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      Anti-Hyperlipidemic Effects and Potential Mechanisms of Action of the Caffeoylquinic Acid-Rich Pandanus tectorius Fruit Extract in Hamsters Fed a High Fat-Diet

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          Abstract

          Hyperlipidemia is considered to be one of the greatest risk factors contributing to the prevalence and severity of cardiovascular diseases. In this work, we investigated the anti-hyperlipidemic effect and potential mechanism of action of the Pandanus tectorius fruit extract in hamsters fed a high fat-diet (HFD). The n-butanol fraction of the P. tectorius fruit ethanol extract (PTF-b) was rich in caffeoylquinic acids (CQAs). Administration of PTF-b for 4 weeks effectively decreased retroperitoneal fat and the serum levels of total cholesterol (TC), triglycerides (TG) and low density lipoprotein–cholesterol (LDL-c) and hepatic TC and TG. The lipid signals (fatty acids, and cholesterol) in the liver as determined by nuclear magnetic resonance (NMR) were correspondingly reduced. Realtime quantitative PCR showed that the mRNA levels of PPARα and PPARα-regulated genes such as ACO, CPT1, LPL and HSL were largely enhanced by PTF-b. The transcription of LDLR, CYP7A1, and PPARγ was also upregulated. Treatment with PTF-b significantly stimulated the activation of AMP-activated protein kinase (AMPK) as well as the activity of serum and hepatic lipoprotein lipase (LPL). Together, these results suggest that administration of the PTF-b enriched in CQAs moderates hyperlipidemia and improves the liver lipid profile. These effects may be caused, at least in part, by increasing the expression of PPARα and its downstream genes and by upregulation of LPL and AMPK activities.

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          Most cited references51

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          ATGL-mediated fat catabolism regulates cardiac mitochondrial function via PPAR-α and PGC-1.

          Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors that regulate genes involved in energy metabolism and inflammation. For biological activity, PPARs require cognate lipid ligands, heterodimerization with retinoic X receptors, and coactivation by PPAR-γ coactivator-1α or PPAR-γ coactivator-1β (PGC-1α or PGC-1β, encoded by Ppargc1a and Ppargc1b, respectively). Here we show that lipolysis of cellular triglycerides by adipose triglyceride lipase (patatin-like phospholipase domain containing protein 2, encoded by Pnpla2; hereafter referred to as Atgl) generates essential mediator(s) involved in the generation of lipid ligands for PPAR activation. Atgl deficiency in mice decreases mRNA levels of PPAR-α and PPAR-δ target genes. In the heart, this leads to decreased PGC-1α and PGC-1β expression and severely disrupted mitochondrial substrate oxidation and respiration; this is followed by excessive lipid accumulation, cardiac insufficiency and lethal cardiomyopathy. Reconstituting normal PPAR target gene expression by pharmacological treatment of Atgl-deficient mice with PPAR-α agonists completely reverses the mitochondrial defects, restores normal heart function and prevents premature death. These findings reveal a potential treatment for the excessive cardiac lipid accumulation and often-lethal cardiomyopathy in people with neutral lipid storage disease, a disease marked by reduced or absent ATGL activity.
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            Lifetime risks of cardiovascular disease.

            The lifetime risks of cardiovascular disease have not been reported across the age spectrum in black adults and white adults. We conducted a meta-analysis at the individual level using data from 18 cohort studies involving a total of 257,384 black men and women and white men and women whose risk factors for cardiovascular disease were measured at the ages of 45, 55, 65, and 75 years. Blood pressure, cholesterol level, smoking status, and diabetes status were used to stratify participants according to risk factors into five mutually exclusive categories. The remaining lifetime risks of cardiovascular events were estimated for participants in each category at each age, with death free of cardiovascular disease treated as a competing event. We observed marked differences in the lifetime risks of cardiovascular disease across risk-factor strata. Among participants who were 55 years of age, those with an optimal risk-factor profile (total cholesterol level, <180 mg per deciliter [4.7 mmol per liter]; blood pressure, <120 mm Hg systolic and 80 mm Hg diastolic; nonsmoking status; and nondiabetic status) had substantially lower risks of death from cardiovascular disease through the age of 80 years than participants with two or more major risk factors (4.7% vs. 29.6% among men, 6.4% vs. 20.5% among women). Those with an optimal risk-factor profile also had lower lifetime risks of fatal coronary heart disease or nonfatal myocardial infarction (3.6% vs. 37.5% among men, <1% vs. 18.3% among women) and fatal or nonfatal stroke (2.3% vs. 8.3% among men, 5.3% vs. 10.7% among women). Similar trends within risk-factor strata were observed among blacks and whites and across diverse birth cohorts. Differences in risk-factor burden translate into marked differences in the lifetime risk of cardiovascular disease, and these differences are consistent across race and birth cohorts. (Funded by the National Heart, Lung, and Blood Institute.).
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              AMPK: a metabolic gauge regulating whole-body energy homeostasis.

              AMP-activated protein kinase (AMPK) is the downstream component of a kinase cascade that acts as a gauge of cellular energy levels. Over the last few years, accumulating evidence has demonstrated that AMPK is also involved in the regulation of energy balance at the whole-body level by responding to hormones and nutrient signals, which leads to changes in energy homeostasis. The physiological relevance of this new role of AMPK is demonstrated by the fact that impairment of AMPK function is associated with metabolic alterations, insulin resistance, obesity, hormonal disorders and cardiovascular disease. Here, we summarize the role of AMPK in the regulation of energy homeostasis. Understanding this key enzyme and its tissue-specific regulation will provide new targets for the treatment of metabolic disorders.
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                Author and article information

                Contributors
                Role: Editor
                Journal
                PLoS One
                PLoS ONE
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, USA )
                1932-6203
                2013
                16 April 2013
                : 8
                : 4
                : e61922
                Affiliations
                [1 ]Pharmacology and Toxicology Research Center, Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China
                [2 ]National Institute of Metrology, Beijing, China
                [3 ]Research Centre on Life Sciences and Environment Sciences, Harbin University of Commerce, Harbin, China
                National Research Council of Italy, Italy
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Conceived and designed the experiments: PG XDX CW. Performed the experiments: CW XPZ HW YS XZ HL YT GS XBS. Analyzed the data: CW PG XDX HW XPZ. Contributed reagents/materials/analysis tools: CW XPZ HW LS YS XZ YT HL GS XBS YJ. Wrote the paper: CW PG XPZ.

                Article
                PONE-D-12-30558
                10.1371/journal.pone.0061922
                3628350
                23613974
                f34ac3b8-e439-470d-9822-8175b6d3b515
                Copyright @ 2013

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 5 October 2012
                : 15 March 2013
                Page count
                Pages: 12
                Funding
                This work was supported by the following grants: 81001437 and 81202994 from National Natural Sciences Foundation of China; 7102111 from Natural Sciences Foundation of Beijing; 2012ZX09301-002-001-026 and 2011ZX09307-002-01 from National S&T Major Project. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Research Article
                Chemistry
                Analytical Chemistry
                Chemical Analysis
                Qualitative Analysis
                Applied Chemistry
                Chemical Properties
                Nuclear Magnetic Resonance
                Physical Chemistry
                Chemical Properties
                Nuclear Magnetic Resonance
                Phytochemistry
                Phytochemicals
                Phytopharmacology
                Medicine
                Drugs and Devices
                Cardiovascular Pharmacology
                Ethnopharmacology
                Pharmacodynamics

                Uncategorized
                Uncategorized

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