Article

Purple sweet potato anthocyanins attenuate hepatic lipid accumulation through activating adenosine monophosphate–activated protein kinase in human HepG2 cells and obese mice

Department of Toxicology, College of Pharmacy, Chungnam National University, Daejeon 305-764, Republic of Korea.
Nutrition research (Impact Factor: 2.47). 12/2011; 31(12):896-906. DOI: 10.1016/j.nutres.2011.09.026
Source: PubMed

ABSTRACT

Purple sweet potato is a functional food rich in anthocyanins that possess disease-preventive properties. Anthocyanins are known to possess potent antidiabetic properties. However, the effect of the anthocyanin fraction (AF) from purple sweet potato on hepatic lipid metabolism remains unclear. Our hypothesis is that AF inhibits hepatic lipid accumulation through the activation of adenosine monophosphate-activated protein kinase (AMPK) signaling pathways in vitro and in vivo. In this study, we evaluated body weight, liver histology, and hepatic lipid content in high-fat diet (HFD)-fed ICR mice treated with AF. In addition, we characterized the underlying mechanism of AF's effects in HepG2 hepatocytes through Western blot analysis. Anthocyanin fraction (200 mg/kg per day) reduced weight gain and hepatic triglyceride accumulation and improved serum lipid parameters in mice fed an HFD for 4 weeks. Anthocyanin fraction significantly increased the phosphorylation of AMPK and acetyl-coenzyme A carboxylase (ACC) in the liver and HepG2 hepatocytes. In addition, AF down-regulated the levels of sterol regulatory element-binding protein 1 and its target genes including ACC and fatty acid synthase (FAS). The specific AMPK inhibitor compound C attenuated the effects of AF on the expression of lipid metabolism-related proteins such as SREBP-1 and FAS in HepG2 hepatocytes. The beneficial effects of AF on HFD-induced hepatic lipid accumulation are thus mediated through AMPK signaling pathways, suggesting a potential target for the prevention of obesity.

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    • "Therefore, there is growing interest in the potential use of plant-derived extracts for disease control as an alternative to chemical treatments as well as their use as promoters of appetite and growth performance in finfish species (Reverter et al., 2014). Anthocyanins, a flavonoid-polyphenol subclass, are found in several vegetables such as purple potatoes, purple carrots, purple corn, black soybean and purple beans (Ha et al., 2010; Hwang et al., 2011; Poudyal et al., 2010; Ramos-Escudero et al., 2012; Zhang et al., 2013a). Previous studies have reported potential health benefits, such as antioxidant , cardio-protective, anti-inflammatory and anti-carcinogenic effects , from dietary intake of anthocyanins in humans and other mammals (Galvano et al., 2004; Vennat et al., 1994; Wallace and Giusti, 2013; Whitehead et al., 1995). "
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    ABSTRACT: There is increasing interest in using plant-derived extracts to promote growth and health in finfish species in recent years. Elucidating the effects of plant secondary metabolites on skeletal muscle growth signaling will contribute to an improved understanding of the effects of feeding carnivorous fish diets supplemented with plant extracts on fish somatic growth. Dietary intake of anthocyanins, a type of flavonoid widely distributed in plants, has long been associated with beneficial effects in both human and animal health; however, their effects in finfish are largely unknown. We conducted an experiment to test the effect of three doses (treatments A, B and C; 1. ×, 2.5. × and 10. ×, respectively) of a mixture of three types of anthocyanidins (peonidin, cyanidin and pelargonidin chloride) on the expression of several genes in primary myogenic cells isolated from the skeletal muscle of rainbow trout (Oncorhynchus mykiss) after 24. h of treatment. The genes of interest analyzed are involved in myogenic programing (pax7, myoD and myogenin), Notch signaling (her6 and hey2) and antioxidant enzymes (sod1, cat and gpx1). Significantly greater expression of pax7 in cells under treatment B compared with the untreated cells was detected. Although no differences in expression of myogenic regulatory factors, myoD and myogenin between test groups or the control were detected, a trend toward significantly lower expression in all groups tested compared with the control group was observed. Moreover, significantly higher expression levels of her6 and hey2 in cells under treatments A and B compared with untreated cells were detected. Although no significant differences in the expression of cat and sod1, significantly greater expression in gpx1 in all treated groups compared with the control group was detected. Collectively, we demonstrated that anthocyanidins enhance the expression of gpx1 in primary myogenic cells, thereby contributing to skeletal muscle tissue defense against oxidative stress in finfish species. Further, anthocyanidins appear to delay myogenic differentiation in primary myogenic cells by up-regulating the expression of pax7 while decreasing myogenic regulatory factors in a Notch signaling-dependent interaction. Whether this effect results a reduced growth performance and/or an increase in feed conversion ratio in fish fed diets supplemented with plant extracts rich in anthocyanins or anthocyanidins needs further study, and the need to better define the potential effects of different polyphenol classes in myogenic differentiation on primary myogenic cells from carnivorous fish is warranted. Statement of relevance: The study contributes to increase our understanding regarding the effect of plant-derived secondary metabolites such as anthocyanidins on myogenic program and antioxidant enzyme defense in differentiating myogenic cells from carnivorous fish. We have demonstrated that anthocyanidins may delay the progress of the myogenic differentiation process and promote antioxidant defense expression in myogenic cells.
    Full-text · Article · Jan 2016 · Aquaculture
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    • "In addition, in some studies, animals were exposed to synthetic ACNs (i.e., cyanidin-3-O-β-glucoside) [50, 52, 56, 57], whereas in others they were exposed to extracts of ACN-rich foods (e.g., sweet potato, berries, and oranges) [27, 49, 58–62]. Mirroring the results obtained in vitro, there is ample convergence supporting an effect of ACNs in reducing hepatic lipid accumulation, that is, steatosis [49, 50, 52, 56–58, 60–63]. In addition, the majority of studies also reported an improvement in hepatic and systemic IR and serum lipids, often related to reduced weight gain [57, 58, 60–62]. "
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    ABSTRACT: Nonalcoholic fatty liver disease (NAFLD), defined by excessive lipid accumulation in the liver, is the hepatic manifestation of insulin resistance and the metabolic syndrome. Due to the epidemics of obesity, NAFLD is rapidly becoming the leading cause of altered liver enzymes in Western countries. NAFLD encompasses a wide spectrum of liver disease ranging from simple uncomplicated steatosis, to steatohepatitis, cirrhosis, and hepatocellular carcinoma. Diet may affect the development of NAFLD either by increasing risk or by providing protective factors. Therefore, it is important to investigate the role of foods and/or food bioactives on the metabolic processes involved in steatohepatitis for preventive strategies. It has been reported that anthocyanins (ACNs) decrease hepatic lipid accumulation and may counteract oxidative stress and hepatic inflammation, but their impact on NAFLD has yet to be fully determined. ACNs are water-soluble bioactive compounds of the polyphenol class present in many vegetable products. Here, we summarize the evidence evaluating the mechanisms of action of ACNs on hepatic lipid metabolism in different experimental setting: in vitro, in vivo, and in human trials. Finally, a working model depicting the possible mechanisms underpinning the beneficial effects of ACNs in NAFLD is proposed, based on the available literature.
    Full-text · Article · Oct 2013 · Oxidative Medicine and Cellular Longevity
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    • "AMPK is a key sensor of cellular energy status [37], and platelet activation is an energy-consuming process. Our group, as well as other laboratories, recently demonstrated that anthocyanins affect AMPK phosphorylation in cells of several distinctive tissues [32], [38], [39], but their effect on platelet AMPK has not been explored. To determine whether Dp-3-g affects the phosphorylation of AMPK, which has recently been implicated in platelet signalling [40], platelet pAMPK levels were examined following collagen activation. "
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    ABSTRACT: Delphinidin-3-glucoside (Dp-3-g) is one of the predominant bioactive compounds of anthocyanins in many plant foods. Although several anthocyanin compounds have been reported to be protective against cardiovascular diseases (CVDs), the direct effect of anthocyanins on platelets, the key players in atherothrombosis, has not been studied. The roles of Dp-3-g in platelet function are completely unknown. The present study investigated the effects of Dp-3-g on platelet activation and several thrombosis models in vitro and in vivo. We found that Dp-3-g significantly inhibited human and murine platelet aggregation in both platelet-rich plasma and purified platelets. It also markedly reduced thrombus growth in human and murine blood in perfusion chambers at both low and high shear rates. Using intravital microscopy, we observed that Dp-3-g decreased platelet deposition, destabilized thrombi, and prolonged the time required for vessel occlusion. Dp-3-g also significantly inhibited thrombus growth in a carotid artery thrombosis model. To elucidate the mechanisms, we examined platelet activation markers via flow cytometry and found that Dp-3-g significantly inhibited the expression of P-selectin, CD63, CD40L, which reflect platelet α- and δ-granule release, and cytosol protein secretion, respectively. We further demonstrated that Dp-3-g downregulated the expression of active integrin αIIbβ3 on platelets, and attenuated fibrinogen binding to platelets following agonist treatment, without interfering with the direct interaction between fibrinogen and integrin αIIbβ3. We found that Dp-3-g reduced phosphorylation of adenosine monophosphate-activated protein kinase, which may contribute to the observed inhibitory effects on platelet activation. Thus, Dp-3-g significantly inhibits platelet activation and attenuates thrombus growth at both arterial and venous shear stresses, which likely contributes to its protective roles against thrombosis and CVDs.
    Full-text · Article · May 2012 · PLoS ONE
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