SYNBIOTIC (Inulin, Lactobacillus, Bifidobacterium and Saccharomyces boulardii) IMPROVES FATTY LIVER DISEASE BY VIRTUE OF ITS ACTION ON LIPID PROFILES, LEPTIN, ADIPONECTIN, AND INFLAMMATORY BIOMARKERS  

Author(s):  
Nazarii Kobyliak
Lipids ◽  
2020 ◽  
Vol 55 (3) ◽  
pp. 271-278
Author(s):  
Christian Lüchtenborg ◽  
Birgit Niederhaus ◽  
Britta Brügger ◽  
Branko Popovic ◽  
Gert Fricker

2018 ◽  
Author(s):  
Patrick J. Connell ◽  
Ian N. Bratz ◽  
Spencer R. Andrei ◽  
Luke Eusebio ◽  
Daniel J. DelloStritto ◽  
...  

AbstractObjectivesTRPV1 channels have been linked to the development and progression of diabetes at multiple levels, including control of appetite and weight, regulation of pancreatic function, thermogenesis, metabolism and energy homeostasis. Despite this, little information is known regarding its role in liver homeostasis and nonalcoholic fatty liver disease (NAFLD).Methods and ResultsTo better understand the role of TRPV1 in liver metabolism, we explored the effects of a high fat/sugar diet (Western, 24-week regimen) in male and female wild type (WT) and TRPV1-null (V1KO) mice. Our data reveal that loss of the TRPV1 gene makes mice susceptible to diet-induced obesity and induces NAFLD. V1KO mice displayed gross phenotypic and gross morphological changes including insulin resistance, glucose intolerance, increased body mass and central adiposity on a western diet compared to WT counterparts. Western fed V1KO mice exhibited gross changes in liver morphology and size compared to western fed WT mice, which were supported with histological H&E and Oil Red O staining. Accompanying the liver changes, Western fed V1KO mice exhibited altered lipid profiles as demonstrated by elevated hepatic triglyceride, cholesterol and free fatty acid levels compared to western fed WT mice. Interestingly, female V1KO mice fed a western diet displayed significant protection against diet-induced obesity and the progression of NAFLD compared to their male counterparts. Taken together, these data suggest that loss of TRPV1 promotes fat accumulation, NAFLD development and changes in liver lipid profiles in male mice, the extent to which is less severe in female V1KO mice.ConclusionIn conclusion, TRPV1 may be a protective therapeutic target for the prevention of NAFLD development in diet-induced obesity.


2021 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Masumeh Norouzpour ◽  
Sayed Mohammad Marandi ◽  
Mohsen Ghanbarzadeh ◽  
Abbasali Zare Maivan

Background: Research evidence shows that non-alcoholic fatty liver disease (NAFLD) is closely related to inflammation. Objectives: This study aimed to evaluate the response of inflammatory biomarkers to 10 weeks of aerobic resistance exercise in inactive postmenopausal women with NAFLD. Methods: In this purposeful quasi-experimental study, conducted in Mahshahr, Iran, in 2019, 24 inactive women aged 50 - 68 years who were diagnosed with fatty liver disease by ultrasound were randomly divided into training or control groups. The training group performed aerobic resistance training for 10 weeks using treadmills and bodybuilding machines. At the beginning and end of the study, serum interleukin 18 (IL18), interleukin 10 (IL10), and other blood parameters were measured, and the subjects underwent liver ultrasound and anthropometric evaluations. Results: The results of intergroup ANCOVA, intragroup paired t-test, and Wilcoxon showed that in response to 10 weeks of training, IL18 levels, anthropometric parameters, insulin resistance (HOMA-IR), liver enzymes, fasting glucose, triglyceride (TG), and liver fat were significantly decreased and plasma IL10 was significantly increased when compared to baseline results (P < 0.05). Also, the results of the Spearman correlation test showed a significant positive relationship between IL18 and waist circumference (WC), alanine aminotransferase (ALT), and HOMA-IR and a significant negative relationship between IL10 and weight, WC, TG, HOMA-IR, and liver fat (P < 0.05). Conclusions: Ten weeks of aerobic resistance training has a significant effect on reducing serum IL18 and increasing IL10 levels in postmenopausal women with fatty liver and can be effective in improving NAFLD by losing weight, improving body composition, and reducing insulin resistance.


Open Medicine ◽  
2018 ◽  
Vol 13 (1) ◽  
pp. 208-213 ◽  
Author(s):  
En Yu ◽  
Hsin-Yin Hsu ◽  
Chun-Yuan Huang ◽  
Lee-Ching Hwang

AbstractBackgroundNon-alcoholic fatty liver disease is an increasing health issue that associates with the development of atherosclerotic cardiovascular disease. This study correlates the association between fatty liver and inflammatory biomarkers with cardiovascular risk scores.MethodologyThis cross-sectional study enrolled 10,181 health examination participants from Northern Taiwan and administered a standardized questionnaire with important biochemical tests and abdominal sonography. To assess concentrations of inflammatory markers high sensitivity C-reactive protein (hs-CRP) and fibrinogen were used.ResultsInflammatory marker levels were significantly increased with increasing fatty liver. In multivariate logistic regression analysis adjusted for major confounding factors, the odds ratios of elevated hs-CRP and fibrinogen were significantly higher in participants with mild or moderate-to-severe fatty liver compared to healthy individuals. The cardiovascular risk scores, above cut-off level 10%, were associated with higher levels of inflammatory biomarkers and fatty liver; odds ratio, 3.52 (2.60-4.77) for non-alcoholic fatty liver disease with hs-CRP, and 2.92 (2.12-4.00) for non-alcoholic fatty liver disease with fibrinogen.ConclusionInflammatory biomarkers (hs-CRP and fibrinogen) are significantly associated with augmentation of fatty liver. Non-alcoholic fatty liver disease may be a predictor of future atherosclerotic cardiovascular disease, and the prediction value increases on adding inflammatory biomarkers levels.


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