Berteroin ameliorates lipid accumulation through AMPK-mediated regulation of hepatic lipid metabolism and inhibition of adipocyte differentiation

Kim, Yeon Ju; Park, Sung Yun; Lee, Ju‐Hee

doi:10.1016/j.lfs.2021.119668

Cited by 16 publications

(8 citation statements)

References 55 publications

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“…Instant fermented teas are shown to heighten energy expenditure by increasing CPT1 expression ( 45 ). Berteroin was found to significantly increase the expression of mitochondrial fatty acid oxidation-related genes CPT1 and PPARγ, and the phosphorylation of AMPK in HepG2 cells ( 46 ). Peroxisome proliferator-activated receptor (HMGR) is a rate-limiting enzyme for cholesterol synthesis.…”

Section: Discussionmentioning

confidence: 99%

Quercetin ameliorates chicken quality by activating the PI3K/PKB/AMPK signaling pathway in broilers

Wang

Zhou

et al. 2022

Front. Vet. Sci.

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This study was conducted to investigate the effects and mechanism of quercetin on chicken quality in broilers. We selected 480 AA broilers (1 day old) and randomly allotted those to four treatments (negative control and 0.2, 0.4, or 0.6 g of quercetin per kg of diet) for 42 days. Compared with the control group, the supplementation with 0.4 g of quercetin significantly increased the pH45min and L* value of the thigh muscle and decreased the shearing force of the thigh muscle and breast muscle and drip loss of the thigh muscle (P < 0.05). The supplementation with 0.6 g/kg of quercetin significantly increased the pH45min and L* value of the thigh muscle, and pH45min of breast muscle and decreased the drip loss of the thigh muscle (P < 0.05). Sensory scores of meat color, tenderness, and juiciness also were improved with increasing quercetin concentration (P < 0.05). The inosinic acid (IMP) content of the breast and thigh muscles of broilers was significantly increased by supplementation with 0.6 g/kg of quercetin (P < 0.05). Supplementation with 0.2, 0.4, and 0.6 g of quercetin significantly reduced mRNA expression of L-FABP (P < 0.05, P < 0.05, and P < 0.05); supplementation with 0.4 and 0.6 g/kg of quercetin significantly increased mRNA expression of PKB and AMPKα1 (P < 0.05 and P < 0.05); supplementation with 0.6 g/kg of quercetin in the diet significantly reduced mRNA expression of SREBP1 and HMGR (P < 0.05 and P < 0.05) and significantly increased mRNA expression of CPT1 and PPARγ (P < 0.05 and P < 0.05); and supplementation with 0.2, 0.4, and 0.6 g/kg of quercetin significantly increased mRNA expression of PI3K, LPL, and Apo A1 and significantly reduced mRNA expression of ACC and FATP1 in the breast muscle of broilers (P > 0.05). PI3k, PKB, AMPK, SREBP1, and L-FABP were significantly and positively correlated with pH45min (P < 0.05); PPARγ was significantly and positively correlated with shear force (P < 0.05); CPT1 was significantly and positively correlated with the L* value (P < 0.05); and HMGR was significantly and positively correlated with drip loss (P < 0.05). In conclusion, quercetin improved the meat quality, protecting it against lipid oxidation and deposition by regulating the PI3K/PKB/AMPKα1 signaling pathway in the breast muscle of broilers.

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Section: Discussionmentioning

confidence: 99%

Quercetin ameliorates chicken quality by activating the PI3K/PKB/AMPK signaling pathway in broilers

Wang

Zhou

et al. 2022

Front. Vet. Sci.

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“…18 An expanding number of studies have indicated that AMPK is related to Ca 2+ signaling 142 and lipid metabolism. 125 In the liver, blockage of the mitochondrial Ca 2+ buffering pathway leads to AMPKmediated elevation of cytoplasmic Ca 2+ , resulting in lipid accumulation. 31 Interestingly, AMPK dephosphorylation rather than aberrant expression of AMPK regulates this process.…”

Section: Mcu Complex In Nafldmentioning

confidence: 99%

“…Mitochondrial Ca 2+ homeostasis under physiological conditions is closely related to the AMPK pathway, 124 which controls numerous lipid metabolism 125,126 and inflammation routes 127,128 . It has been demonstrated that hepatocyte lipid deposition is associated with abnormal MCU expression.…”

Section: Pathological Role Of Mcu Complex In Metabolic Diseasesmentioning

confidence: 99%

“…It is well known that AMPK can sense cellular energy demand to be activated and regulate energy metabolism 18 . An expanding number of studies have indicated that AMPK is related to Ca 2+ signaling 142 and lipid metabolism 125 . In the liver, blockage of the mitochondrial Ca 2+ buffering pathway leads to AMPK‐mediated elevation of cytoplasmic Ca 2+ , resulting in lipid accumulation 31 .…”

Section: Pathological Role Of Mcu Complex In Metabolic Diseasesmentioning

confidence: 99%

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Implications of MCU complex in metabolic diseases

Li,

Sun,

Zhang

et al. 2023

The FASEB Journal

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Metabolic diseases are considered the primary culprit for physical and mental health of individuals. Although the diagnosis of these diseases is relatively easy, more effective and convenient potent drugs are still being explored. Ca 2+ across the inner mitochondrial membrane is a vital intracellular messenger that regulates energy metabolism and cellular Ca 2+ homeostasis and is involved in cell death. Mitochondria rely on a selective mitochondrial Ca 2+ unidirectional transport complex (MCU complex) in their inner membrane for Ca 2+ uptake. We found that the channel contains several subunits and undergoes dramatic transformations in various pathological processes, especially in metabolic diseases. In this way, we believe that the MCU complex becomes a target with significant potential for these diseases. However, there is no review linking the two factors, thus hindering the possibility of new drug production. Here, we highlight the connection between MCU complex-related Ca 2+ transport and the pathophysiology of metabolic diseases, adding understanding and insight at the molecular level to provide new insights for targeting MCU to reverse metabolism-related diseases.

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“…CPT1 expression is significantly inhibited during liver injury and fat accumulation, and CPT1 knockdown in mice results in severe liver fat accumulation and inflammation [ 13 ]. The decrease of mitochondrial β-oxidation caused by reduced CPT1 expression may be a key event in the pathogenesis of hepatic steatosis in mice [ 14 ]. ATP-binding cassette transporter A1 (ABCA1) is a membrane protein that uses ATP as energy for the transport of molecules, such as cholesterol and phospholipids, and plays an important role in the initial steps of cholesterol reversal transport (RCT) and high-density lipoprotein (HDL) generation [ 15 , 16 ].…”

Section: Introductionmentioning

confidence: 99%

A nanodrug system overexpressed circRNA_0001805 alleviates nonalcoholic fatty liver disease via miR-106a-5p/miR-320a and ABCA1/CPT1 axis

Tang

et al. 2021

J Nanobiotechnol

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Our study aimed to explore the function of circRNA_0001805 in the pathogenesis of NAFLD and the underlying mechanism. A nanodrug system (GA-RM/GZ/PL) was constructed to overexpress circRNA_0001805 specifically in hepatocytes for the treatment of NAFLD. Fat droplet accumulation in cultured cells and mouse hepatic tissues was detected using Oil Red O or H&E staining. The relative expression of circRNAs, genes associated with lipogenesis was quantified by qRT-PCR. Interactions between circRNA_0001805 and miR-106a-5p/miR-320a, between miR-106a-5p/miR-320a and ABCA1/CPT1 were confirmed by dual-luciferase reporter assay. A novel metalorganic framework nanocarrier (GZ) was prepared from glycyrrhizic acid and zinc ions (Zn2+), and this nanocarrier was loaded with the circRNA_0001805 plasmid to construct a nanocore (GZ/PL). Then, this GZ/PL was coated with a galactose-modified RBC membrane (GA-RM) to generate GA-RM/GZ/PL. CircRNA_0001805 expression was downregulated in FFA-challenged primary hepatocytes, HFD-fed mice and NAFLD patients. Overexpressed circRNA_0001805 attenuated NAFLD development by suppressing lipid metabolism disorder and inflammation. CircRNA_0001805 targeted miR-106a-5p/miR-320a, which served as an upstream inhibitor of ABCA1/CPT1 and collaboratively regulated NAFLD progression. GA-RM/GZ/PL targeted hepatocytes, overexpressed circRNA_0001805, released glycyrrhizic acid to reduce the accumulation of lipids in the liver and played a synergistic role against NAFLD-induced lipid metabolism disorder. Graphical Abstract

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Berteroin ameliorates lipid accumulation through AMPK-mediated regulation of hepatic lipid metabolism and inhibition of adipocyte differentiation

Cited by 16 publications

References 55 publications

Quercetin ameliorates chicken quality by activating the PI3K/PKB/AMPK signaling pathway in broilers

Quercetin ameliorates chicken quality by activating the PI3K/PKB/AMPK signaling pathway in broilers

Implications of MCU complex in metabolic diseases

A nanodrug system overexpressed circRNA_0001805 alleviates nonalcoholic fatty liver disease via miR-106a-5p/miR-320a and ABCA1/CPT1 axis

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