling / Zhou, Yujia / Pang, Nengzhi / Luo, Jing / Tang, Zhaoyang / Zhang, Zhenfeng / Yang, Lili

Frontiers in pharmacology

2021 Volume 12, Page(s) 724747

Abstract: Alcohol abuse and high-fat diet-induced liver diseases have been the most prevalent chronic liver diseases and the leading reasons for liver transplantation around the world. Cannabidiol (CBD) is a botanical component extracted from marijuana plants ... ...

Abstract	Alcohol abuse and high-fat diet-induced liver diseases have been the most prevalent chronic liver diseases and the leading reasons for liver transplantation around the world. Cannabidiol (CBD) is a botanical component extracted from marijuana plants without psychoactive impact. In our previous reports, we found that CBD can prevent fatty liver induced by Lieber-DeCarli ethanol diet or non-alcoholic fatty liver disease (NAFLD) induced by high-fat high-cholesterol diet. The current work is a further study on whether CBD can alleviate liver injuries induced by ethanol plus high-fat high-cholesterol diet (EHFD), which is a model simulating heavy alcohol drinkers in a Western diet. A mice liver injury model induced by EHFD for 8 weeks was applied to explore the protective properties of CBD and the underlying mechanisms. We found that CBD prevented liver steatosis and oxidative stress induced by EHFD. CBD treatment inhibited macrophage recruitment and suppressed activation of NFκB-NLRP3-pyroptosis pathway in mice livers. The hepatoprotective property of CBD in the current model might be a result of inhibition of inflammation via alleviating activation of the hepatic NFκB-NLRP3 inflammasome-pyroptosis pathway by CBD.
Language	English
Publishing date	2021-09-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2021.724747
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Article ; Online: Nicotinamide Adenine Dinucleotide Precursor Suppresses Hepatocellular Cancer Progression in Mice.

Pang, Nengzhi / Hu, Qianrong / Zhou, Yujia / Xiao, Ying / Li, Wenli / Ding, Yijie / Chen, Yunan / Ye, Mingtong / Pei, Lei / Li, Qiuyan / Gu, Yingying / Sun, Yan / Fang, Evandro Fei / Chen, Mianrong / Zhang, Zhenfeng / Yang, Lili

Nutrients

2023 Volume 15, Issue 6

Abstract: Targeting Nicotinamide adenine dinucleotide (NAD) metabolism has emerged as a promising anti-cancer strategy; we aimed to explore the health benefits of boosting NAD levels with nicotinamide riboside (NR) on hepatocellular carcinoma (HCC). We established ...

Abstract	Targeting Nicotinamide adenine dinucleotide (NAD) metabolism has emerged as a promising anti-cancer strategy; we aimed to explore the health benefits of boosting NAD levels with nicotinamide riboside (NR) on hepatocellular carcinoma (HCC). We established three in vivo tumor models, including subcutaneous transplantation tumor model in both Balb/c nude mice (xenograft), C57BL/6J mice (allograft), and hematogenous metastatic neoplasm in nude mice. NR (400 mg/kg bw) was supplied daily in gavage. In-situ tumor growth or noninvasive bioluminescence were measured to evaluate the effect of NR on the HCC process. HepG2 cells were treated with transforming growth factor-β (TGF-β) in the absence/presence of NR in vitro. We found that NR supplementation alleviated malignancy-induced weight loss and metastasis to lung in nude mice in both subcutaneous xenograft and hematogenous metastasis models. NR supplementation decreased metastasis to the bone and liver in the hematogenous metastasis model. NR supplementation also significantly decreased the size of allografted tumors and extended the survival time in C57BL/6J mice. In vitro experiments showed that NR intervention inhibited the migration and invasion of HepG2 cells triggered by TGF-β. In summary, our results supply evidence that boosting NAD levels by supplementing NR alleviates HCC progression and metastasis, which may serve as an effective treatment for the suppression of HCC progression.
MeSH term(s)	Mice ; Humans ; Animals ; NAD/metabolism ; Carcinoma, Hepatocellular/drug therapy ; Mice, Nude ; Liver Neoplasms/drug therapy ; Mice, Inbred C57BL ; Niacinamide/pharmacology ; Transforming Growth Factor beta
Chemical Substances	NAD (0U46U6E8UK) ; Niacinamide (25X51I8RD4) ; Transforming Growth Factor beta
Language	English
Publishing date	2023-03-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu15061447
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Article ; Online: Cyanidin-3-O-β-glucoside inactivates NLRP3 inflammasome and alleviates alcoholic steatohepatitis via SirT1/NF-κB signaling pathway.

Zhou, Yujia / Wang, Sufan / Wan, Ting / Huang, Yuanling / Pang, Nengzhi / Jiang, Xuye / Gu, Yingying / Zhang, Zhenfeng / Luo, Jing / Yang, Lili

Free radical biology & medicine

2020 Volume 160, Page(s) 334–341

Abstract: Alcoholic liver disease (ALD) is a major cause of liver disease worldwide. In patients with ALD, an increased level of hepatic inflammasome components was observed, together with an increased circulating pro-inflammatory cytokines. Cyanidin-3-O-β- ... ...

Abstract	Alcoholic liver disease (ALD) is a major cause of liver disease worldwide. In patients with ALD, an increased level of hepatic inflammasome components was observed, together with an increased circulating pro-inflammatory cytokines. Cyanidin-3-O-β-glucoside (Cy-3-G) is a bioactive compound belonging to the anthocyanin group, which widely exists in deep-colored fruits and vegetables. Consumption of Cy-3-G is associated with lower risks of non-alcoholic fatty liver disease (NAFLD), liver fibrosis, obesity, atherosclerosis, and inflammation. However, whether Cy-3-G has effects on inflammasome formation and activation thereby protects against alcohol-induced liver damage remain elusive. In this study, we identified that dietary provision of Cy-3-G remarkably attenuated liver damage caused by excess energy intake and alcohol consumption. Supplement with Cy-3-G mediated NAD
MeSH term(s)	Anthocyanins/pharmacology ; Fatty Liver, Alcoholic/drug therapy ; Humans ; Inflammasomes ; NF-kappa B/genetics ; NF-kappa B/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; Signal Transduction ; Sirtuin 1/genetics
Chemical Substances	Anthocyanins ; Inflammasomes ; NF-kappa B ; NLR Family, Pyrin Domain-Containing 3 Protein ; cyanidin-3-O-beta-glucopyranoside ; SIRT1 protein, human (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-)
Language	English
Publishing date	2020-08-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2020.08.006
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Article ; Online: Cannabidiol protects livers against nonalcoholic steatohepatitis induced by high-fat high cholesterol diet via regulating NF-κB and NLRP3 inflammasome pathway.

Huang, Yuanling / Wan, Ting / Pang, Nengzhi / Zhou, Yujia / Jiang, Xuye / Li, Bangyan / Gu, Yingying / Huang, Yufeng / Ye, Xiaodie / Lian, Hui / Zhang, Zhenfeng / Yang, Lili

Journal of cellular physiology

2019 Volume 234, Issue 11, Page(s) 21224–21234

Abstract: Cannabidiol (CBD), an abundant nonpsychoactive constituent of marijuana, has been reported previously to protect against hepatic steatosis. In this study, we studied further the functions and mechanisms of CBD on liver inflammation induced by HFC diet. ... ...

Abstract	Cannabidiol (CBD), an abundant nonpsychoactive constituent of marijuana, has been reported previously to protect against hepatic steatosis. In this study, we studied further the functions and mechanisms of CBD on liver inflammation induced by HFC diet. Mice feeding an HFC diet for 8 weeks were applied to test the protective effect of CBD on livers. RAW264.7 cells were incubated with LPS + ATP ± CBD to study the mechanisms of the effect of CBD against inflammasome activation. We found that CBD alleviated liver inflammation induced by HFC diet. CBD significantly inhibited the nuclear factor-κappa B (NF-κB) p65 nuclear translocation and the activation of nucleotide-binding domain like receptor protein 3 (NLRP3) inflammasome both in vivo and in vitro studies, which lead to the reduction of the expression of inflammation-related factors in our studies. In addition, Inhibitor of activation of NF-κB partly suppressed the NLRP3 inflammasome activation, while adding CBD further inhibited NF-κB activation and correspondingly suppressed the NLRP3 inflammasome activation in macrophages. In conclusion, the suppression of the activation of NLRP3 inflammasome through deactivation of NF-κB in macrophages by CBD might be one mechanism of its anti-inflammatory function in the liver.
MeSH term(s)	Animals ; Cannabidiol/pharmacology ; Diet, High-Fat/adverse effects ; Inflammasomes/drug effects ; Inflammasomes/metabolism ; Macrophages/drug effects ; Macrophages/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; NF-kappa B/drug effects ; NF-kappa B/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/drug effects ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Non-alcoholic Fatty Liver Disease/metabolism ; RAW 264.7 Cells ; Signal Transduction/drug effects
Chemical Substances	Inflammasomes ; NF-kappa B ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nlrp3 protein, mouse ; Cannabidiol (19GBJ60SN5)
Language	English
Publishing date	2019-04-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/jcp.28728
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Article: Oxidized Vitamin C (DHA) Overcomes Resistance to EGFR-targeted Therapy of Lung Cancer through Disturbing Energy Homeostasis.

Ye, Mingtong / Pang, Nengzhi / Wan, Ting / Huang, Yuanling / Wei, Tianyi / Jiang, Xuye / Zhou, Yujia / Huang, Yufeng / Yang, Hainan / Zhang, Zhenfeng / Yang, Lili

Journal of Cancer

2019 Volume 10, Issue 3, Page(s) 757–764

Abstract: Switching aerobic respiration to anaerobic glycolysis of cancer cells plays an important role in development and progression of acquired resistance. Since vitamin C enabled the inhibition of glycolysis of cancer cells, and erlotinib-resistant sub-line of ...

Abstract	Switching aerobic respiration to anaerobic glycolysis of cancer cells plays an important role in development and progression of acquired resistance. Since vitamin C enabled the inhibition of glycolysis of cancer cells, and erlotinib-resistant sub-line of HCC827 (ER6 cells) switched its metabolic features to higher glycolysis for survival, we hypothesize that vitamin C is able to inhibit glycolysis of ER6 cells. In this study, we found that both reduced vitamin C and oxidized vitamin C (DHA) could selectively suppress the viability of ER6 cells. DHA was efficient in inhibiting glycolysis and leading to energy crisis, which could be one mechanism for overcoming drug resistance to erlotinib of ER6 cells. Our data suggest that applying DHA could be a novel treatment strategy for NSCLC with acquired resistance to targeted therapy.
Language	English
Publishing date	2019-01-01
Publishing country	Australia
Document type	Journal Article
ZDB-ID	2573318-7
ISSN	1837-9664
ISSN	1837-9664
DOI	10.7150/jca.28087
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