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Protein expression of CYP450 (cytochrome P450) and COX (cyclo-oxygenase) enzymes in renal microvessels was studied in obese and lean Zucker rats at 20–21 weeks of age. Body weight and blood glucose averaged 649±13 g and 142±10 mg\u002Fdl in obese Zucker rats compared with 437±10 g and 111±5 mg\u002Fdl in age-matched lean Zucker rats. Renal microvascular CYP4A and COX-2 protein levels were increased and CYP2C protein levels decreased in obese Zucker rats. TX (thromboxane) B2 excretion was 2-fold higher and PG (prostaglandin) E2 excretion significantly lower in obese Zucker rats. Additional studies investigated the ability of the COX-2 inhibitor, rofecoxib, to slow the progression of renal injury in obese Zucker rats. Rofecoxib treatment decreased urinary PGF2α and 8-isoprostane levels in obese Zucker rats. Renal microvessel mRNA expression of pro-inflammatory chemokines was decreased in COX-2-inhibitor-treated obese Zucker rats. Urinary albumin excretion, an index of kidney damage, averaged 95±11 mg\u002Fday in vehicle-treated and 9±1 mg\u002Fday in rofecoxib-treated obese Zucker rats. Glomerulosclerosis, characterized by mesangial expansion, tubulo-interstitial fibrosis and extracellular matrix accumulation, was prominent in obese Zucker rats compared with a lack of damage in age-matched lean Zucker rats and rofecoxib-treated obese Zucker rats. 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J. Gender-Specific Med., 1, 10",{},{"id":24,"text":1069,"url":24,"identifiers":1070},"Cevenini, 2010, Systems biology and longevity: an emerging approach to identify innovative anti-aging targets and Strategies, Curr. Pharm. Des., 16, 802, 10.2174\u002F138161210790883660",{"doi":1071},"10.2174\u002F138161210790883660",{"id":24,"text":1073,"url":24,"identifiers":1074},"Regitz-Zagrosek, 2012, Sex and gender differences in health, EMBO Rep., 13, 596, 10.1038\u002Fembor.2012.87",{"doi":1075},"10.1038\u002Fembor.2012.87",{"id":24,"text":1077,"url":24,"identifiers":1078},"Franceschi, 2000, Do men and women follow different trajectories to reach extreme longevity? Italian Multicenter Study on Centenarians (IMUSCE), Aging (Milano), 12, 77",{},{"id":24,"text":1080,"url":24,"identifiers":1081},"Passarino, 2002, Male\u002Ffemale ratio in centenarians: a possible role played by population genetic structure, Exp. Gerontol., 37, 1283, 10.1016\u002FS0531-5565(02)00140-7",{"doi":1082},"10.1016\u002FS0531-5565(02)00140-7",{"id":24,"text":1084,"url":24,"identifiers":1085},"Barford, 2006, Life expectancy: women now on top everywhere, BMJ, 332, 808, 10.1136\u002Fbmj.332.7545.808",{"doi":1086},"10.1136\u002Fbmj.332.7545.808",{"id":24,"text":1088,"url":24,"identifiers":1089},"Livi Bacci, 2015, La differenza di genere nella longevità: si attenua il vantaggio delle donne, Longevità, Vecchiaia, Salute, 34",{},{"id":24,"text":1091,"url":24,"identifiers":1092},"Wisser, 2014, The sex differential in mortality: a historical comparison of the adult-age pattern of the ratio and the difference, MPIDR Working Paper WP 2014-005",{},{"id":24,"text":1094,"url":24,"identifiers":1095},"Beltrán-Sánchez, 2015, Twentieth century surge of excess adult male mortality, Proc. Natl. Acad. Sci. 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Int., 2014, 560340, 10.1155\u002F2014\u002F560340",{"doi":1598},"10.1155\u002F2014\u002F560340",{"id":24,"text":1600,"url":24,"identifiers":1601},"Austad, 2006, Why women live longer than men: sex differences in longevity, Gend. Med., 3, 79, 10.1016\u002FS1550-8579(06)80198-1",{"doi":1602},"10.1016\u002FS1550-8579(06)80198-1",{"id":24,"text":1604,"url":24,"identifiers":1605},"Bittel, 2008, Comparison of X-chromosome inactivation patterns in multiple tissues from human females, J. Med. Genet., 45, 309, 10.1136\u002Fjmg.2007.055244",{"doi":1606},"10.1136\u002Fjmg.2007.055244",{"id":24,"text":1608,"url":24,"identifiers":1609},"Deng, 2014, X chromosome regulation: diverse patterns in development, tissues and disease, Nat. Rev. Genet., 15, 367, 10.1038\u002Fnrg3687",{"doi":1610},"10.1038\u002Fnrg3687",{"id":24,"text":1612,"url":24,"identifiers":1613},"Ozcelik, 2008, X chromosome inactivation and female predisposition to autoimmunity, Clin. Rev. Allergy Immunol., 34, 348, 10.1007\u002Fs12016-007-8051-0",{"doi":1614},"10.1007\u002Fs12016-007-8051-0",{"id":24,"text":1616,"url":24,"identifiers":1617},"Gentilini, 2012, Age-dependent skewing of X chromosome inactivation appears delayed in centenarians’ offspring: is there a role for allelic imbalance in healthy aging and longevity?, Aging Cell, 11, 277, 10.1111\u002Fj.1474-9726.2012.00790.x",{"doi":1618},"10.1111\u002Fj.1474-9726.2012.00790.x",{"id":24,"text":1620,"url":24,"identifiers":1621},"Gentilini, 2015, Stochastic epigenetic mutations (DNA methylation) increase exponentially in human aging and correlate with X chromosome inactivation skewing in females, Aging (Albany NY), 7, 568, 10.18632\u002Faging.100792",{"doi":1622},"10.18632\u002Faging.100792",{"id":24,"text":1624,"url":24,"identifiers":1625},"Sgarbi, 2014, Mitochondria hyperfusion and elevated autophagic activity are key mechanisms for cellular bioenergetic preservation in centenarians, Aging (Albany NY), 6, 296, 10.18632\u002Faging.100654",{"doi":1626},"10.18632\u002Faging.100654",{"id":24,"text":1628,"url":24,"identifiers":1629},"Raule, 2014, The co-occurrence of mtDNA mutations on different oxidative phosphorylation subunits, not detected by haplogroup analysis, affects human longevity and is population specific, Aging Cell, 13, 401, 10.1111\u002Facel.12186",{"doi":1630},"10.1111\u002Facel.12186",{"id":24,"text":1632,"url":24,"identifiers":1633},"Rose, 2007, The mitochondrial DNA control region shows genetically correlated levels of heteroplasmy in leukocytes of centenarians and their offspring, BMC Genomics, 8, 293, 10.1186\u002F1471-2164-8-293",{"doi":1634},"10.1186\u002F1471-2164-8-293",{"id":24,"text":1636,"url":24,"identifiers":1637},"Rose, 2010, Somatic point mutations in mtDNA control region are influenced by genetic background and associated with healthy aging: a GEHA study, PLoS One, 5, e13395, 10.1371\u002Fjournal.pone.0013395",{"doi":1638},"10.1371\u002Fjournal.pone.0013395",{"id":24,"text":1640,"url":24,"identifiers":1641},"Giuliani, 2014, Transmission from centenarians to their offspring of mtDNA heteroplasmy revealed by ultra-deep sequencing, Aging (Albany NY), 6, 454, 10.18632\u002Faging.100661",{"doi":1642},"10.18632\u002Faging.100661",{"id":24,"text":1644,"url":24,"identifiers":1645},"Achilli, 2011, Mitochondrial DNA backgrounds might modulate diabetes complications rather than T2DM as a whole, PLoS One, 6, e21029, 10.1371\u002Fjournal.pone.0021029",{"doi":1646},"10.1371\u002Fjournal.pone.0021029",{"id":24,"text":1648,"url":24,"identifiers":1649},"Chinnery, 2010, Mitochondrial DNA haplogroups and risk of transient ischaemic attack and ischaemic stroke: a genetic association study, Lancet. Neurol., 9, 498, 10.1016\u002FS1474-4422(10)70083-1",{"doi":1650},"10.1016\u002FS1474-4422(10)70083-1",{"id":24,"text":1652,"url":24,"identifiers":1653},"Gaweda-Walerych, 2008, Mitochondrial DNA haplogroups and subhaplogroups are associated with Parkinson's disease risk in a Polish PD cohort, J. Neural. Transm., 115, 1521, 10.1007\u002Fs00702-008-0121-9",{"doi":1654},"10.1007\u002Fs00702-008-0121-9",{"id":24,"text":1656,"url":24,"identifiers":1657},"Lee, 2010, Has the microbiota played a critical role in the evolution of the adaptive immune system?, Science, 330, 1768, 10.1126\u002Fscience.1195568",{"doi":1658},"10.1126\u002Fscience.1195568",{"id":24,"text":1660,"url":24,"identifiers":1661},"Mueller, 2006, Differences in fecal microbiota in different European study populations in relation to age, gender, and country: a cross-sectional study, Appl. Environ. Microbiol., 72, 1027, 10.1128\u002FAEM.72.2.1027-1033.2006",{"doi":1662},"10.1128\u002FAEM.72.2.1027-1033.2006",{"id":24,"text":1664,"url":24,"identifiers":1665},"Biagi, 2010, Through ageing, and beyond: gut microbiota and inflammatory status in seniors and centenarians, PLoS One, 5, e10667, 10.1371\u002Fjournal.pone.0010667",{"doi":1666},"10.1371\u002Fjournal.pone.0010667",{"id":24,"text":1668,"url":24,"identifiers":1669},"Anon, 2010, Putting gender on the agenda, Nature, 465, 665, 10.1038\u002F465665a",{"doi":1670},"10.1038\u002F465665a",{"id":24,"text":1672,"url":24,"identifiers":1673},"Schiebinger, 2014, Scientific research must take gender into account, Nature, 507, 9, 10.1038\u002F507009a",{"doi":1674},"10.1038\u002F507009a",{"id":1676,"createTime":1677,"updateTime":1677,"relativeEntities":1678,"slug":1679,"properties":1680,"entityType":110,"verifyStatus":111,"verifyTime":1677,"verifyNote":112,"syncStatus":23,"languages":1694,"translateLanguages":24,"viewCount":25,"primaryUrl":1695,"fullTextUrl":24,"authors":1696,"publicationType":266,"publisherRelationship":1912,"citationCount":1945,"citationInfo":1946,"publishDate":1948,"publishYear":1949,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":24,"openAccess":24,"references":1950,"isForceReanalyzing":537},"faaafd15-0293-4e16-8e2d-04535db535b3","2024-09-24T22:51:33.452+00:00",[],"Red-wine-polyphenols-prevent-endothelial-dysfunction-induced-by-endothelin-1-in-rat-aorta-role-of-NADPH-oxidase",{"mag":1681,"keywords":1683,"openalex":1684,"abstract":1686,"title":1688,"pm":1690,"doi":1692},{"VOID":1682},"2100581807",{},{"VOID":1685},"W2100581807",{"EN":1687},"\u003Cjats:p>RWPs (red wine polyphenols) exert antihypertensive effects and improve endothelial function by reducing the plasma levels of ET-1 (endothelin-1) and the subsequent vascular production of O2•− (superoxide anion). Our present study was designed to evaluate whether RWPs act directly in the vascular wall improving endothelial dysfunction and O2•− production induced by ET-1 and to analyse the compounds responsible for these protective effects. We incubated rat isolated aortic rings in the presence or absence of ET-1 (10 nM) and RWPs (10−4 to 10−2 g\u002Fl) or catechin (0.2 μM), epicatechin (10 μM) and resveratrol (0.1 μM). ET-1 reduced the relaxant responses to acetylcholine, increased intracellular O2•− production, NADPH oxidase activity and protein expression of NADPH oxidase subunit p47phox. All these changes were prevented by RWPs. The preventive effects of RWPs were unaffected by co-incubation with either ICI-182780, an ER (oestrogen receptor) antagonist, or GW9662, a PPARγ (peroxisome-proliferator-activated receptor γ) antagonist. RWPs inhibited the phosphorylation of the mitogen-activated protein kinase, ERK1\u002F2 (extracellular signal-regulated kinase 1\u002F2), a key regulator of p47phox expression in response to ET-1. When the isolated polyphenols were tested, at the concentrations found in 10−2 g\u002Fl RWPs, only epicatechin prevented endothelial dysfunction and all biochemical changes induced by ET-1 in the vascular wall. Taken together, these results indicate that RWPs prevent ET-1-induced vascular O2•− production by reducing overexpression of p47phox and the subsequent increased NADPH oxidase activity, leading to improvement in endothelial function. The effects of RWPs appear to be independent of ER and PPARγ activation and are related to ERK1\u002F2 inhibition.\u003C\u002Fjats:p>",{"EN":1689},"Red wine polyphenols prevent endothelial dysfunction induced by endothelin-1 in rat aorta: role of NADPH 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of Pharmacology, School of Pharmacy, University of Granada, 18071 Granada, Spain",{"openalex":1713,"orcid":1715,"title":1717},{"VOID":1714},"A5011420908",{"VOID":1716},"https:\u002F\u002Forcid.org\u002F0000-0002-9423-817X",{"EN":1718},"R López-Sepúlveda",{"id":1720,"sortIndex":1721,"researcher":24,"roles":1722,"affiliations":1723,"properties":1730},"3f16540b-70be-4cb0-bb90-a82413d9c223",11,[],[1724],{"id":1725,"sortIndex":25,"affiliation":1726,"properties":24},"31ec0f28-2c81-4c44-a9c6-c6248e426f2f",{"id":1704,"createTime":1705,"updateTime":1706,"relativeEntities":1727,"slug":1708,"properties":1728,"entityType":45,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},[],{"title":1729},{"VI":1711},{"openalex":1731,"orcid":1733,"title":1735},{"VOID":1732},"A5021273363",{"VOID":1734},"https:\u002F\u002Forcid.org\u002F0000-0003-3872-2669",{"EN":1736},"Rosario 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Res., 71, 794, 10.1016\u002Fj.cardiores.2006.05.022",{"doi":2103},"10.1016\u002Fj.cardiores.2006.05.022",{"id":24,"text":2105,"url":24,"identifiers":2106},"Sumi, 2003, 17β-Estradiol inhibits NADPH oxidase activity through the regulation of p47phox mRNA and protein expression in THP-1 cells, Biochim. Biophys. Acta, 1640, 113, 10.1016\u002FS0167-4889(03)00026-0",{"doi":2107},"10.1016\u002FS0167-4889(03)00026-0",{"id":24,"text":2109,"url":24,"identifiers":2110},"Liang, 2001, Suppression of inducible cyclooxygenase and nitric oxide synthase through activation of peroxisome proliferator-activated receptor-gamma by flavonoids in mouse macrophages, FEBS Lett., 496, 12, 10.1016\u002FS0014-5793(01)02393-6",{"doi":2111},"10.1016\u002FS0014-5793(01)02393-6",{"id":24,"text":2113,"url":24,"identifiers":2114},"Mehta, 2003, Pioglitazone inhibits LOX-1 expression in human coronary artery endothelial cells by reducing intracellular superoxide radical generationArterioscler, Thromb. Vasc. Biol., 23, 2203, 10.1161\u002F01.ATV.0000094411.98127.5F",{"doi":2115},"10.1161\u002F01.ATV.0000094411.98127.5F",{"id":24,"text":2117,"url":24,"identifiers":2118},"Foschi, 1997, Biphasic activation of p21ras by endothelin-1 sequentially activates the ERK cascade and phosphatidylinositol 3-kinase, EMBO J., 16, 6439, 10.1093\u002Femboj\u002F16.21.6439",{"doi":2119},"10.1093\u002Femboj\u002F16.21.6439",{"id":24,"text":2121,"url":24,"identifiers":2122},"Daou, 2004, Reactive oxygen species mediate endothelin-1-induced activation of ERK1\u002F2, PKB, and Pyk2 signaling, as well as protein synthesis, in vascular smooth muscle cells, Free Radical Biol. Med., 37, 208, 10.1016\u002Fj.freeradbiomed.2004.04.018",{"doi":2123},"10.1016\u002Fj.freeradbiomed.2004.04.018",{"id":24,"text":2125,"url":24,"identifiers":2126},"Yogi, 2007, Endothelin-1, but not Ang II, activates MAP kinases through c-Src independent Ras–Raf dependent pathways in vascular smooth muscle cells, Arterioscler. Thromb. Vasc. Biol., 27, 1960, 10.1161\u002FATVBAHA.107.146746",{"doi":2127},"10.1161\u002FATVBAHA.107.146746",{"id":24,"text":2129,"url":24,"identifiers":2130},"Pearson, 2001, Mitogen-activated protein kinase pathways: regulation and physiological functions, Endocr. Rev., 22, 153",{},{"id":24,"text":2132,"url":24,"identifiers":2133},"Sparwel, 2009, Differential effects of red and white wines on inhibition of the platelet-derived growth factor receptor: impact of the mash fermentation, Cardiovasc. Res., 81, 758, 10.1093\u002Fcvr\u002Fcvn340",{"doi":2134},"10.1093\u002Fcvr\u002Fcvn340",{"id":2136,"createTime":2137,"updateTime":2137,"relativeEntities":2138,"slug":2139,"properties":2140,"entityType":110,"verifyStatus":111,"verifyTime":2137,"verifyNote":112,"syncStatus":23,"languages":2154,"translateLanguages":24,"viewCount":25,"primaryUrl":2155,"fullTextUrl":24,"authors":2156,"publicationType":266,"publisherRelationship":2312,"citationCount":2344,"citationInfo":2345,"publishDate":2351,"publishYear":2352,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":24,"openAccess":24,"references":2353,"isForceReanalyzing":537},"2c65ec46-3862-4571-89f9-31c56b016f29","2024-09-01T22:44:22.938+00:00",[],"Looking-to-the-horizon-the-role-of-bilirubin-in-the-development-and-prevention-of-age-related-chronic-diseases",{"mag":2141,"keywords":2143,"openalex":2144,"abstract":2146,"title":2148,"pm":2150,"doi":2152},{"VOID":2142},"2038172495",{},{"VOID":2145},"W2038172495",{"EN":2147},"\u003Cjats:p>Bilirubin, the principal tetrapyrrole, bile pigment and catabolite of haem, is an emerging biomarker of disease resistance, which may be related to several recently documented biological functions. Initially believed to be toxic in infants, the perception of bilirubin has undergone a transformation: it is now considered to be a molecule that may promote health in adults. Data from the last decade demonstrate that mildly elevated serum bilirubin levels are strongly associated with reduced prevalence of chronic diseases, particularly cardiovascular diseases (CVDs), as well as CVD-related mortality and risk factors. Recent data also link bilirubin to other chronic diseases, including cancer and Type 2 diabetes mellitus, and to all-cause mortality. Therefore, there is evidence to suggest that bilirubin is a biomarker for reduced chronic disease prevalence and a predictor of all-cause mortality, which is of important clinical significance. In the present review, detailed information on the association between bilirubin and all-cause mortality, as well as the pathological conditions of CVD, cancer, diabetes and neurodegenerative diseases, is provided. The mechanistic background concerning how bilirubin and its metabolism may influence disease prevention and its clinical relevance is also discussed. Given that the search for novel biomarkers of these diseases, as well as for novel therapeutic modalities, is a key research objective for the near future, bilirubin represents a promising candidate, meeting the criteria of a biomarker, and should be considered more carefully in clinical practice as a molecule that might provide insights into disease resistance. Clearly, however, greater molecular insight is warranted to support and strengthen the conclusion that bilirubin can prevent disease, with future research directions also proposed.\u003C\u002Fjats:p>",{"EN":2149},"Looking to the horizon: the role of bilirubin in the development and prevention of age-related chronic 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Res., 560, 1, 10.1016\u002Fj.mrgentox.2004.01.010",{"doi":3145},"10.1016\u002Fj.mrgentox.2004.01.010",{"id":24,"text":3147,"url":24,"identifiers":3148},"Wallner, 2013, Anti-genotoxic potential of bilirubin in vivo: damage to DNA in hyperbilirubinemic human and animal models, Cancer Prev. Res., 6, 1056, 10.1158\u002F1940-6207.CAPR-13-0125",{"doi":3149},"10.1158\u002F1940-6207.CAPR-13-0125",{"id":24,"text":3151,"url":24,"identifiers":3152},"Kim, 1997, UDP-glucuronosyltransferase-mediated protection against in vitro DNA oxidation and micronucleus formation initiated by phenytoin and its embryotoxic metabolite 5-(p-hydroxyphenyl)-5-phenylhydantoin, J. Pharmacol. Exp. 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Res., 287, 293, 10.1016\u002F0027-5107(93)90022-8",{"doi":3163},"10.1016\u002F0027-5107(93)90022-8",{"id":24,"text":881,"url":24,"identifiers":3165},{},{"id":24,"text":3167,"url":24,"identifiers":3168},"Orlov, 2014, Circular dichroism study of the interaction between mutagens and bilirubin bound to different binding sites of serum albumins, Spectrochim. Acta A Mol. Biol. Spectrosc., 126, 68, 10.1016\u002Fj.saa.2014.01.139",{"doi":3169},"10.1016\u002Fj.saa.2014.01.139",{"id":24,"text":3171,"url":24,"identifiers":3172},"Molzer, 2013, Interaction between TNFone and tetrapyrroles may account for their anti-genotoxic effects–a novel mechanism for DNA-protection, J. Porphyrins Phthalocyanines, 17, 1157, 10.1142\u002FS1088424613500995",{"doi":3173},"10.1142\u002FS1088424613500995",{"id":24,"text":3175,"url":24,"identifiers":3176},"Keshavan, 2004, Unconjugated bilirubin induces apoptosis in colon cancer cells by triggering mitochondrial depolarization, Int. J. Cancer, 112, 433, 10.1002\u002Fijc.20418",{"doi":3177},"10.1002\u002Fijc.20418",{"id":24,"text":3179,"url":24,"identifiers":3180},"Ollinger, 2007, Bilirubin inhibits tumor cell growth via activation of ERK, Cell Cycle, 6, 3078, 10.4161\u002Fcc.6.24.5022",{"doi":3181},"10.4161\u002Fcc.6.24.5022",{"id":24,"text":3183,"url":24,"identifiers":3184},"Molzer, 2013, In vitro DNA-damaging effects of intestinal and related tetrapyrroles in human cancer cells, Exp. Cell Res., 319, 536, 10.1016\u002Fj.yexcr.2012.12.003",{"doi":3185},"10.1016\u002Fj.yexcr.2012.12.003",{"id":24,"text":3187,"url":24,"identifiers":3188},"Markesbery, 2007, Damage to lipids, proteins, DNA, and RNA in mild cognitive impairment, Arch. 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Sci., 18, 69, 10.1007\u002FBF01999565",{"doi":3215},"10.1007\u002FBF01999565",{"id":24,"text":3217,"url":24,"identifiers":3218},"Li, 2014, Decreased serum bilirubin is associated with silent cerebral infarction, Arterioscler. Thromb. Vasc. Biol., 34, 946, 10.1161\u002FATVBAHA.113.303003",{"doi":3219},"10.1161\u002FATVBAHA.113.303003",{"id":24,"text":2685,"url":24,"identifiers":3221},{"doi":2687},{"id":24,"text":3223,"url":24,"identifiers":3224},"Ilzecka, 2003, Serum bilirubin concentration in patients with amyotrophic lateral sclerosis, Clin. Neurol. Neurosurg., 105, 237, 10.1016\u002FS0303-8467(03)00031-3",{"doi":3225},"10.1016\u002FS0303-8467(03)00031-3",{"id":24,"text":3227,"url":24,"identifiers":3228},"Muller, 1991, Coincidence of schizophrenia and hyperbilirubinemia, Pharmacopsychiatr, 24, 225, 10.1055\u002Fs-2007-1014472",{"doi":3229},"10.1055\u002Fs-2007-1014472",{"id":24,"text":3231,"url":24,"identifiers":3232},"Miyaoka, 2000, Schizophrenia-associated idiopathic unconjugated hyperbilirubinemia (Gilbert's syndrome), J. Clin. Psychiatry, 61, 868, 10.4088\u002FJCP.v61n1110",{"doi":3233},"10.4088\u002FJCP.v61n1110",{"id":24,"text":3235,"url":24,"identifiers":3236},"Yao, 1998, Reduced status of plasma total antioxidant capacity in schizophrenia, Schizophr. Res., 32, 1, 10.1016\u002FS0920-9964(98)00030-9",{"doi":3237},"10.1016\u002FS0920-9964(98)00030-9",{"id":24,"text":3239,"url":24,"identifiers":3240},"Pae, 2004, Decreased plasma antioxidants in schizophrenia, Neuropsychobiology, 50, 54, 10.1159\u002F000077942",{"doi":3241},"10.1159\u002F000077942",{"id":24,"text":3243,"url":24,"identifiers":3244},"Vitek, 2010, Serum bilirubin levels and UGT1A1 promoter variations in patients with schizophrenia, Psychiatry. Res., 178, 449, 10.1016\u002Fj.psychres.2009.12.008",{"doi":2683},{"id":24,"text":3246,"url":24,"identifiers":3247},"Oren, 2002, Effects of light on low nocturnal bilirubin in winter depression: a preliminary report, Biol. Psychiatry, 51, 422, 10.1016\u002FS0006-3223(01)01254-9",{"doi":3248},"10.1016\u002FS0006-3223(01)01254-9",{"id":24,"text":3250,"url":24,"identifiers":3251},"Oren, 1998, Tweaking the human circadian clock with light, Science, 279, 333, 10.1126\u002Fscience.279.5349.333",{"doi":3252},"10.1126\u002Fscience.279.5349.333",{"id":24,"text":3254,"url":24,"identifiers":3255},"Seta, 2006, Heme oxygenase-2 is a critical determinant for execution of an acute inflammatory and reparative response, Am. J. Pathol., 169, 1612, 10.2353\u002Fajpath.2006.060555",{"doi":3256},"10.2353\u002Fajpath.2006.060555",{"id":24,"text":3258,"url":24,"identifiers":3259},"Biomarkers Definitions Working Group, 2001, Biomarkers and surrogate endpoints: preferred definitions and conceptual framework, Clin. Pharmacol. Ther., 69, 89, 10.1067\u002Fmcp.2001.113989",{"doi":3260},"10.1067\u002Fmcp.2001.113989",{"id":24,"text":3262,"url":24,"identifiers":3263},"Knasmuller, 2008, Use of conventional and -omics based methods for health claims of dietary antioxidants: a critical overview, Br. J. Nutr., 99, ES3, 10.1017\u002FS0007114508965752",{"doi":3264},"10.1017\u002FS0007114508965752",{"id":24,"text":3266,"url":24,"identifiers":3267},"Weber, 2006, Role of B-type natriuretic peptide (BNP) and NT-proBNP in clinical routine, Heart, 92, 843, 10.1136\u002Fhrt.2005.071233",{"doi":3268},"10.1136\u002Fhrt.2005.071233",{"id":24,"text":3270,"url":24,"identifiers":3271},"Gillett, 2009, International Expert Committee report on the role of the A1c assay in the diagnosis of diabetes: Diabetes Care 2009;32(7):1327–1334, Clin. Biochem. Rev., 30, 197",{},{"id":24,"text":3273,"url":24,"identifiers":3274},"Keller, 2009, Sensitive troponin I assay in early diagnosis of acute myocardial infarction, N. Engl. J. Med., 361, 868, 10.1056\u002FNEJMoa0903515",{"doi":3275},"10.1056\u002FNEJMoa0903515",{"id":24,"text":3277,"url":24,"identifiers":3278},"Ridker, 2003, Clinical application of C-reactive protein for cardiovascular disease detection and prevention, Circulation, 107, 363, 10.1161\u002F01.CIR.0000053730.47739.3C",{"doi":3279},"10.1161\u002F01.CIR.0000053730.47739.3C",{"id":24,"text":3281,"url":24,"identifiers":3282},"European Food Safety Authority (EFSA) Panel on Dietetic Products, 2011, Guidance on the scientific requirements for health claims related to antioxidants, oxidative damage and cardiovascular health, EFSA J., 9, 2474, 10.2903\u002Fj.efsa.2011.2474",{"doi":3283},"10.2903\u002Fj.efsa.2011.2474",{"id":24,"text":3285,"url":24,"identifiers":3286},"Sistrom, 2004, Proportions, odds, and risk, Radiology, 230, 12, 10.1148\u002Fradiol.2301031028",{"doi":3287},"10.1148\u002Fradiol.2301031028",{"id":24,"text":3289,"url":24,"identifiers":3290},"Kundur, 2015, Bilirubin, platelet activation and heart disease: a missing link to cardiovascular protection in Gilbert's syndrome?, Atherosclerosis, 239, 73, 10.1016\u002Fj.atherosclerosis.2014.12.042",{"doi":3291},"10.1016\u002Fj.atherosclerosis.2014.12.042",{"id":24,"text":3293,"url":24,"identifiers":3294},"Dore, 1999, Bilirubin, formed by activation of heme oxygenase-2, protects neurons against oxidative stress injury, Proc. Natl. Acad. Sci. U.S.A., 96, 2445, 10.1073\u002Fpnas.96.5.2445",{"doi":3295},"10.1073\u002Fpnas.96.5.2445",{"id":24,"text":3297,"url":24,"identifiers":3298},"Baranano, 2002, Biliverdin reductase: a major physiologic cytoprotectant, Proc. Natl. Acad. Sci. U.S.A., 99, 16093, 10.1073\u002Fpnas.252626999",{"doi":3299},"10.1073\u002Fpnas.252626999",{"id":24,"text":3301,"url":24,"identifiers":3302},"Sedlak, 2004, Bilirubin benefits: cellular protection by a biliverdin reductase antioxidant cycle, Pediatrics, 113, 1776, 10.1542\u002Fpeds.113.6.1776",{"doi":3303},"10.1542\u002Fpeds.113.6.1776",{"id":3305,"createTime":3306,"updateTime":3306,"relativeEntities":3307,"slug":3308,"properties":3309,"entityType":110,"verifyStatus":111,"verifyTime":3306,"verifyNote":112,"syncStatus":23,"languages":3323,"translateLanguages":24,"viewCount":25,"primaryUrl":3324,"fullTextUrl":24,"authors":3325,"publicationType":266,"publisherRelationship":3362,"citationCount":3394,"citationInfo":3395,"publishDate":3397,"publishYear":3398,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":24,"openAccess":24,"references":3399,"isForceReanalyzing":537},"e4f3e643-2c2e-4555-9a31-38aa73ddab9e","2024-10-02T22:43:37.832+00:00",[],"Non-esterified-fatty-acids-may-regulate-human-leucocyte-sodium-pump-activity",{"mag":3310,"keywords":3312,"openalex":3313,"abstract":3315,"title":3317,"pm":3319,"doi":3321},{"VOID":3311},"2409741355",{},{"VOID":3314},"W2409741355",{"EN":3316},"\u003Cjats:p>1. Human leucocyte sodium pump activity was studied in normal fasting subjects by measuring the ouabain-sensitive 22Na+ efflux rate constants.\u003C\u002Fjats:p>\n               \u003Cjats:p>2. This 22Na+ efflux rate constant was inversely related to the fasting plasma non-esterified fatty acid level (rs = −0.73, P < 0.0001).\u003C\u002Fjats:p>\n               \u003Cjats:p>3. An oral glucose load (40 g\u002Fm2 surface area) led to an increase in the leucocyte ouabain-sensitive 22Na+ efflux rate constant after 2 h (1.97 ± 0.25 to 2.44 ± 0.19 h−1, P < 0.0001, n = 11). There was a concomitant fall in the plasma non-esterified fatty acid level.\u003C\u002Fjats:p>\n               \u003Cjats:p>4. Incubation of leucocytes in vitro with 100 μmol\u002Fl linoleic acid inhibited the leucocyte ouabain-sensitive 22Na+ efflux rate constant (1.52 ± 0.27 vs 0.84 ± 0.24 h−1, P < 0.001, n = 8).\u003C\u002Fjats:p>\n               \u003Cjats:p>5. The leucocyte Na+,K+-dependent adenosine triphosphatase (Na+,K+-ATPase) activity was inhibited in vitro by long chain non-esterified fatty acids, especially when unsaturated.\u003C\u002Fjats:p>\n               \u003Cjats:p>6. Non-esterified fatty acids may account for some of the Na+,K+-ATPase inhibitory activity of plasma.\u003C\u002Fjats:p>",{"EN":3318},"Non-esterified fatty acids may regulate human leucocyte sodium pump activity",{"VOID":3320},"3024900",{"VOID":3322},"10.1042\u002Fcs0710737",[114],"https:\u002F\u002Fportlandpress.com\u002Fclinsci\u002Farticle\u002F71\u002F6\u002F737\u002F73984\u002FNon-esterified-fatty-acids-may-regulate-human",[3326,3347],{"id":3327,"sortIndex":25,"researcher":24,"roles":3328,"affiliations":3329,"properties":3340},"0a0b64f2-9c6e-4737-8aae-27006ed02319",[],[3330],{"id":3331,"sortIndex":25,"affiliation":3332,"properties":24},"2874bea3-e07a-49d6-b62f-b913ba1b19e4",{"id":3333,"createTime":3334,"updateTime":3334,"relativeEntities":3335,"slug":3336,"properties":3337,"entityType":45,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},"986d277e-6143-4e43-8d91-e7270e9b11bb","2024-10-02T22:43:37.855+00:00",[],"Sheikh-Rashid-Diabetes-Unit-Radcliffe-Infirmary-Oxford-U-K-",{"title":3338},{"EN":3339},"Sheikh Rashid Diabetes Unit, Radcliffe Infirmary, Oxford, U.K.",{"openalex":3341,"orcid":3343,"title":3345},{"VOID":3342},"A5091305818",{"VOID":3344},"https:\u002F\u002Forcid.org\u002F0000-0002-6553-5749",{"EN":3346},"Leong L. Ng",{"id":3348,"sortIndex":119,"researcher":24,"roles":3349,"affiliations":3350,"properties":3357},"d224b66c-c90f-47c2-83df-2b19a72097e0",[],[3351],{"id":3352,"sortIndex":25,"affiliation":3353,"properties":24},"a03793d7-d134-48bc-bccc-fed47bfda9bb",{"id":3333,"createTime":3334,"updateTime":3334,"relativeEntities":3354,"slug":3336,"properties":3355,"entityType":45,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},[],{"title":3356},{"EN":3339},{"openalex":3358,"title":3360},{"VOID":3359},"A5052208535",{"EN":3361},"T. D. R. Hockaday",{"url":24,"publisher":3363,"properties":3388},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":3364,"slug":10,"properties":3365,"entityType":22,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25,"subjectFields":3371,"manageAffiliations":3372,"indexDatabases":3373,"url":86,"thumbnailPath":24,"statistic":24,"gsStatistic":24,"type":24,"analyzePriority":24},[],{"country":3366,"issn":3367,"introduce":3368,"eissn":3369,"title":3370},{"VOID":13},{"VOID":15},{"EN":17},{"VOID":19},{"EN":21},[],[],[3374,3381],{"id":49,"indexDatabase":3375,"url":64,"indexYears":24,"academicFieldIds":3380,"indexDatabaseRanking":24},{"id":51,"createTime":52,"updateTime":53,"relativeEntities":3376,"label":3377,"description":3378,"key":60,"publicationTags":3379,"standard":24},[],{"EN":56,"VI":56},{"VI":58,"EN":59},[62,63],[66],{"id":68,"indexDatabase":3382,"url":81,"indexYears":82,"academicFieldIds":3387,"indexDatabaseRanking":85},{"id":70,"createTime":71,"updateTime":72,"relativeEntities":3383,"label":3384,"description":3385,"key":78,"publicationTags":3386,"standard":24},[],{"EN":75,"VI":75},{"EN":75,"VI":77},[80],[84],{"volume":3389,"pages":3391,"issue":3393},{"VOID":3390},"71",{"VOID":3392},"737-742",{"VOID":299},25,{"total":3394,"publishYear":24,"statisticByYear":3396},{"2015":119},"1986-12-01",1986,[],{"id":3401,"createTime":3402,"updateTime":3402,"relativeEntities":3403,"slug":3404,"properties":3405,"entityType":110,"verifyStatus":111,"verifyTime":3402,"verifyNote":112,"syncStatus":23,"languages":3419,"translateLanguages":24,"viewCount":25,"primaryUrl":3420,"fullTextUrl":24,"authors":3421,"publicationType":266,"publisherRelationship":3499,"citationCount":3531,"citationInfo":3532,"publishDate":3536,"publishYear":3537,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":24,"openAccess":24,"references":3538,"isForceReanalyzing":537},"63ef3524-2fa5-4dc3-b3a5-af472efb94a1","2024-09-20T22:41:55.455+00:00",[],"The-renin-angiotensin-aldosterone-system-in-pre-eclampsia-the-delicate-balance-between-good-and-bad",{"mag":3406,"keywords":3408,"openalex":3409,"abstract":3411,"title":3413,"pm":3415,"doi":3417},{"VOID":3407},"2128998689",{},{"VOID":3410},"W2128998689",{"EN":3412},"\u003Cjats:p>Pregnancy demands major changes of the cardiovascular system, and this involves, among others, activation of the RAAS (renin–angiotensin–aldosterone system), allowing an aldosterone-dependent increase in volume. Remarkably, a relative resistance to the pressor response of AngII (angiotensin II) develops simultaneously to prevent the increase in blood pressure that would normally accompany RAAS activation. The increase in volume, the degree of RAAS activation and the diminished pressor response to AngII are less pronounced in pre-eclampsia. However, animal models displaying excessive RAAS activation also result in a pre-eclampsia-like syndrome, and the aldosterone\u002Frenin ratio is elevated in pre-eclampsia compared with a normal pregnancy. New insights into the pathogenesis of pre-eclampsia have revealed a major role for VEGF (vascular endothelial growth factor), VEGF-inactivating sFlt-1 (soluble fms-like tyrosine kinase-1) and AT1 (angiotensin II type 1) receptor autoantibodies. The last mentioned activate AT1 receptors, thereby potentially suppressing circulating renin and aldosterone. VEGF, both directly and indirectly (by increasing capillary density), affects adrenal aldosterone synthesis. The present review summarizes all of the recent findings regarding RAAS regulation in pre-eclampsia compared with normal pregnancy, concluding that factors such as sFlt-1 and AT1 receptor autoantibodies disturb the delicate balance that normally results in a volume increase and a diminished vasoconstrictor response to AngII in pregnant women. It is possible that there are non-parallel changes in the circulating and renal RAAS in pre-eclampsia, which are potentially reflected by the urinary levels of renin.\u003C\u002Fjats:p>",{"EN":3414},"The renin–angiotensin–aldosterone system in pre-eclampsia: the delicate balance between good and bad",{"VOID":3416},"24400721",{"VOID":3418},"10.1042\u002Fcs20130455",[114],"https:\u002F\u002Fportlandpress.com\u002Fclinsci\u002Farticle\u002F126\u002F8\u002F537\u002F69212\u002FThe-renin-angiotensin-aldosterone-system-in-pre",[3422,3443,3465,3482],{"id":3423,"sortIndex":119,"researcher":24,"roles":3424,"affiliations":3425,"properties":3436},"c5b3dc45-6b37-4323-8169-d91c4ba0e2c3",[],[3426],{"id":3427,"sortIndex":25,"affiliation":3428,"properties":24},"44c2f144-4852-4b6b-beb5-4532d4abf720",{"id":3429,"createTime":3430,"updateTime":3430,"relativeEntities":3431,"slug":3432,"properties":3433,"entityType":45,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},"5de2e0a1-6135-4b9f-882e-1da4a18c49de","2024-09-20T22:41:55.489+00:00",[],"Department-of-Obstetrics-and-Gynecology-Division-Obstetrics-Prenatal-Medicine-Erasmus-MC-Rotterdam-The-Netherlands",{"title":3434},{"EN":3435},"Department of Obstetrics and Gynecology, Division Obstetrics & Prenatal Medicine, Erasmus MC, Rotterdam, The Netherlands",{"openalex":3437,"orcid":3439,"title":3441},{"VOID":3438},"A5038074463",{"VOID":3440},"https:\u002F\u002Forcid.org\u002F0000-0002-5248-863X",{"EN":3442},"W. 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J. Hypertens., 5, 366, 10.1093\u002Fajh\u002F5.6.366",{"doi":3759},"10.1093\u002Fajh\u002F5.6.366",{"id":24,"text":3761,"url":24,"identifiers":3762},"Seva-Pessôa, 2012, Key developments in renin–angiotensin–aldosterone system inhibition, Nat. Rev. Nephrol., 9, 26, 10.1038\u002Fnrneph.2012.249",{"doi":3763},"10.1038\u002Fnrneph.2012.249",{"id":24,"text":3765,"url":24,"identifiers":3766},"Verdonk, 2011, Do angiotensin II type 2 receptors mediate the enhanced angiotensin II constrictor response in pre-eclampsia?, Hypertension, 58, E40",{},{"id":24,"text":3768,"url":24,"identifiers":3769},"Florijn, 1991, Plasma immunoreactive endothelin-1 in pregnant women with and without pre-eclampsia, J. Cardiovasc. Pharmacol., 17, S446, 10.1097\u002F00005344-199100177-00128",{"doi":3770},"10.1097\u002F00005344-199100177-00128",{"id":24,"text":3772,"url":24,"identifiers":3773},"Krop, 2013, The (pro)renin receptor. A decade of research: what have we learned?, Pflügers Arch., 465, 87, 10.1007\u002Fs00424-012-1105-z",{"doi":3774},"10.1007\u002Fs00424-012-1105-z",{"id":24,"text":3776,"url":24,"identifiers":3777},"van den Heuvel, 2011, Urinary renin, but not angiotensinogen or aldosterone, reflects the renal renin–angiotensin–aldosterone system activity and the efficacy of renin–angiotensin–aldosterone system blockade in the kidney, J. Hypertens., 29, 2147, 10.1097\u002FHJH.0b013e32834bbcbf",{"doi":3778},"10.1097\u002FHJH.0b013e32834bbcbf",{"id":24,"text":3780,"url":24,"identifiers":3781},"Persson, 2013, Urinary renin and angiotensinogen in type 2 diabetes: added value beyond urinary albumin?, J. Hypertens., 31, 1646, 10.1097\u002FHJH.0b013e328362217c",{"doi":3782},"10.1097\u002FHJH.0b013e328362217c",{"id":3784,"createTime":3785,"updateTime":3785,"relativeEntities":3786,"slug":3787,"properties":3788,"entityType":110,"verifyStatus":111,"verifyTime":3785,"verifyNote":112,"syncStatus":23,"languages":3802,"translateLanguages":24,"viewCount":25,"primaryUrl":3803,"fullTextUrl":24,"authors":3804,"publicationType":266,"publisherRelationship":3909,"citationCount":3941,"citationInfo":3942,"publishDate":3945,"publishYear":3946,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":24,"openAccess":24,"references":3947,"isForceReanalyzing":537},"ed200461-d75c-4e7c-b401-01128e8ba83a","2024-12-05T21:36:18.232+00:00",[],"Comparative-effects-of-telmisartan-sitagliptin-and-metformin-alone-or-in-combination-on-obesity-insulin-resistance-and-liver-and-pancreas-remodelling-in-C57BL-6-mice-fed-on-a-very-high-fat-diet",{"mag":3789,"keywords":3791,"openalex":3792,"abstract":3794,"title":3796,"pm":3798,"doi":3800},{"VOID":3790},"1992316317",{},{"VOID":3793},"W1992316317",{"EN":3795},"\u003Cjats:p>The aim of the present study was to evaluate the effects of monotherapies and combinations of drugs on insulin sensitivity, adipose tissue morphology, and pancreatic and hepatic remodelling in C57BL\u002F6 mice fed on a very HF (high-fat) diet. Male C57BL\u002F6 mice were fed on an HF (60% lipids) diet or SC (standard chow; 10% lipids) diet for 10 weeks, after which time the following drug treatments began: HF-T (HF diet treated with telmisartan; 5.2 mg·kg−1 of body weight·day−1), HF-S (HF diet treated with sitagliptin; 1.08 g·kg−1 of body weight·day−1), HF-M (HF diet treated with metformin; 310.0 mg·kg−1 of body weight·day−1), HF-TM (HF diet treated with telmisartan+metformin), HF-TS (HF diet treated with telmisartan+sitagliptin) and HF-SM (HF diet treated with sitagliptin+metformin). Treated groups also had free access to the HF diet, and treatments lasted for 6 weeks. Morphometry, stereological tools, immunostaining, ELISA, Western blot analysis and electron microscopy were used. The HF diet yielded an overweight phenotype, an increase in oral glucose intolerance, hyperinsulinaemia, hypertrophied islets and adipocytes, stage 2 steatosis (>33%), and reduced liver PPAR-α (peroxisome-proliferator-activated receptor-α) and GLUT-2 (glucose transporter-2) levels, concomitant with enhanced SREBP-1 (sterol-regulatory-element-binding protein-1) expression (P<0.0001). Conversely, all drug treatments resulted in significant weight loss, a reversal of insulin resistance, islet and adipocyte hypertrophy, and alleviated hepatic steatosis. Only the HF-T and HF-TS groups had body weights similar to the SC group at the end of the experiment, and the latter treatment reversed hepatic steatosis. Increased PPAR-α immunostaining in parallel with higher GLUT-2 and reduced SREBP-1 expression may explain the favourable hepatic outcomes. Restoration of adipocyte size was consistent with higher adiponectin levels and lower TNF-α (tumour necrosis factor-α) levels (P<0.0001) in the drug-treated groups. In conclusion, all of the drug treatments were effective in controlling the metabolic syndrome. The best results were achieved using telmisartan and sitagliptin as monotherapies or as a dual treatment, combining partial PPAR-γ agonism and PPAR-α activation in the liver with extended incretin action.\u003C\u002Fjats:p>",{"EN":3797},"Comparative effects of telmisartan, sitagliptin and metformin alone or in combination on obesity, insulin resistance, and liver and pancreas remodelling in C57BL\u002F6 mice fed on a very high-fat diet",{"VOID":3799},"20415664",{"VOID":3801},"10.1042\u002Fcs20100061",[114],"https:\u002F\u002Fportlandpress.com\u002Fclinsci\u002Farticle\u002F119\u002F6\u002F239\u002F68767\u002FComparative-effects-of-telmisartan-sitagliptin-and",[3805,3826,3841,3858,3875,3892],{"id":3806,"sortIndex":119,"researcher":24,"roles":3807,"affiliations":3808,"properties":3819},"6b6d3b36-5b03-4d54-8ccc-098a7c545842",[],[3809],{"id":3810,"sortIndex":25,"affiliation":3811,"properties":24},"12c523a5-1f28-415f-8fcf-43ed95e3f868",{"id":3812,"createTime":3813,"updateTime":3813,"relativeEntities":3814,"slug":3815,"properties":3816,"entityType":45,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},"ca2fa996-964a-4134-8cec-8ab30aa1660b","2024-12-05T21:36:18.267+00:00",[],"Laboratory-of-Morphometry-Biomedical-Center-Institute-of-Biology-State-University-of-Rio-de-Janeiro-20551-030-Rio-de-Janeiro-RJ-Brazil",{"title":3817},{"EN":3818},"Laboratory of Morphometry, Biomedical Center, Institute of Biology, State University of Rio de Janeiro, 20551-030 Rio de Janeiro, RJ, Brazil",{"openalex":3820,"orcid":3822,"title":3824},{"VOID":3821},"A5056682088",{"VOID":3823},"https:\u002F\u002Forcid.org\u002F0000-0001-8138-7734",{"EN":3825},"Bianca Martins Gregório",{"id":3827,"sortIndex":140,"researcher":24,"roles":3828,"affiliations":3829,"properties":3836},"79381270-babb-4431-8579-04f49ad6e2d9",[],[3830],{"id":3831,"sortIndex":25,"affiliation":3832,"properties":24},"f9a2190b-abbd-407a-bf62-674cdd3f8217",{"id":3812,"createTime":3813,"updateTime":3813,"relativeEntities":3833,"slug":3815,"properties":3834,"entityType":45,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},[],{"title":3835},{"EN":3818},{"openalex":3837,"title":3839},{"VOID":3838},"A5098038533",{"EN":3840},"Fernando S. 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2006, Abdominal obesity and metabolic syndrome, Nature, 444, 881, 10.1038\u002Fnature05488",{"doi":3951},"10.1038\u002Fnature05488",{"id":24,"text":3953,"url":24,"identifiers":3954},"Marchesini, 2001, Nonalcoholic fatty liver disease: a feature of the metabolic syndrome, Diabetes, 50, 1844, 10.2337\u002Fdiabetes.50.8.1844",{"doi":3955},"10.2337\u002Fdiabetes.50.8.1844",{"id":24,"text":3957,"url":24,"identifiers":3958},"Pitt, 2007, Hepato-pancreato-biliary fat: the good, the bad and the ugly, HPB, 9, 92, 10.1080\u002F13651820701286177",{"doi":3959},"10.1080\u002F13651820701286177",{"id":24,"text":3961,"url":24,"identifiers":3962},"Duvnjak, 2007, Pathogenesis and management issues for non-alcoholic fatty liver disease, World J. 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Cienc., 75, 469, 10.1590\u002FS0001-37652003000400006",{"doi":4007},"10.1590\u002FS0001-37652003000400006",{"id":24,"text":4009,"url":24,"identifiers":4010},"Araki, 2006, Telmisartan prevents obesity and increases the expression of uncoupling protein 1 in diet-induced obese mice, Hypertension, 48, 51, 10.1161\u002F01.HYP.0000225402.69580.1d",{"doi":4011},"10.1161\u002F01.HYP.0000225402.69580.1d",{"id":24,"text":4013,"url":24,"identifiers":4014},"Cohen, 2004, Effects of insulin-sensitising agents in mice with hepatic insulin resistance, Diabetologia, 47, 407, 10.1007\u002Fs00125-003-1320-4",{"doi":4015},"10.1007\u002Fs00125-003-1320-4",{"id":24,"text":4017,"url":24,"identifiers":4018},"Lamont, 2008, Differential antidiabetic efficacy of incretin agonists versus DPP-4 inhibition in high fat fed mice, Diabetes, 57, 190, 10.2337\u002Fdb07-1202",{"doi":4019},"10.2337\u002Fdb07-1202",{"id":24,"text":4021,"url":24,"identifiers":4022},"Benson, 2004, Identification of telmisartan as a unique angiotensin II receptor antagonist with selective PPARγ-modulating activity, Hypertension, 43, 993, 10.1161\u002F01.HYP.0000123072.34629.57",{"doi":4023},"10.1161\u002F01.HYP.0000123072.34629.57",{"id":24,"text":4025,"url":24,"identifiers":4026},"Zanchi, 2007, Telmisartan prevents the glitazone-induced weight gain without interfering with its insulin-sensitizing properties, Am. 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