14-Deoxy-11,12-didehydroandrographolide suppresses adipogenesis of 3 T3-L1 preadipocytes by inhibiting CCAAT/enhancer-binding protein β activation and AMPK-mediated mitotic clonal expansion

Li, Chien−Chun; Yen, Chih-Ching; Fan, Ciou-Ting; Chuang, Wei-Ting; Huang, Chin-Shiu; Chen, Haw‐Wen; Lii, Chong‐Kuei

doi:10.1016/j.taap.2018.09.028

Cited by 9 publications

(11 citation statements)

References 59 publications

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“…Li and colleagues found that 14‐deoxy‐11,12‐didehydroandrographolide, isolated from Andrographis paniculata , exerts its effect through the protein kinase A‐cAMP response element‐binding protein‐C/EBPβ and activated protein kinase/mammalian target of rapamycin (mTOR) pathways, leading to downregulate C/EBPβ‐driven lipogenic protein expression and halting mitotic clonal expansion progression in 3 T3‐L1 cells (Li et al, ). Moreover, carnosic acid lowered insulin, leptin, and TG concentrations in ovariectomized or sham‐operated and in HFD mice.…”

Section: Resultsmentioning

confidence: 99%

“…Therefore, substances that can modulate these two proteins may be used to control obesity (Wang et al, ). In this context, research findings indicated that diterpenes such as carnosic acid (Gaya et al, ; Lee et al, ; Romo‐Vaquero, Larrosa, et al, ), kahweol (Kim, Lee, Kang, Kwon, & Nam, 2017), and 14‐deoxy‐11,12‐didehydroandrographolide (Li et al, ), were found to downregulate C/EBPβ and/or PPARγ expressions. In addition, 16 α ‐hydroxycleroda‐3, 13 (14) Z‐dien‐15, 16‐olide, a clerodane diterpene isolated from P. longifolia , exhibited remarkable antiadipogenic activity and less toxicity in differentiating adipocytes and lowered expression levels of PPARγ, C/EBPα, and glucose transporter type 4 during differentiation in a time‐ and concentration‐dependent manner.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, there is evidence that liver steatosis occurs through AMPK/mTOR‐dependent pathway, where PPARδ reduces intrahepatic lipid content and stimulates β‐oxidation in the liver and hepatic cells by an autophagy‐lysosomal pathway involving AMPK/mTOR signaling (Tong et al, ). Along this line, the diterpenoid 14‐deoxy‐11,12‐didehydroandrographolide (Li et al, ) and carnosic acid are known to act through (Lee et al, ) AMPK/mTOR signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

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Anti‐obesity effect of plant diterpenes and their derivatives: A review

Islam

Ali

Mubarak

2020

Phytotherapy Research

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Obesity is a medical condition in which excess body fat is accumulated by a combination of excessive food intake, lack of physical activity, and genetic susceptibility. Obesity increases the risk of various diseases and conditions, including cardiovascular diseases, diabetes, cancer, and depression. This review focuses on most recent reports pertaining to the antiobesity activity of plant-derived diterpenes in different databases. For this, a search (until August 2019) was conducted in the PubMed and Science Direct databases with the following keywords: "plant diterpenes" or "plant diterpenoids" paired with "obesity" or "antiobesity effects." Overall, 729 references that used the aforementioned keywords were selected, among which 34 articles have been included in this review. Results from this search suggest that a number of diterpenes and their derivatives have been found to exert antiobesity effects through various mechanisms, such as overweight reduction or modification of body mass index, protein-tyrosine phosphatase 1B inhibition, lipase activity inhibition, antiadipogenesis effect, among others. Carnosic acid, carnosol and the derivatives of abietic acid, steviol, and andrographolide are examples of important antiobesity diterpenes and their derivatives. Of note, plant-derived diterpenes may be potential candidates for managing obesity and obesity-related diseases and disorders in human and other animals. K E Y W O R D S metabolic diseases, obesity, plant diterpenes

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Anti‐obesity effect of plant diterpenes and their derivatives: A review

Islam

Ali

Mubarak

2020

Phytotherapy Research

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“…1,36 In addition, some studies have reported that AMPK activators can induce cell cycle arrest, resulting in cell proliferation in 3T3-L1 cells during MCE. [40][41][42] Recently, the activation of AMPK was reported to suppress adipogenesis by reducing adipogenesis-associated target genes, such as those of the C/EBP family and PPARr, during MCE. .…”

Section: Discussionmentioning

confidence: 99%

“…Consequently, the suppression of MCE progression is crucial to inhibit adipogenesis. [40][41][42] Recently, the activation of AMPK was reported to suppress adipogenesis by reducing adipogenesis-associated target genes, such as those of the C/EBP family and PPARr, during MCE. 23,43 Consistent with these reports, our results showed that ezetimibe-mediated inhibition of MCE led to a reduction in lipid accumulation by activating AMPK in adipocytes.…”

Section: Discussionmentioning

confidence: 99%

Ezetimibe ameliorates lipid accumulation during adipogenesis by regulating the AMPK–mTORC1 pathway

et al. 2019

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Adipogenesis, a critical process that converts adipocyte precursors into adipocytes, is considered a potential therapeutic target for the treatment of obesity. Ezetimibe, a drug approved by the United States Food and Drug Administration, is used for the treatment of hypercholesterolemia. Recently, it was reported to ameliorate high fat diet‐induced dyslipidemia in mice and reduce lipid accumulation in hepatocytes through the activation of AMPK. However, the anti‐adipogenic effects of ezetimibe and the underlying molecular mechanism have not yet been elucidated. Here, we found that ezetimibe reduced lipid accumulation via activating AMPK during the early phase of adipogenesis. We also observed that ezetimibe inhibited peroxisome proliferator‐activated receptor γ, which is a major transcription factor of adipogenesis. Furthermore, ezetimibe‐mediated AMPK activation reduced lipid accumulation by inhibiting mTORC1 signaling, leading to the downregulation of lipogenesis‐related genes. Mitotic clonal expansion, required for adipogenesis, accelerates cell cycle progression and cell proliferation. We additionally observed that ezetimibe prevented the progression of mitotic clonal expansion by arresting the cell cycle at the G0/G1 phase, which was followed by the inhibition of cell proliferation. Collectively, ezetimibe‐mediated inhibition of adipogenesis is dependent on the AMPK–mTORC1 pathway. Thus, we suggest that ezetimibe might be a promising drug for the treatment of obesity.

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Quercetin-3-O-rutinoside from Moringa oleifera Downregulates Adipogenesis and Lipid Accumulation and Improves Glucose Uptake by Activation of AMPK/Glut-4 in 3T3-L1 Cells

Ganjayi

Karunakaran

Gandham

et al. 2023

Rev. Bras. Farmacogn.

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Natural product-based therapeutic alternatives have drawn immense interest to deal with growing incidence of metabolic disorders. Rutin (quercetin-3- O -rutinoside) is found in a variety of fruits, vegetables, and plant beverages. In the present study, rutin was isolated from Moringa oleifera Lam., leaves and its anti-lipidemic and anti-adipogenic activity was evaluated through inhibition of key digestive enzymes and in vitro cell culture experiments using 3T3-L1 adipocytes. Rutin treatment substantially reduced α-glucosidase and pancreatic lipase activities with IC 50 values of 40 and 35 μg/ml, respectively. MTT assay with 3T3-L1 cells demonstrated the non-toxic effect of rutin up to 160 μg/ml. Oil Red O-stained images of rutin-treated 3T3-L1 cells depicted that rutin considerably reduced lipid content and adipogenesis (79.9%), and enhanced glycerol release in 3T3-L1 cells when compared to untreated cells. Rutin significantly ( p < 0.05) enhanced glucose uptake in 3T3-L1 adipocytes and also led to reduced levels of leptin but enhanced levels of adiponectin. Western blot analysis of rutin-treated (40 µg/ml) adipocytes showed phosphorylation of AMPK, upregulated expression of Glut-4 (1.31-fold) and UCP-1 (1.47-fold), but downregulated expression of PPAR-γ by 0.73-fold. At transcriptional level, similar trends were observed in the mRNA expression of the above genes, except AMPK. Our results demonstrate that rutin isolated from M. oleifera significantly alleviates lipid content and adipogenesis, and improves glucose uptake through regulating PPAR-γ and AMPK signaling pathways; thus, rutin can be considered as a potential therapeutic agent against adiposity and glucose intolerance. Graphical Abstract

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14-Deoxy-11,12-didehydroandrographolide suppresses adipogenesis of 3 T3-L1 preadipocytes by inhibiting CCAAT/enhancer-binding protein β activation and AMPK-mediated mitotic clonal expansion

Cited by 9 publications

References 59 publications

Anti‐obesity effect of plant diterpenes and their derivatives: A review

Anti‐obesity effect of plant diterpenes and their derivatives: A review

Ezetimibe ameliorates lipid accumulation during adipogenesis by regulating the AMPK–mTORC1 pathway

Quercetin-3-O-rutinoside from Moringa oleifera Downregulates Adipogenesis and Lipid Accumulation and Improves Glucose Uptake by Activation of AMPK/Glut-4 in 3T3-L1 Cells

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