Nutrition: a promising route for prevention and management of obesity-related nonalcoholic fatty liver disease

Tarantino, Giovanni

doi:10.1515/hmbci-2014-0034

Cited by 4 publications

(4 citation statements)

References 15 publications

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“…Although fatty liver was proven to be induced efficiently by feeding experimental animals with high fat diet, we applied here a somewhat novel and attractive model based on deficiency of the essential components methionine and choline in diet, which was also applied by other authors (Ding et al, 2015;Jha et al, 2014). This model is also relevant to human NAFLD as it was proven recently that a complex interplay among methionine, choline, and other factors is essential for proper lipid metabolism in the liver, and that deficiency of methionine or choline in human diet is a leading factor to fatty liver progression (Tarantino, 2014;Veena et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Protective effect of ursodeoxycholic acid, resveratrol, andN-acetylcysteine on nonalcoholic fatty liver disease in rats

Ali

Messiha

Abdellatif

2015

Pharmaceutical Biology

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(2016) Protective effect of ursodeoxycholic acid, resveratrol, and Nacetylcysteine on nonalcoholic fatty liver disease in rats, Pharmaceutical Biology, 54:7, 1198-1208, DOI: 10.3109/13880209.2015 -a), glucose, albumin, renal functions (urea, creatinine), lipid profile (total cholesterol; TC, triglycerides, high density lipoproteins, low density lipoproteins; LDL-C, very low density lipoproteins, leptin), and oxidative stress markers (hepatic malondialdehyde; MDA, glutathione; GSH, glutathione-S-transferase; GST) were measured using automatic analyzer, colorimetric kits, and ELISA kits, supported by a liver histopathological study.Results: RSV and NAC administration significantly improved liver index (RSV only), alanine transaminase (52, 52%), TNF-a (70, 70%), glucose (69, 80%), albumin (122, 114%), MDA (55, 63%), GSH (160, 152%), GST (84, 84%), TC (86, 86%), LDL-C (83, 81%), and leptin (59, 70%) levels compared with steatosis control values. A combination of RSV or NAC with UDCA seems to ameliorate their effects. Discussion and conclusion: RSV and NAC are effective on NAFLD through antioxidant, antiinflammatory, and lipid-lowering potentials, where as RSV seems better than UDCA or NAC.

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Section: Discussionmentioning

confidence: 99%

Protective effect of ursodeoxycholic acid, resveratrol, andN-acetylcysteine on nonalcoholic fatty liver disease in rats

Ali

Messiha

Abdellatif

2015

Pharmaceutical Biology

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“…The liver is an organ deeply implicated in insulin resistance [6]. Indeed, ectopic lipid accumulation in liver and peripheral tissues due to obesity results in insulin resistance, a key risk factor for developing T2DM [7,8]. In humans, higher concentrations of free fatty acids in plasma induce insulin desensitization [9].…”

Section: Introductionmentioning

confidence: 99%

Sulforaphane Prevents Hepatic Insulin Resistance by Blocking Serine Palmitoyltransferase 3-Mediated Ceramide Biosynthesis

Teng

et al. 2019

Nutrients

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Sulforaphane (SFA), a naturally active isothiocyanate compound from cruciferous vegetables used in clinical trials for cancer treatment, was found to possess potency to alleviate insulin resistance. But its underlying molecular mechanisms are still incompletely understood. In this study, we assessed whether SFA could improve insulin sensitivity and glucose homeostasis both in vitro and in vivo by regulating ceramide production. The effects of SFA on glucose metabolism and expression levels of key proteins in the hepatic insulin signaling pathway were evaluated in insulin-resistant human hepatic carcinoma HepG2 cells. The results showed that SFA dose-dependently increased glucose uptake and intracellular glycogen content by regulating the insulin receptor substrate 1 (IRS-1)/protein kinase B (Akt) signaling pathway in insulin-resistant HepG2 cells. SFA also reduced ceramide contents and downregulated transcription of ceramide-related genes. In addition, knockdown of serine palmitoyltransferase 3 (SPTLC3) in HepG2 cells prevented ceramide accumulation and alleviated insulin resistance. Moreover, SFA treatment improved glucose tolerance and insulin sensitivity, inhibited SPTLC3 expression and hepatic ceramide production and reduced hepatic triglyceride content in vivo. We conclude that SFA recovers glucose homeostasis and improves insulin sensitivity by blocking ceramide biosynthesis through modulating SPTLC3, indicating that SFA may be a potential candidate for prevention and amelioration of hepatic insulin resistance via a ceramide-dependent mechanism.

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“…7 The available evidence suggests an inverse relationship between the lipid liver content and insulin sensitivity. 8,9 Indeed, ectopic lipid accumulation in the liver is associated with IR, and therefore the increase in the fat content in obesity is a risk factor for developing T2D. 9,10 Interestingly, free fatty acids may exert different effects on insulin signaling depending on the degree of saturation.…”

Section: Introductionmentioning

confidence: 99%

“…8,9 Indeed, ectopic lipid accumulation in the liver is associated with IR, and therefore the increase in the fat content in obesity is a risk factor for developing T2D. 9,10 Interestingly, free fatty acids may exert different effects on insulin signaling depending on the degree of saturation. 7 The clinical trials on the effects of n-3 PUFA on glucose metabolism are controversial, tending to point to no effect.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of fish oil on pre-diabetes: a lipidomic analysis of liver ceramides in rats

et al. 2016

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A high intake of fat and sucrose can dramatically increase bioactive lipids such as ceramides in tissues. Ceramides regulate several steps in the insulin signal pathway. The effects of n-3 PUFA on insulin resistance are inconsistent, especially in liver. We investigated the effect of n-3 PUFA (EPA/DHA 1 : 1) from fish oil on hepatic ceramides in a pre-diabetic animal model. Three groups of rats were fed standard feed, high fat high sucrose feed (HFHS) or HFHS enriched with n-3 PUFA. We investigated by lipidomic analysis how supplementation of a HFHS diet with n-3 PUFA modifies the hepatic ceramide profile triggered by a HFHS diet. Our results show that n-3 PUFA modified the ceramide profile of the liver and reduced their total content in pre-diabetic rats. Significant linear correlations were observed between ceramides and biochemical insulin parameters. Long chain ceramide 18:1/18:0 showed a positive correlation with the HOMA index. Very long chain ceramide 18:1/24:0 showed a negative correlation with insulin and the HOMA index. Finally, very long chain ceramide 18:1/20:0 correlated negatively with glucose levels, plasmatic insulin levels and the HOMA index. In conclusion, the modulation of the ceramide profile in pre-diabetic rats may explain the protective action of n-3 PUFA against liver insulin resistance (IR) caused by an HFHS diet. We confirm the protective role of very long chain ceramide 18:1/24:0 and the harmful role of long chain ceramide 18:1/18:0 in the pre-diabetic state and propose ceramide 18:1/20:0 as a biomarker of early liver IR in rats.

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Nutrition: a promising route for prevention and management of obesity-related nonalcoholic fatty liver disease

Cited by 4 publications

References 15 publications

Protective effect of ursodeoxycholic acid, resveratrol, andN-acetylcysteine on nonalcoholic fatty liver disease in rats

Protective effect of ursodeoxycholic acid, resveratrol, andN-acetylcysteine on nonalcoholic fatty liver disease in rats

Sulforaphane Prevents Hepatic Insulin Resistance by Blocking Serine Palmitoyltransferase 3-Mediated Ceramide Biosynthesis

Protective effects of fish oil on pre-diabetes: a lipidomic analysis of liver ceramides in rats

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