2007
DOI: 10.1038/sj.jhh.1002148
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Hypertension and fatty liver: guilty by association?

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Cited by 44 publications
(56 citation statements)
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“…ICV administration of TUDCA over 3 days lowered arterial pressure and heart rate in DIO mice, a response that was evident within 24-48 hours, with blood pressure and heart rate in ICV TUDCA-treated DIO mice returning to normal chow levels within 72 hours ( Figure 2, H and I). Thus, brain ER stress contributes to obesity-induced hypertension, an abnormality that commonly occurs in concert with NAFLD (27,28).…”
Section: Resultsmentioning
confidence: 99%
See 1 more Smart Citation
“…ICV administration of TUDCA over 3 days lowered arterial pressure and heart rate in DIO mice, a response that was evident within 24-48 hours, with blood pressure and heart rate in ICV TUDCA-treated DIO mice returning to normal chow levels within 72 hours ( Figure 2, H and I). Thus, brain ER stress contributes to obesity-induced hypertension, an abnormality that commonly occurs in concert with NAFLD (27,28).…”
Section: Resultsmentioning
confidence: 99%
“…In addition to contributing to NAFLD, obesity is also associated with an increased risk for the development of cardiovascular diseases, including hypertension (27,28). Emerging evidence also indicates that nonobese hypertensive patients are prone to the development of NAFLD (46).…”
Section: Discussionmentioning
confidence: 99%
“…11,[17][18][19] Risk factors for macrovesicular steatosis include alcoholism, diabetes mellitus, hypertension, obesity, various drugs (such as amiodarone and methotrexate), cellular toxins, malnutrition, and anoxia. [20][21][22][23][24] The posttransplant effects of steatosis are not completely understood but are thought to be associated with greater susceptibility to ischemia. 25 Buildup of fat deposits in the hepatocytes results in an increased cell volume, which may cause sinusoidal obstruction and is more frequently found in the elderly.…”
Section: Macrovesicular Steatosismentioning
confidence: 99%
“…Teori "multiple hit" merupakan teori yang paling banyak diterima untuk menjelaskan patogenesis perlemakan hati nonalkoholik dan progresivitasnya dari simple steatosis menjadi non-alcoholic steatohepatitis (NASH). 2,11,12 Peningkatan aktivitas sistem renin, angiotensin, dan juga aldosteron pada hipertensi yang menginduksi resistensi insulin dianggap memiliki peranan penting dalam perkembangan perlemakan hati nonalkoholik. 2,13 USG merupakan pemeriksaan tidak invasif, tanpa radiasi dengan ketersediaan yang luas dan biaya terjangkau serta memiliki sensitivitas dan spesifisitas yang cukup tinggi dalam mendiagnosis perlemakan hati nonalkoholik.…”
Section: Pendahuluanunclassified