High fat diet and liver damage induced by biliary obstruction in the rat

1995 ◽  
Vol 15 (2) ◽  
pp. 125-128 ◽  
Author(s):  
Pablo Muriel
Keyword(s):  
Liver Damage ◽  
High Fat Diet ◽  
Biliary Obstruction ◽  
High Fat

scholarly journals Choline Supplementation Protects against Liver Damage by Normalizing Cholesterol Metabolism in Pemt/Ldlr Knockout Mice Fed a High-Fat Diet

2013 ◽  
Vol 144 (3) ◽  
pp. 252-257 ◽  
Author(s):  
Ala Al Rajabi ◽  
Gabriela S. F. Castro ◽  
Robin P. da Silva ◽  
Randy C. Nelson ◽  
Aducio Thiesen ◽  
...  
Keyword(s):  
Liver Damage ◽  
Knockout Mice ◽  
High Fat Diet ◽  
Cholesterol Metabolism ◽  
High Fat

scholarly journals Protein hydrolysate from potato confers hepatic-protection in hamsters against high fat diet induced apoptosis and fibrosis by suppressing Caspase-3 and MMP2/9 and by enhancing Akt-survival pathway

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Shibu Marthandam Asokan ◽  
Tsu-Han Hung ◽  
Zong-Yan Li ◽  
Wen-Dee Chiang ◽  
Wan-Teng Lin
Keyword(s):  
Liver Damage ◽  
High Fat Diet ◽  
Interstitial Fibrosis ◽  
Protein Hydrolysate ◽  
Serum Markers ◽  
Tunel Staining ◽  
High Fat ◽  
Molecular Events ◽  
Extracellular Signal ◽  
Induced Apoptosis

Abstract Background A potato protein hydrolysate, APPH is a potential anti-obesity diet ingredient. Since, obesity leads to deterioration of liver function and associated liver diseases, in this study the effect of APPH on high fat diet (HFD) associated liver damages was investigated. Methods Six week old male hamsters were randomly separated to six groups (n = 8) as control, HFD (HFD fed obese), L-APPH (HFD + 15 mg/kg/day of APPH), M-APPH (HFD + 30 mg/kg/day), H-APPH (HFD + 75 mg/kg/day of APPH) and PB (HFD + 500 mg/kg/day of probucol). HFD fed hamsters were administered with APPH 50 days through oral gavage. The animals were euthanized and the number of apoptotic nuclei in liver tissue was determined by TUNEL staining and the extent of interstitial fibrosis was determined by Masson’s trichrome staining. Modulation in the molecular events associated with apoptosis and fibrosis were elucidated from the western blotting analysis of the total protein extracts. Results Hamsters fed with high fat diet showed symptoms of liver damage as measured from serum markers like alanine aminotransferase and aspartate aminotransferase levels. However a 50 day long supplementation of APPH effectively ameliorated the effects of HFD. HFD also modulated the expression of survival and apoptosis proteins in the hamster liver. Further the HFD groups showed elevated levels of fibrosis markers in liver. The increase in fibrosis and apoptosis was correlated with the increase in the levels of phosphorylated extracellular signal-regulated kinases (pERK1/2) revealing a potential role of ERK in the HFD mediated liver damage. However APPH treatment reduced the effect of HFD on the apoptosis and fibrosis markers considerably and provided hepato-protection. Conclusion APPH can therefore be considered as an efficient therapeutic agent to ameliorate high fat diet related liver damages.

scholarly journals SRT1720 attenuates obesity and insulin resistance but not liver damage in the offspring due to maternal and postnatal high-fat diet consumption

2018 ◽  
Vol 315 (2) ◽  
pp. E196-E203 ◽  
Author(s):  
Long The Nguyen ◽  
Hui Chen ◽  
Crystal Mak ◽  
Amgad Zaky ◽  
Carol Pollock ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Liver Damage ◽  
High Fat Diet ◽  
Metabolic Disorders ◽  
Maternal Obesity ◽  
Liver Toxicity ◽  
Sirtuin 1 ◽  
High Fat ◽  
Stress Markers

Recent studies indicate that sirtuin-1 (SIRT1), an important metabolic sensor and regulator of life span, plays a mechanistic role in maternal obesity-induced programming of metabolic disorders in the offspring. In this study we investigate whether SIRT1 activation in early childhood can mitigate metabolic disorders due to maternal and postnatal high-fat feeding in mice. Male offspring born to chow-fed (MC) or high fat diet-fed dams (MHF) were weaned onto postnatal chow or high-fat diet and treated with SRT1720 (25 mg/kg ip every 2 days) or vehicle control for 6 wk and examined for metabolic disorders. MHF exacerbated offspring body weight and insulin resistance in the offspring exposed to postnatal HFD (OHF). These metabolic changes were associated with reduced hepatic lipid droplet accumulation but increased plasma levels of alanine aminotransferase (ALT), a marker of liver damage. SRT1720 significantly decreased offspring body weight, adiposity, glucose intolerance, and hyperleptinemia due to OHF and reversed hyperinsulinemia and adipocyte hypertrophy due to the additive effects of MHF. Although SRT1720 suppresses liver lipogenesis, inflammation, and oxidative stress markers, it also reduces antioxidants and increased liver collagen deposition in OHF offspring independent of MHF. Hepatic steatosis was attenuated only in MC/OHF offspring in association with elevated plasma ALT levels. The study suggests that postnatal SRT1720 administration can mitigate obesity and insulin resistance in the offspring due to maternal and postnatal HFD exposure. However, the possibility of liver toxicity needs to be further examined.

scholarly journals Alleviation of High-Fat Diet-Induced Fatty Liver Damage in Group IVA Phospholipase A2-Knockout Mice

PLoS ONE ◽  
2009 ◽  
Vol 4 (12) ◽  
pp. e8089 ◽  
Author(s):  
Hiromi Ii ◽  
Naoki Yokoyama ◽  
Shintaro Yoshida ◽  
Kae Tsutsumi ◽  
Shinji Hatakeyama ◽  
...  
Keyword(s):  
Fatty Liver ◽  
Phospholipase A2 ◽  
Liver Damage ◽  
Knockout Mice ◽  
High Fat Diet ◽  
High Fat ◽  
Group Iva

scholarly journals Phenethylamine in chlorella alleviates high-fat diet-induced mouse liver damage by regulating generation of methylglyoxal

2021 ◽  
Vol 5 (1) ◽  
Author(s):  
Yifeng Zheng ◽  
Agustin Martin-Morales ◽  
Jing Wang ◽  
Masaki Fujishima ◽  
Eri Okumura ◽  
...  
Keyword(s):  
Oral Administration ◽  
Liver Damage ◽  
High Fat Diet ◽  
Mouse Liver ◽  
Water Extract ◽  
Dihydroxyacetone Phosphate ◽  
High Fat ◽  
Hepatic Lipid Accumulation ◽  
Protein Levels ◽  
Gapdh Protein

AbstractThis study examined the effects of oral administration of water extract of chlorella (WEC) (100 mg/kg bodyweight) and phenethylamine (10 μg/kg bodyweight) on high-fat diet (HFD)-induced liver damage in mice. Phenethylamine significantly mitigated HFD-induced lipid oxidation (generation of malondialdehyde) and liver damage without markedly decreasing hepatic lipid accumulation. WEC exerted similar effects although with decreased efficacy. In addition, WEC and phenethylamine decreased the methylglyoxal levels and increased the glyceraldehyde 3-phosphate dehydrogenase (GAPDH) protein levels in the liver. Methylglyoxal is generated from substrates of GAPDH, dihydroxyacetone phosphate and glyceraldehyde 3-phosphate. These facts indicate that methylglyoxal triggers oxidation of accumulated lipid, which generates malondialdehyde and consequently induces liver damage. Suppression of generation of toxic aldehydes by WEC and phenethylamine was also confirmed by maintaining hepatic cysteine, highly reactive to aldehydes. Thus, trace amounts of phenethylamine alleviate HFD-induced liver damage by regulating methylglyoxal via increase of GAPDH.

scholarly journals Morphological evaluation of the effects of exercise on high-fat-diet-induced liver damage in rats

2020 ◽  
Vol 31 (9) ◽  
pp. 626-632
Author(s):  
Merve Acikel Elmas ◽  
◽  
Nilsu Atay ◽  
Ozlem Bingol Ozakpinar ◽  
Serap Arbak ◽  
...  
Keyword(s):  
Liver Damage ◽  
High Fat Diet ◽  
High Fat ◽  
Morphological Evaluation

scholarly journals Soybean Oil-Derived Poly-Unsaturated Fatty Acids Enhance Liver Damage in NAFLD Induced by Dietary Cholesterol

Nutrients ◽  
2018 ◽  
Vol 10 (9) ◽  
pp. 1326 ◽  
Author(s):  
Janin Henkel ◽  
Eugenia Alfine ◽  
Juliana Saín ◽  
Korinna Jöhrens ◽  
Daniela Weber ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Soybean Oil ◽  
Liver Damage ◽  
High Fat Diet ◽  
Unsaturated Fatty Acids ◽  
Saturated Fatty Acids ◽  
Dietary Cholesterol ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
The Impact

While the impact of dietary cholesterol on the progression of atherosclerosis has probably been overestimated, increasing evidence suggests that dietary cholesterol might favor the transition from blunt steatosis to non-alcoholic steatohepatitis (NASH), especially in combination with high fat diets. It is poorly understood how cholesterol alone or in combination with other dietary lipid components contributes to the development of lipotoxicity. The current study demonstrated that liver damage caused by dietary cholesterol in mice was strongly enhanced by a high fat diet containing soybean oil-derived ω6-poly-unsaturated fatty acids (ω6-PUFA), but not by a lard-based high fat diet containing mainly saturated fatty acids. In contrast to the lard-based diet the soybean oil-based diet augmented cholesterol accumulation in hepatocytes, presumably by impairing cholesterol-eliminating pathways. The soybean oil-based diet enhanced cholesterol-induced mitochondrial damage and amplified the ensuing oxidative stress, probably by peroxidation of poly-unsaturated fatty acids. This resulted in hepatocyte death, recruitment of inflammatory cells, and fibrosis, and caused a transition from steatosis to NASH, doubling the NASH activity score. Thus, the recommendation to reduce cholesterol intake, in particular in diets rich in ω6-PUFA, although not necessary to reduce the risk of atherosclerosis, might be sensible for patients suffering from non-alcoholic fatty liver disease.

scholarly journals Protective effects of various ratios of DHA/EPA supplementation on high-fat diet-induced liver damage in mice

2017 ◽  
Vol 16 (1) ◽  
Author(s):  
Tingting Shang ◽  
Liang Liu ◽  
Jia Zhou ◽  
Mingzhen Zhang ◽  
Qinling Hu ◽  
...  
Keyword(s):  
Liver Damage ◽  
High Fat Diet ◽  
Protective Effects ◽  
High Fat
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