Curcumin promotes cholesterol efflux from adipocytes related to PPARgamma–LXRalpha–ABCA1 passway

Dong, Shuying; Zhao, Shui‐Ping; Wu, Zhihong; Yang, Jun; Xie, Xiang-Zhu; Yu, Bo; Nie, Shaoping

doi:10.1007/s11010-011-0978-z

Cited by 57 publications

(41 citation statements)

References 31 publications

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“…Increased PPARγ expression has been shown to promote cholesterol efflux through LXRα in macrophages [54] and adipocytes [55]. LXRs act as cholesterol sensors, inducing the transcription of genes that protect cells from cholesterol overload, regulating reverse cholesterol transport (RCT), cholesterol biosynthesis and cholesterol absorption/excretion [56].…”

Section: Discussionmentioning

confidence: 99%

The deleterious effect of cholesterol and protection by quercetin on mitochondrial bioenergetics of pancreatic β-cells, glycemic control and inflammation: In vitro and in vivo studies

et al. 2016

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Studying rats fed high cholesterol diet and a pancreatic β-cell line (Min6), we aimed to determine the mechanisms by which quercetin protects against cholesterol-induced pancreatic β-cell dysfunction and impairments in glycemic control. Quercetin prevented the increase in total plasma cholesterol, but only partially prevented the high cholesterol diet-induced alterations in lipid profile. Quercetin prevented cholesterol-induced decreases in pancreatic ATP levels and mitochondrial bioenergetic dysfunction in Min6 cells, including decreases in mitochondrial membrane potentials and coupling efficiency in the mitochondrial respiration (basal and maximal oxygen consumption rate (OCR), ATP-linked OCR and reserve capacity). Quercetin protected against cholesterol-induced apoptosis of Min6 cells by inhibiting caspase-3 and -9 activation and cytochrome c release. Quercetin prevented the cholesterol-induced decrease in antioxidant defence enzymes from pancreas (cytosolic and mitochondrial homogenates) and Min6 cells and the cholesterol-induced increase of cellular and mitochondrial oxidative status and lipid peroxidation. Quercetin counteracted the cholesterol-induced activation of the NFκB pathway in the pancreas and Min6 cells, normalizing the expression of pro-inflammatory cytokines. Quercetin inhibited the cholesterol-induced decrease in sirtuin 1 expression in the pancreas and pancreatic β-cells. Taken together, the anti-apoptotic, antioxidant and anti-inflammatory properties of quercetin, and its ability to protect and improve mitochondrial bioenergetic function are likely to contribute to its protective action against cholesterol-induced pancreatic β-cell dysfunction, thereby preserving glucose-stimulated insulin secretion (GSIS) and glycemic control. Specifically, the improvement of ATP-linked OCR and the reserve capacity are important mechanisms for protection of quercetin. In addition, the inhibition of the NFκB pathway is an important mechanism for the protection of quercetin against cytokine mediated cholesterol-induced glycemic control impairment. In summary, our data highlight cellular, molecular and bioenergetic mechanisms underlying quercetin's protective effects on β-cells in vitro and in vivo, and provide a scientifically tested foundation upon which quercetin can be developed as a nutraceutical to preserve β-cell function.

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Section: Discussionmentioning

confidence: 99%

The deleterious effect of cholesterol and protection by quercetin on mitochondrial bioenergetics of pancreatic β-cells, glycemic control and inflammation: In vitro and in vivo studies

et al. 2016

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“…When 3T3-L1 adipocytes were treated with 5, 10 and 20 µM of curcumin, the palmitic acid oxidation was 1.1-, 1.3-, and 2.0-fold higher than it in control 3T3-L1 cells, respectively; and mRNA expression levels of CPT-1 were 1.8-, 3.4-, and 3.8-fold higher than them in control 3T3-L1 cells, respectively [136]. In addition, Dong et al demonstrated that curcumin increases cholesterol efflux by activating and up-regulating the expression of liver X receptor (LXR) and ATP-binding cassette A1 (ABCA1) in subcutaneous adipocytes isolated from rabbits [135]. …”

Section: Curcuminmentioning

confidence: 99%

“…Recruitment and infiltration of macrophages into expanded adipose tissue can increased its local inflammatory response. Inhibitory effect of curcumin on chemotaxis and release of MCP-1 from adipocytes [130, 135] may partially contribute to its anti-inflammatory activity. When RAW 264.7 macrophages were treated with adipose tissue-conditioned medium containing 0.1 to 10 µM curcumin, the migration of macrophages was inhibited in a dose-dependent manner [142].…”

Section: Curcuminmentioning

confidence: 99%

Novel insights of dietary polyphenols and obesity

Wang

Moustaid‐Moussa

Chen

et al. 2014

The Journal of Nutritional Biochemistry

774

575

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Prevalence of obesity has steadily increased over the past three decades both in the United States and worldwide. Recent studies have shown the role of dietary polyphenols in the prevention of obesity and obesity-related chronic diseases. Here we evaluated the impact of commonly consumed polyphenols, including green tea catechins and epigallocatechin gallates, resveratrol, and curcumin, on obesity and obesity-related-inflammation. Cellular studies demonstrated that these dietary polyphenols reduce viability of adipocytes and proliferation of preadipocytes, suppress adipocyte differentiation and triglyceride accumulation, stimulate lipolysis and fatty acid β-oxidation, and reduce inflammation. Concomitantly, the polyphenols modulate signaling pathways including the AMP-activated protein kinase, peroxisome proliferator activated receptor γ, CCAAT/enhancer binding protein α, PPAR gamma activator 1-alpha, sirtuin 1, sterol regulatory element binding protein-1c, uncoupling proteins 1 and 2, and nuclear factor kappa B that regulate adipogenesis, antioxidant and anti-inflammatory responses. Animal studies strongly suggest that commonly consumed polyphenols described in this review have a pronounced effect on obesity as shown by lower body weight, fat mass, and triglycerides through enhancing energy expenditure and fat utilization, and modulating glucose hemostasis. Limited human studies have been conducted in this area, and are inconsistent about the anti-obesity impact of dietary polyphenols, probably due to the various study designs and lengths, variation among subjects (age, gender, ethnicity), chemical forms of the dietary polyphenols used and confounding factors such as other weight reducing agents. Future randomized controlled trials are warranted to reconcile the discrepancies between preclinical efficacies and inconclusive clinic outcomes of these polyphenols.

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“…In a mouse macrophage study, Zhou et al (2014) found that curcumin prevents a decrease in thrombospondin-4 induced by oxidized low-density lipoprotein (ox-LDL) to inhibit cell interaction. Furthermore, Dong et al (2011) found that curcumin can affect the cholesterol efflux from adipocytes by regulating the PPAR-LXR-ABCA1 pathway. On the basis of this study, Zhao et al (2012) demonstrated that curcumin reduces cholesterol accumulation in foam cell development by downregulating SR-A and upregulating ATP-binding cassette transporter 1 (ABCA1) using proteasome-and liver X receptor alpha (LXRa)-dependent pathways, respectively.…”

Section: Introductionmentioning

confidence: 99%

Curcumin Enhanced Cholesterol Efflux by Upregulating ABCA1 Expression Through AMPK-SIRT1-LXRα Signaling in THP-1 Macrophage-Derived Foam Cells

Lin

Liu

et al. 2015

DNA and Cell Biology

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Curcumin, a traditional Chinese derivative from the rhizomes of Curcuma longa, is beneficial to health by modulating lipid metabolism and suppressing atherogenesis. A key part of atherosclerosis is the failure of macrophages to restore their cellular cholesterol homeostasis and the formation of foam cells. In this study, results showed that curcumin dramatically increased the expression of ATP-binding cassette transporter 1 (ABCA1), promoted cholesterol efflux from THP-1 macrophage-derived foam cells, and reduced cellular cholesterol levels. Curcumin activated AMP-activated protein kinase (AMPK) and SIRT1, and then activated LXRα in THP-1 macrophage-derived foam cells. Inhibiting AMPK/SIRT1 activity by its specific inhibitor or by small interfering RNA could inhibit LXRα activation and abolish curcumin-induced ABCA1 expression and cholesterol efflux. Thus, curcumin enhanced cholesterol efflux by upregulating ABCA1 expression through activating AMPK-SIRT1-LXRα signaling in THP-1 macrophage-derived foam cells. This study describes a possible mechanism for understanding the antiatherogenic effects of curcumin on attenuating the progression of atherosclerosis.

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Curcumin promotes cholesterol efflux from adipocytes related to PPARgamma–LXRalpha–ABCA1 passway

Cited by 57 publications

References 31 publications

The deleterious effect of cholesterol and protection by quercetin on mitochondrial bioenergetics of pancreatic β-cells, glycemic control and inflammation: In vitro and in vivo studies

The deleterious effect of cholesterol and protection by quercetin on mitochondrial bioenergetics of pancreatic β-cells, glycemic control and inflammation: In vitro and in vivo studies

Novel insights of dietary polyphenols and obesity

Curcumin Enhanced Cholesterol Efflux by Upregulating ABCA1 Expression Through AMPK-SIRT1-LXRα Signaling in THP-1 Macrophage-Derived Foam Cells

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