Nuciferine ameliorates hepatic steatosis in high‐fat diet/streptozocin‐induced diabetic mice through a PPARα/PPARγ coactivator‐1α pathway

Zhang, Chao; Deng, Jianjun; Liú, Dan; Tuo, Xingxia; Xiao, Lei; Lai, Baochang; Yao, Qinyu; Liu, Jia; Yang, Haixia; Wang, Nanping

doi:10.1111/bph.14482

Cited by 153 publications

(105 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…For example, exposure of myotubes to palmitic acid leads to attenuated insulin signaling, but exposure to oleic acid does not cause these changes; in addition, co‐incubation of palmitic acid–exposed cells with a lower concentration of oleic acid reverses the effects of the latter . In our in vitro study, we used palmitate to induce insulin resistance, which is a classic insulin resistance model that has been used in many studies . Although we did not determine whether stearate and oleate have the same effects on mitochondria in our experiment, it would be interesting and worth further investigation.…”

Section: Discussionmentioning

confidence: 94%

Increased Dynamin‐Related Protein 1–Dependent Mitochondrial Fission Contributes to High‐Fat‐Diet‐Induced Cardiac Dysfunction and Insulin Resistance by Elevating Tafazzin in Mouse Hearts

Chang

Xiao

et al. 2019

Molecular Nutrition Food Res

View full text Add to dashboard Cite

Scope: High fat (HF)-diet-induced insulin resistance is a major contributor to the pathogenesis of cardiovascular diseases. However, the molecular mechanisms that regulate cardiac insulin signaling are not fully understood. The regulatory role of tafazzin in the hearts of HF-diet-fed mice is investigated. Methods and results: Mice are fed a HF diet or low fat (LF) diet for up to 24 weeks. After 24 weeks, it is found that HF-diet-induced cardiac dysfunction is linked to overexpression of the mitochondrial protein tafazzin. Increased tafazzin promotes mitochondrial fission and impairs insulin signaling, which is mediated by dynamin-related protein 1 (Drp-1) translocation from the cytosol to the mitochondria. Furthermore, knockdown of tafazzin with siRNA inhibits palmitic-acid-induced mitochondrial fission and restores insulin sensitivity. Moreover, miR-125b-5p as an upstream regulator targeting tafazzin is identified and palmitate-induced insulin resistance further rescued. Conclusion: In HF-diet-fed mouse hearts, increased tafazzin contributes to insulin resistance via mediating Drp-1 translocation to the mitochondria, and a small non-coding RNA, miR-125b-5p, at least partially regulates this signaling pathway and alleviates insulin resistance.

show abstract

Section: Discussionmentioning

confidence: 94%

Increased Dynamin‐Related Protein 1–Dependent Mitochondrial Fission Contributes to High‐Fat‐Diet‐Induced Cardiac Dysfunction and Insulin Resistance by Elevating Tafazzin in Mouse Hearts

Chang

Xiao

et al. 2019

Molecular Nutrition Food Res

View full text Add to dashboard Cite

show abstract

“…To monitor the kidney and liver function, the concentrations of creatinine, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in plasma were determined using an Auto Chemistry Analyzer (Hitachi 7180, Tokyo, Japan) as described previously [16,17].…”

Section: Kidney and Liver Functionmentioning

confidence: 99%

High plasma levels of pro-inflammatory factors interleukin-17 and interleukin-23 are associated with poor outcome of cardiac-arrest patients: a single center experience

Zhuang

Chen

Zhou

et al. 2020

BMC Cardiovasc Disord

View full text Add to dashboard Cite

Background: Systemic inflammation is an important feature of post-cardiac arrest syndrome (PCAS). This study was designed to determine whether the plasma concentrations of some circulating pro-inflammatory cytokines , IL-22, IL-23 and IL-33) are of value in predicting the outcome of patients after return of spontaneous circulation (ROSC) during the post-cardiac arrest period. Methods: This was a prospective observational clinical study. In total, 21 patients (survivors, n = 10; non-survivors, n = 11) who experienced cardiac arrest and successful ROSC with expected survival of at least 7 days were consecutively enrolled from January 2016 to December 2017. Of the 21 enrolled patients, ten survived were designated "survivors". The other eleven patients died between 2 days and 1 months post ROSC. Venous blood was drawn at three time-points: baseline (< 1 h post ROSC), 2 days post ROSC and 7 days post ROSC. Plasma IL-8, IL-22, IL-23 and IL-33 were determined using commercial enzyme-linked immunosorbent assays. Results: Plasma creatinine levels, but aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, were elevated in non-survivors compared with survivors. Plasma levels of IL-17, IL-22, IL-23 and IL-33 of the 21 total patients did not change at 2 or 7 days post ROSC compared to baseline. In survivors, the plasma levels of IL-17 and IL-23 at 2 or 7 days post ROSC were lower than baseline. In non-survivors, plasma levels of IL-17 increased compared with baseline. Receiver operating characteristic curve analysis showed that the plasma levels of IL-17 and IL-23 at 2 or 7 days post ROSC were able to predict the mortality of PCAS patients, and positively correlated with Acute Physiology and Chronic Health Evaluation (APACHE)-II score and time to ROSC.Conclusion: These results provide the first evidence that the elevated plasma IL-17 and IL-23 levels are associated with poor outcome in PCAS patients. The role of IL-17/IL-23 axis post ROSC is worth paying attention to in PCAS patients.Trial registration: Clinicaltrial.gov NCT02297776, 2014-11-21.

show abstract

“…[30,31]. The main pharmacological effects of nuciferine include hyperlipidemia amelioration, stimulation of insulin secretion and vasodilation, hypotension induction, and anti-hepatic steatosis activity [32,33,34,35]. However, the effect of lotus leaf on adipocyte differentiation and its action mechanism remain unclear.…”

Section: Introductionmentioning

confidence: 99%

Lotus Leaf Ethanol Extract and Nuciferine Suppress Adipocyte Differentiation by Regulating Akt-mTORC1 Signaling in 3T3-L1 Cells

Yoo¹,

Jang²,

Ahn³

et al. 2019

JFNR

View full text Add to dashboard Cite

Lotus leaf has been reported to exert anti-inflammatory, hypolipidemic, and hepatoprotective effects. However, the effect of lotus leaf on adipocyte differentiation and its action mechanism have not been clarified. In this study, 3T3-L1 preadipocytes were incubated with or without lotus leaf ethanol extract (EEN) for 8 days. Microscopic inspection and Oil Red O staining indicated that EEN treatment significantly reduced adipogenesis in 3T3-L1 cells. EEN also downregulated the protein levels of adipogenic transcription factors including sterol regulatory element binding protein 1 (SREBP1), peroxisome proliferator-activated receptor-gamma (PPARγ), and CCAAT/enhancer binding protein α (C/EBPα), and target genes such as adipocyte binding protein 2 (aP2) and fatty acid synthase (FAS) in a dose-dependent manner. In order to understand whether nuciferine, the primary active component of EEN contributed to the anti-adipogenic activity of EEN, we examined the effect of nuciferine on adipogenesis related gene expression. Nuciferine significantly reduced expression of adipogenic transcription factors and target genes. Notably, nuciferine downregulated the phosphorylation of Akt, mammalian target of rapamycin complex 1 (mTORC1), S6K, and 4EBP1. These results suggest that lotus leaf ethanol extract exerts anti-adipogenic activity, and could be partially mediated through the regulation of the Akt-mTORC1 signaling pathway by nuciferine.

show abstract

Nuciferine ameliorates hepatic steatosis in high‐fat diet/streptozocin‐induced diabetic mice through a PPARα/PPARγ coactivator‐1α pathway

Abstract: Nuciferine improved lipid profile and attenuated hepatic steatosis in HFD/STZ-induced diabetic mice by activating the PPARα/PGC1α pathway. Nuciferine may be a potentially important candidate in improving hepatic steatosis and the management of T2DM.

Cited by 153 publications

References 50 publications

Increased Dynamin‐Related Protein 1–Dependent Mitochondrial Fission Contributes to High‐Fat‐Diet‐Induced Cardiac Dysfunction and Insulin Resistance by Elevating Tafazzin in Mouse Hearts

Increased Dynamin‐Related Protein 1–Dependent Mitochondrial Fission Contributes to High‐Fat‐Diet‐Induced Cardiac Dysfunction and Insulin Resistance by Elevating Tafazzin in Mouse Hearts

High plasma levels of pro-inflammatory factors interleukin-17 and interleukin-23 are associated with poor outcome of cardiac-arrest patients: a single center experience

Lotus Leaf Ethanol Extract and Nuciferine Suppress Adipocyte Differentiation by Regulating Akt-mTORC1 Signaling in 3T3-L1 Cells

Contact Info

Product

Resources

About