Central energy metabolism remains robust in acute steatotic hepatocytes challenged by a high free fatty acid load

Niklas, Jens; Bonin, Anne; Mangin, Stefanie; Bucher, J.B.; Kopacz, Stephanie; Matz‐Soja, Madlen; Thiel, Carlo; Gebhardt, Rolf; Hofmann, Ute; Mauch, Klaus

doi:10.5483/bmbrep.2012.45.7.070

Cited by 15 publications

(6 citation statements)

References 28 publications

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“…64 2004). Literature data confirmed the induction of steatosis in mice (Malhi et al 2006, Niklas et al 2012), goose (Pan et al 2011) and in human (Joshi-Barve et al 2007) hepatocytes exposed to palmitic and/or oleic acids in primary cultures as well as in immortalized hepatocyte cell lines (Gómez-Lechón et al 2007, Mantzaris et al 2011, Ricchi et al 2009, Rogue et al 2014, Swagell et al 2005. The intracellular accumulation of triacylglycerols (TAG) was proportional to the final concentration of fatty acids in the culture medium (Ricchi et al 2009).…”

Section: Introductionmentioning

confidence: 83%

The Effect of Oleic and Palmitic Acid on Induction of Steatosis and Cytotoxicity on Rat Hepatocytes in Primary Culture

Moravcová

Červinková²,

Kučera³

et al. 2015

Physiol Res

126

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In vitro models serve as a tool for studies of steatosis. Palmitic and oleic acids can induce steatosis in cultured hepatocytes. The aim of our study was to verify steatogenic and cytotoxic effects of palmitic acid (PA), oleic acid (OA) and their combinations as well as their impact on functional capacity of rat primary hepatocytes. Hepatocytes were exposed to OA or PA (0.125-2 mmol/l) or their combination at ratios of 3:1, 2:1 or 1:1 at the final concentrations of 0.5-1 mmol/l. Both OA and PA caused a dose-dependent increase in triacylglycerol content in hepatocytes. PA was more steatogenic at 0.25 and 0.5 mmol/l while OA at 0.75 and 1 mmol/l. PA exhibited a dose-dependent cytotoxic effect associated with ROS production, present markers of apoptosis and necrosis and a decrease in albumin production.OA induced a damage of the cytoplasmic membrane from 1 mM concentration. Mixture of OA and PA induced lower cytotoxicity with less weakened functional capacity than did PA alone. Extent of steatosis was comparable to that after exposure to OA alone.In conclusion, OA or combination of OA with PA is more suitable for simulation of simple steatosis than PA alone.

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Section: Introductionmentioning

confidence: 83%

The Effect of Oleic and Palmitic Acid on Induction of Steatosis and Cytotoxicity on Rat Hepatocytes in Primary Culture

Moravcová

Červinková²,

Kučera³

et al. 2015

Physiol Res

126

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“…Under physiological conditions, intracellular fatty acid levels are low as a result of mitochondrial β-oxidation or esterification to triglycerides [164-166]. Oleic acid and palmitic acid are often used in in vitro to induce fat accumulation in cultured cells, with the former acting more potent than the latter [163, 167]. Common concentrations of oleic acid and palmitic acid used can range from 0.05 to 2 mM, depending on the duration of exposure [163, 168-170].…”

Section: Strategies In Nafld Researchmentioning

confidence: 99%

“…Nevertheless, they can be of value to experimental liver steatosis research. Cultures of primary C57BL/6 mouse hepatocytes simultaneously exposed to oleic acid and palmitic acid preferably take up the former and show intracellular lipid droplets [167, 207]. When mixed, more steatosis is observed compared to oleic acid and palmitic acid alone [163, 208, 209].…”

Section: Models In Nafld Researchmentioning

confidence: 99%

Strategies, models and biomarkers in experimental non-alcoholic fatty liver disease research

Willebrords¹,

Pereira

Maes³

et al. 2015

Progress in Lipid Research

148

130

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Non-alcoholic fatty liver disease encompasses a spectrum of liver diseases, including simple steatosis, steatohepatitis, liver fibrosis and cirrhosis and hepatocellular carcinoma. Non-alcoholic fatty liver disease is currently the most dominant chronic liver disease in Western countries due to the fact that hepatic steatosis is associated with insulin resistance, type 2 diabetes mellitus, obesity, metabolic syndrome and drug-induced injury. A variety of chemicals, mainly drugs, and diets is known to cause hepatic steatosis in humans and rodents. Experimental non-alcoholic fatty liver disease models rely on the application of a diet or the administration of drugs to laboratory animals or the exposure of hepatic cell lines to these drugs. More recently, genetically modified rodents or zebrafish have been introduced as non-alcoholic fatty liver disease models. Considerable interest now lies in the discovery and development of novel non-invasive biomarkers of non-alcoholic fatty liver disease, with specific focus on hepatic steatosis. Experimental diagnostic biomarkers of non-alcoholic fatty liver disease, such as (epi)genetic parameters and '-omics'-based read-outs are still in their infancy, but show great promise. In this paper, the array of tools and models for the study of liver steatosis is discussed. Furthermore, the current state-of-art regarding experimental biomarkers such as epigenetic, genetic, transcriptomic, proteomic and metabonomic biomarkers will be reviewed.

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“…Palmitic acid and monounsaturated oleic acid represents the two most abundant FFA present in high-fat diets [ 6 ]. Intake of high levels of oleic acid and palmitic acids from food sources has been shown to induce steatosis in hepatocytes of different organisms [ 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 ].…”

Section: Introductionmentioning

confidence: 99%

Tri-Herbal Medicine Divya Sarva-Kalp-Kwath (Livogrit) Regulates Fatty Acid-Induced Steatosis in Human HepG2 Cells through Inhibition of Intracellular Triglycerides and Extracellular Glycerol Levels

et al. 2020

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Steatosis is characterized by excessive triglycerides accumulation in liver cells. Recently, application of herbal formulations has gained importance in treating complex diseases. Therefore, this study explores the efficacy of tri-herbal medicine Divya Sarva-Kalp-Kwath (SKK; brand name, Livogrit) in treating free fatty acid (FFA)-induced steatosis in human liver (HepG2) cells and rat primary hepatocytes. Previously, we demonstrated that cytosafe SKK ameliorated CCl4-induced hepatotoxicity. In this study, we evaluated the role of SKK in reducing FFA-induced cell-death, and steatosis in HepG2 through analysis of cell viability, intracellular lipid and triglyceride accumulation, extracellular free glycerol levels, and mRNA expression changes. Plant metabolic components fingerprinting in SKK was performed via High Performance Thin Layer Chromatography (HPTLC). Treatment with SKK significantly reduced the loss of cell viability induced by 2 mM-FFA in a dose-dependent manner. SKK also reduced intracellular lipid, triglyceride accumulation, secreted AST levels, and increased extracellular free glycerol presence in the FFA-exposed cells. SKK normalized the FFA-stimulated overexpression of SREBP1c, FAS, C/EBPα, and CPT1A genes associated with the induction of steatosis. In addition, treatment of rat primary hepatocytes with FFA and SKK concurrently, reduced intracellular lipid accumulation. Thus, SKK showed efficacy in reducing intracellular triglyceride accumulation and increasing extracellular glycerol release, along with downregulation of related key genetic factors for FFA-associated steatosis.

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Central energy metabolism remains robust in acute steatotic hepatocytes challenged by a high free fatty acid load

Cited by 15 publications

References 28 publications

The Effect of Oleic and Palmitic Acid on Induction of Steatosis and Cytotoxicity on Rat Hepatocytes in Primary Culture

The Effect of Oleic and Palmitic Acid on Induction of Steatosis and Cytotoxicity on Rat Hepatocytes in Primary Culture

Strategies, models and biomarkers in experimental non-alcoholic fatty liver disease research

Tri-Herbal Medicine Divya Sarva-Kalp-Kwath (Livogrit) Regulates Fatty Acid-Induced Steatosis in Human HepG2 Cells through Inhibition of Intracellular Triglycerides and Extracellular Glycerol Levels

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