Nonalcoholic Fatty Liver Disease

Puri, Puneet; Sanyal, Arun J.

doi:10.1016/b978-1-4377-0881-3.00053-x

Cited by 9 publications

(15 citation statements)

References 255 publications

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“…Non-alcoholic fatty liver disease (NAFLD) is one of the most common diseases in developed countries, and (5,6). Of all of these, vitamin E antioxidant therapy and/or statins may be effective options for NAFLD treatment.…”

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confidence: 99%

Retinol Status and Expression of Retinol-Related Proteins in Methionine-Choline Deficient Rats

Miyazaki

Takitani

Koh

et al. 2014

J Nutr Sci Vitaminol

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Vitamin A (retinol) plays an important role in vision and has pleiotropic functions in immune response, hematopoiesis, fertility, cell differentiation, growth, and morphogenesis (1). Both retinol deficiency and excessive doses of retinol cause malformations in the embryos of many vertebrate species, demonstrating that retinol plays an important role in embryogenesis. Retinoic acids, derivatives of retinol, act as the ligands of retinoic acid receptors (RAR) and retinoid X receptors (RXR), which are members of the nuclear receptor superfamily and are ligand-dependent transcriptional factors (2). RAR and RXR have subtypes (a, b, and g), and 9-cis retinoic acid (an isomer of retinoic acid) binds RARs and RXRs, whereas all-trans retinoic acid binds only RARs. Both types of retinoic acid receptors transcriptionally regulate the expression of target genes and exert multiple physiological functions.Dietary retinol has 2 major forms: retinyl esters derived from animal sources and provitamin A carotenoids, mainly in the form of b-carotene, derived from plants (3,4). Dietary retinyl esters are emulsified with fatty acids and bile salts and then micellized before hydrolysis in the lumen of the small intestine for retinol uptake. In the enterocytes, retinol is rapidly re-esterified with long-chain fatty acids. b-Carotene is absorbed in intestinal mucosal cells and then cleaved for retinal formation. b-Carotene 15,15′-monooxygenase (BCMO), the key enzyme of this process, cleaves b-carotene into 2 molecules of retinal, which are then esterified to retinyl ester in the intestine (4). Retinyl esters that are incorporated into chylomicrons are secreted from enterocytes and transferred to the liver through the lymphatic circulation. Chylomicrons containing retinyl esters are taken up by the liver and transferred to hepatic stellate cells (HSCs) for storage. Retinol in the liver is esterified by the enzyme lecithin:retinol acyltransferase (LRAT) to form retinyl esters. The transfer of retinol in the liver is mediated by cellular retinol binding protein (CRBP)-I, which delivers retinol to retinol binding protein (RBP) for secretion into the circulation. Retinoic acid levels are tightly regulated at the biosynthesis and oxidation stages (3). Retinol is reversibly oxidized to retinal by retinol dehydrogenases, and retinal is irreversibly oxidized to retinoic acid by members of the retinal dehydrogenase (ALDH) family. As mentioned above, the biological actions of retinoic acid isomers (all-trans and 9-cis forms) are conducted through their role as RAR and RXR ligands. Retinoic acids are oxidized by the cytochrome P450 26 family (CYP26A1, CYP26B1, and CYP26C1), following which their metabolites are conjugated with glucuronic acid.Non-alcoholic fatty liver disease (NAFLD) is one of the most common diseases in developed countries, and Pediatrics, Osaka Rosai Hospital, 1179-3 Nagasone-cho, Kita-ku, Sakai, Osaka 591-8025, Japan (Received October 9, 2013 Summary Retinol and its derivative, retinoic acid, have pleiotropic functions includ...

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mentioning

confidence: 99%

Retinol Status and Expression of Retinol-Related Proteins in Methionine-Choline Deficient Rats

Miyazaki

Takitani

Koh

et al. 2014

J Nutr Sci Vitaminol

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“…Simple hepatic steatosis, or fatty liver, is often seen in patients with obesity, diabetes mellitus, dyslipidemia and metabolic syndrome in the developed and developing countries (reviewed in [ 1 , 2 , 3 , 4 , 5 ]). Among them, the patients who never drink alcohol, or drink less than 70 g/week for women and 140 g/week for men are defined as nonalcoholic fatty liver disease (NAFLD) if the patients do not have any drug history, negative HBV- or HCV-related markers or negative markers for autoimmune liver diseases, and fatty liver is observed by hepatic echography, CT or MRI (reviewed in [ 1 , 2 , 3 , 4 , 5 , 6 ]). NAFLD is seen in 9% to 37% of the general population, and is currently emerging in both developed and developing countries due to changing life-styles (reviewed in [ 1 , 2 , 3 , 4 , 5 , 6 ]).…”

Section: Introductionmentioning

confidence: 99%

“…Nonalcoholic hepatitis (NASH) reported by Ludwig et al in 1980 [ 7 ], has been clarified to be a severe form of NAFLD; 13% to 31% cases of NAFLD progress to NASH (reviewed in [ 4 , 5 ]). NASH is very similar to alcoholic hepatitis (ASH) in pathology (reviewed in [ 1 , 2 , 3 , 4 , 5 , 6 , 7 ]). Its prognosis is somehow better than that of ASH (reviewed in [ 1 ]), but 9% to 20% of NASH patients usually progress to liver cirrhosis (reviewed in [ 3 , 4 , 5 , 6 , 8 ]).…”

Section: Introductionmentioning

confidence: 99%

“…NAFLD include a large spectrum of chronic liver diseases from simple hepatic steatosis or fatty liver, through NASH, to cirrhosis post-NASH. As NASH progresses to cirrhosis, steatosis progressively disappears with the development of fibrosis to cirrhosis, a phenomenon known as “burn-out NASH” [ 8 ], and such cases may present as cryptogenic cirrhosis ([ 9 ], reviewed in [ 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 ]). As it is difficult to discriminate NASH among NAFLDs, scoring of histological findings by liver biopsy has been developed [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

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Fibrogenesis and Carcinogenesis in Nonalcoholic Steatohepatitis (NASH): Involvement of Matrix Metalloproteinases (MMPs) and Tissue Inhibitors of Metalloproteinase (TIMPs)

Okazaki

Noro

Tsutsui

et al. 2014

Cancers

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Nonalcoholic steatohepatitis (NASH) is emerging worldwide because life-styles have changed to include much over-eating and less physical activity. The clinical and pathophysiological features of NASH are very different from those of HBV- and HCV-chronic liver diseases. The prognosis of NASH is worse among those with nonalcoholic fatty liver diseases (NAFLD), and some NASH patients show HCC with or without cirrhosis. In the present review we discuss fibrogenesis and the relationship between fibrosis and HCC occurrence in NASH to clarify the role of MMPs and TIMPs in both mechanisms. Previously we proposed MMP and TIMP expression in the multi-step occurrence of HCC from the literature based on viral-derived HCC. We introduce again these expressions during hepatocarcinogenesis and compare them to those in NASH-derived HCC, although the relationship with hepatic stem/progenitor cells (HPCs) invasion remains unknown. Signal transduction of MMPs and TIMPs is also discussed because it is valuable for the prevention and treatment of NASH and NASH-derived HCC.

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“…Неалкогольная жировая болезнь печени (НАЖБП) характеризуется высокой распространенностью и увеличивает общую смертность у больных по сравнению с общей популяцией того же возраста и пола [2]. Интересно, что основными причинами смертности среди пациентов с НАЖБП являются сердечно-сосудистые заболевания (ССЗ) (25%) [16].…”

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Parameters of Carbohydrate Metabolism and Expression of Liver Steatosis in Patients with Nonalcoholic Fatty Liver Disease and Hypertensive Depending on Lipid Parameters

Babak¹,

Bashkirova²

2019

Ukr. ž. med. bìol. sportu

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Целью исследования стало изучение концентрации эндотелиальной липазы крови, как ведущего регулятора концентрации липопротеинов высокой плотности, в группах, распределенных по уровню липопротеинов высокой плотности, необходимых для понимания патогенетических соотношений у больных с неалкогольной жировой болезнью печени и гипертонической болезнью.Было обследовано 50 больных с неалкогольной жировой болезнью печени на фоне гипертонической болезни. Пациенты были распределены на группы с учетом показателей уровней липопротеинов высокой плотности. Все пациенты прошли общеклинические исследования, а также определение концентрации в сыворотке крови эндотелиальной липазы и определение степени стеатоза с помощью NAFLD liver fat score.Анализ липидного профиля демонстрировал достоверное (р < 0,05) отличие между всеми группами по уровню липопротеинов высокой плотности. Концентрация общего холестерина не отличалась в группах. При этом достоверно (р < 0,05) ниже уровень триглицеридов и липопротеинов низкой плотности отмечался у лиц с высоким уровнем липопротеинов высокой плотности, а уровень эндотелиальной липазы наоборот был выше в той же самой группе.Выраженность стеатоза печени по уровню трансаминаз и индексу стеатоза NAFLD liver fat score достоверно (р<0,05) больше у лиц с низким уровнем липопротеинов высокой плотности. Наиболее высокая инсулинорезистентность по индексу HOMA-IR наблюдалась у лиц с низкими уровня-ми липопротеинов высокой плотности по сравнению с теми, кто имеет протективную их концентрацию.Уровни липопротеинов низкой плотности у пациентов с неалкогольной жировой болезнью печени на фоне гипертонической болезни имеют прямую пропорциональность с концентрацией общего холестерина, индексом массы тела и абдоминальным жирораспределением и ассоциируются с повышением систолического и диастолического артериального давления.Изучение зависимостей концентрации эндотелиальной липазы с показателями липидограммы выявило положительную связь только с уровнем общего холестерина и отрицательныйс уровнем липопротеинов низкой плотности. Таким образом, концентрация эндотелиальной липазы не показала прямой связи с уровнем липопротеинов высокой плотности в плазме, что определяет ее дополнительную роль в метаболизме липопротеинов низкой плотности в условиях стеатоза печени на фоне инсулинорезистентности.Ключевые слова: неалкогольная жировая болезнь печени, гипертоническая болезнь, липиды, эндотелиальная липаза, инсулинорезистентность.Связь работы с научными программами, планами, темами. Работа выполнена на базе Национального института терапии им. Л. Т. Малой НАМН Украины в рамках научно-исследовательской работы кафедры внутренней медицины № 1 Харьковского национального медицинского КЛІНІЧНА МЕДИЦИНА

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Nonalcoholic Fatty Liver Disease

Cited by 9 publications

References 255 publications

Retinol Status and Expression of Retinol-Related Proteins in Methionine-Choline Deficient Rats

Retinol Status and Expression of Retinol-Related Proteins in Methionine-Choline Deficient Rats

Fibrogenesis and Carcinogenesis in Nonalcoholic Steatohepatitis (NASH): Involvement of Matrix Metalloproteinases (MMPs) and Tissue Inhibitors of Metalloproteinase (TIMPs)

Parameters of Carbohydrate Metabolism and Expression of Liver Steatosis in Patients with Nonalcoholic Fatty Liver Disease and Hypertensive Depending on Lipid Parameters

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