scholarly journals Hepatic Unsaturated Fatty Acids Are Linked to Lower Degree of Fibrosis in Non-alcoholic Fatty Liver Disease

2022 ◽  
Vol 8 ◽  
Author(s):  
Michael Fridén ◽  
Fredrik Rosqvist ◽  
Håkan Ahlström ◽  
Heiko G. Niessen ◽  
Christian Schultheis ◽  
...  

Background: The hepatic lipidome of patients with early stages of non-alcoholic fatty liver disease (NAFLD) has been fairly well-explored. However, studies on more progressive forms of NAFLD, i.e., liver fibrosis, are limited.Materials and methods: Liver fatty acids were determined in cholesteryl esters (CE), phospholipids (PL), and triacylglycerols (TAG) by gas chromatography. Cross-sectional associations between fatty acids and biopsy-proven NAFLD fibrosis (n = 60) were assessed using multivariable logistic regression models. Stages of fibrosis were dichotomized into none-mild (F0–1) or significant fibrosis (F2–4). Models were adjusted for body-mass index (BMI), age and patatin-like phospholipase domain-containing protein 3 (PNPLA3 rs738409) (I148M) genotype. A secondary analysis examined whether associations from the primary analysis could be confirmed in the corresponding plasma lipid fractions.Results: PL behenic acid (22:0) was directly associated [OR (95% CI): 1.86 (1.00, 3.45)] whereas PL docosahexaenoic acid (22:6n-3) [OR (95% CI): 0.45 (0.23, 0.89)], TAG oleic acid (18:1n-9) [OR (95% CI): 0.52 (0.28, 0.95)] and 18:1n-9 and vaccenic acid (18:1n-7) (18:1) [OR (95% CI): 0.52 (0.28, 0.96)] were inversely associated with liver fibrosis. In plasma, TAG 18:1n-9 [OR (95% CI): 0.55 (0.31, 0.99)], TAG 18:1 [OR (95% CI): 0.54 (0.30, 0.97)] and PL 22:0 [OR (95% CI): 0.46 (0.25, 0.86)] were inversely associated with liver fibrosis.Conclusion: Higher TAG 18:1n-9 levels were linked to lower fibrosis in both liver and plasma, possibly reflecting an altered fatty acid metabolism. Whether PL 22:6n-3 has a protective role, together with a potentially adverse effect of hepatic 22:0, on liver fibrosis warrants large-scale studies.

Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3372
Author(s):  
Kátia Cansanção ◽  
Marta Citelli ◽  
Nathalie Carvalho Leite ◽  
María-Carmen López de las Hazas ◽  
Alberto Dávalos ◽  
...  

Non-alcoholic fatty liver disease (NAFLD) is a chronic disease affecting up to 25% of the population worldwide. n-3 long-chain polyunsaturated fatty acids (n-3 PUFA) have been associated with improved clinical parameters of NAFLD. Our purpose was to conduct a pilot study to evaluate the effects of n-3 PUFA supplementation in a randomized, double-blind, placebo-controlled clinical study performed on NAFLD individuals diagnosed by ultrasound. Patients received n-3 PUFA (n = 13) or placebo (n = 11) supplementation for six months. Circulating miR-122 expression (determined by quantitative real time-polymerase chain reaction (qRT-PCR), liver fibrosis (FibroScan®), red blood cells (RBC) fatty acids (gas chromatography), and biochemical tests were performed at baseline and after intervention. After the intervention, in the n-3 PUFA group, docosahexaenoic acid (DHA) and omega index increased significantly in RBC (p = 0.022 and p = 0.012, respectively), in addition to a significant reduction in alkaline phosphatase (ALP) (p = 0.002) and liver fibrosis (p = 0.039). However, there was no change in the expression of circulating miR-122 in both groups. Our results showed that omega-3 PUFA were incorporated in erythrocytes after six months of fish oil supplementary intake, and that n-3 PUFA were effective in reducing ALP and liver fibrosis without altering the expression of circulating miR-122 in individuals with NAFLD.


2010 ◽  
Vol 75 (2) ◽  
pp. e102-e107 ◽  
Author(s):  
J.R. van Werven ◽  
T.C.M.A. Schreuder ◽  
A.J. Nederveen ◽  
C. Lavini ◽  
P.L.M. Jansen ◽  
...  

Choonpa Igaku ◽  
2020 ◽  
Vol 47 (6) ◽  
pp. 241-248
Author(s):  
Hirohito TAKEUCHI ◽  
Katsutoshi SUGIMOTO ◽  
Hisashi OSHIRO ◽  
Kunio IWATSUKA ◽  
Shin KONO ◽  
...  

2018 ◽  
Vol 49 (3) ◽  
pp. 296-303 ◽  
Author(s):  
Kenichi Tanaka ◽  
Hirokazu Takahashi ◽  
Hideyuki Hyogo ◽  
Masafumi Ono ◽  
Noriko Oza ◽  
...  

2021 ◽  
Vol 15 (7) ◽  
pp. 1936-1939
Author(s):  
Shahla Mohammed Saeed Rasul ◽  
Ali Khalaf Salim ◽  
Hiwa Abubakr Hussein

Background: Nowadays, generating shear waves and simulation of the liver tissue is done using point shear-wave elastographic (pSWE) techniques which uess acoustic radiation force impulse (ARFI). Objective: This study aimed to evaluate the correlation between pSWE and liver function tests (LFTs) to predict liver fibrosis in patients with non-alcoholic fatty liver disease (NAFLD). Materials and methods: It was a cross sectional study conducted in an Ultrasound Clinic in Suleymaniya city. The duration of the study was from 1st of November, 2018 to 30th of June, 2019 which conducted on 50 NAFLD patients. After confirming NAFLD diagnosis, the patients were referred to Ultrasound Clinic to go under pSWE test. Results: The data showed that the mean PSWE of NAFLD patient was 4.12±0.87 Kpa; and 18% of them had high PSWE (> 4.6). Elastography fibrosis score was distributed to F0 (82%), F1 (6%), F2 (8%) and F3 (4%). There was a significant association between high APRI and high Aspartate Aminotransferase/Alanine Aminotransferase(AST/ALT) ratio (p=0.04). There was also a highly significant association between elastography fibrosis score and APRI fibrosis score among NAFLD patients (p<0.001). Conclusion: This study showed that the pSWE is a valuable noninvasive diagnostic technique for predicting liver fibrosis among NAFLD patients and there is significant correlation between APRI and pSWE scores. Keywords: Non-alcoholic fatty liver disease, Point shears wave elastography, Liver fibrosis.


2018 ◽  
Vol 68 ◽  
pp. S838
Author(s):  
A. Dalbeni ◽  
A. Mantovani ◽  
A. Tagetti ◽  
S. Bonafini ◽  
V. Paon ◽  
...  

2020 ◽  
Vol 21 (9) ◽  
pp. 3308 ◽  
Author(s):  
Carla Cremonese ◽  
Robert Schierwagen ◽  
Frank Erhard Uschner ◽  
Sandra Torres ◽  
Olaf Tyc ◽  
...  

Non-alcoholic fatty liver disease (NAFLD) is gaining in importance and is linked to obesity. Especially, the development of fibrosis and portal hypertension in NAFLD patients requires treatment. Transgenic TGR(mREN2)27 rats overexpressing mouse renin spontaneously develop NAFLD with portal hypertension but without obesity. This study investigated the additional role of obesity in this model on the development of portal hypertension and fibrosis. Obesity was induced in twelve-week old TGR(mREN2)27 rats after receiving Western diet (WD) for two or four weeks. Liver fibrosis was assessed using standard techniques. Hepatic expression of transforming growth factor-β1 (TGF-β1), collagen type Iα1, α-smooth muscle actin, and the macrophage markers Emr1, as well as the chemoattractant Ccl2, interleukin-1β (IL1β) and tumor necrosis factor-α (TNFα) were analyzed. Assessment of portal and systemic hemodynamics was performed using the colored microsphere technique. As expected, WD induced obesity and liver fibrosis as confirmed by Sirius Red and Oil Red O staining. The expression of the monocyte-macrophage markers, Emr1, Ccl2, IL1β and TNFα were increased during feeding of WD, indicating infiltration of macrophages into the liver, even though this increase was statistically not significant for the EGF module-containing mucin-like receptor (Emr1) mRNA expression levels. Of note, portal pressure increased with the duration of WD compared to animals that received a normal chow. Besides obesity, WD feeding increased systemic vascular resistance reflecting systemic endothelial and splanchnic vascular dysfunction. We conclude that transgenic TGR(mREN2)27 rats are a suitable model to investigate NAFLD development with liver fibrosis and portal hypertension. Tendency towards elevated expression of Emr1 is associated with macrophage activity point to a significant role of macrophages in NAFLD pathogenesis, probably due to a shift of the renin–angiotensin system towards a higher activation of the classical pathway. The hepatic injury induced by WD in TGR(mREN2)27 rats is suitable to evaluate different stages of fibrosis and portal hypertension in NAFLD with obesity.


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