Ovulation mitigates fatty liver associated with reproductive suppression and oxidative stress in Damaraland mole-rats (Fukomys damarensis)

2020 ◽  
Vol 32 (10) ◽  
pp. 923
Author(s):  
Christina M. Schmidt ◽  
Sandra Arbi ◽  
Nigel C. Bennett
Keyword(s):  
Oxidative Damage ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Lipid Droplets ◽  
Reproductive Suppression ◽  
Alcoholic Fatty Liver ◽  
Reproductive Females ◽  
Inflammatory Infiltrates ◽  
And Oxidative Stress ◽  
Alcoholic Fatty Liver Disease

Oxidative damage is often linked to reproduction; however, reproducing female Damaraland mole-rats (Fukomys damarensis) exhibit a reduction in oxidative damage relative to their non-reproductive, anovulatory, cohorts. Specifically, liver concentrations of malondialdehyde, a biomarker for lipid peroxidation, are significantly lower in reproducing females. We examined liver histology in reproductive, anovulatory and recently ovulating non-reproductive females, demonstrating an accumulation of lipid droplets only in the livers of anovulatory females and no fibrosis, cell death or inflammatory infiltrates in any group. Our observations suggest that anovulatory females experience a form of non-alcoholic fatty liver disease, which is reversed once they commence ovulation. We propose hormonal interactions that may underlie our observations.

scholarly journals Addressing the liver progenitor cell response and hepatic oxidative stress in experimental non-alcoholic fatty liver disease/non-alcoholic steatohepatitis using amniotic epithelial cells

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Mihiri Goonetilleke ◽  
Nathan Kuk ◽  
Jeanne Correia ◽  
Alex Hodge ◽  
Gregory Moore ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Epithelial Cells ◽  
Fatty Liver ◽  
Progenitor Cells ◽  
Fatty Liver Disease ◽  
Hepatic Inflammation ◽  
Alcoholic Fatty Liver ◽  
And Oxidative Stress ◽  
Alcoholic Fatty Liver Disease

Abstract Background Non-alcoholic fatty liver disease is the most common liver disease globally and in its inflammatory form, non-alcoholic steatohepatitis (NASH), can progress to cirrhosis and hepatocellular carcinoma (HCC). Currently, patient education and lifestyle changes are the major tools to prevent the continued progression of NASH. Emerging therapies in NASH target known pathological processes involved in the progression of the disease including inflammation, fibrosis, oxidative stress and hepatocyte apoptosis. Human amniotic epithelial cells (hAECs) were previously shown to be beneficial in experimental models of chronic liver injury, reducing hepatic inflammation and fibrosis. Previous studies have shown that liver progenitor cells (LPCs) response plays a significant role in the development of fibrosis and HCC in mouse models of fatty liver disease. In this study, we examined the effect hAECs have on the LPC response and hepatic oxidative stress in an experimental model of NASH. Methods Experimental NASH was induced in C57BL/6 J male mice using a high-fat, high fructose diet for 42 weeks. Mice received either a single intraperitoneal injection of 2 × 106 hAECs at week 34 or an additional hAEC dose at week 38. Changes to the LPC response and oxidative stress regulators were measured. Results hAEC administration significantly reduced the expansion of LPCs and their mitogens, IL-6, IFNγ and TWEAK. hAEC administration also reduced neutrophil infiltration and myeloperoxidase production with a concurrent increase in heme oxygenase-1 production. These observations were accompanied by a significant increase in total levels of anti-fibrotic IFNβ in mice treated with a single dose of hAECs, which appeared to be independent of c-GAS-STING activation. Conclusions Expansion of liver progenitor cells, hepatic inflammation and oxidative stress associated with experimental NASH were attenuated by hAEC administration. Given that repeated doses did not significantly increase efficacy, future studies assessing the impact of dose escalation and/or timing of dose may provide insights into clinical translation.

scholarly journals The Bisphenol A Induced Oxidative Stress in Non-Alcoholic Fatty Liver Disease Male Patients: A Clinical Strategy to Antagonize the Progression of the Disease

2020 ◽  
Vol 17 (10) ◽  
pp. 3369 ◽  
Author(s):  
Alessandro Federico ◽  
Marcello Dallio ◽  
Antonietta Gerarda Gravina ◽  
Nadia Diano ◽  
Sonia Errico ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Bisphenol A ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Free Form ◽  
Alcoholic Fatty Liver ◽  
Male Patients ◽  
And Oxidative Stress ◽  
Alcoholic Fatty Liver Disease

Introduction: Bisphenol A (BPA) exposure has been correlated to non-alcoholic fatty liver disease (NAFLD) development and progression. We investigated, in a clinical model, the effects of the administration of 303 mg of silybin phospholipids complex, 10 μg of vitamin D, and 15 mg of vitamin E (RealSIL, 100D, IBI-Lorenzini, Aprilia, Italy) in male NAFLD patients exposed to BPA on metabolic, hormonal, and oxidative stress-related parameters. Methods: We enrolled 32 male patients with histologic diagnosis of NAFLD and treated them with Realsil 100D twice a day for six months. We performed at baseline clinical, biochemical, and food consumption assessments as well as the evaluation of physical exercise, thiobarbituric acid reactive substances (TBARS), plasmatic and urinary BPA and estrogen levels. The results obtained were compared with those of healthy control subjects and, in the NAFLD group, between baseline and the end of treatment. Results: A direct proportionality between TBARS levels and BPA exposure was shown (p < 0.0001). The therapy determined a reduction of TBARS levels (p = 0.011), an improvement of alanine aminotransferase, aspartate aminotransferase, insulinemia, homeostatic model assessment insulin resistance, C reactive protein, tumor necrosis factor alpha (p < 0.05), an increase of conjugated BPA urine amount, and a reduction of its free form (p < 0.0001; p = 0.0002). Moreover, the therapy caused an increase of plasmatic levels of the native form of estrogens (p = 0.03). Conclusions: We highlighted the potential role of BPA in estrogen oxidation and oxidative stress in NAFLD patients. The use of Realsil 100D could contribute to fast BPA detoxification and to improve cellular antioxidant power, defending the integrity of biological estrogen-dependent pathways.

Tu1052 Insulin Resistance is Associated With Increased Apoptosis and Oxidative Stress in Non-Alcoholic Fatty Liver Disease

2012 ◽  
Vol 142 (5) ◽  
pp. S-1021 ◽  
Author(s):  
Billur Canbakan ◽  
Hakan Senturk ◽  
Murat Tuncer ◽  
Ibrahim Hatemi ◽  
Yusuf Erzin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Alcoholic Fatty Liver ◽  
And Oxidative Stress ◽  
Alcoholic Fatty Liver Disease

scholarly journals Lipid droplets associated perilipins protein insights into finding a therapeutic target approach to cure non-alcoholic fatty liver disease (NAFLD)

2022 ◽  
Vol 8 (1) ◽  
Author(s):  
Aman Sharma
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Therapeutic Target ◽  
Fatty Liver Disease ◽  
Lipid Droplets ◽  
Alcoholic Fatty Liver ◽  
The World ◽  
Associated Proteins ◽  
Pharmacological Target ◽  
Alcoholic Fatty Liver Disease

Abstract Background Non-alcoholic fatty liver disease (NAFLD) is now the most common form of chronic liver disease in the world, and it’s linked to a slew of other risk factors including diabetes, obesity, dysbiosis and inflammatory bowel disease. More than 30 years ago, a patient was diagnosed with fatty liver with excessive fat accumulation in hepatocytes, a disorder known as hepatosteatosis. There will be no promising therapeutic medicines available from 1980 to 2021 which can reverse the fatty liver to normal liver state. In this review, we highlighted on lipid droplet associated protein which play a major role in accumulation of fat in liver cells and how these cellular pathway could be a promising therapeutic approach to treat the fatty liver disease. Main body Over the last few decades, Western countries follow a high-fat diet and change their lifestyle pattern due to certain metabolic disorders prevalence rate is very high all over the world. NAFLD is a major health issue and burden globally nowadays. Researchers are trying to find out the potential therapeutic target to combat the disease. The exact pathophysiology of the disease is still unclear. In the present decades. There is no Food and Drug Administration approved drugs are available to reverse the chronic condition of the disease. Based on literature survey, lipid droplets and their associated protein like perilipins play an eminent role in body fat regulation. In this review, we explain all types of perilipins such as perilipin1-5 (PLIN1-5) and their role in the pathogenesis of fatty liver which will be helpful to find the novel pharmacological target to treat the fatty liver. Conclusion In this review, majorly focussed on how fat is get deposited into hepatocytes follow the cellular signalling involved during lipid droplet biogenesis and leads to NAFLD. However, up to date still there mechanism of action is unclear. In this review, we hypothesized that lipid droplets associated proteins like perilipins could be better pharmacological target to reverse the chronic stage of fatty liver disease and how these lipid droplets associated proteins hide a clue to maintain the normal lipid homeostasis in the human body.

scholarly journals Protection of hepatocyte mitochondrial function by blueberry juice and probiotics via SIRT1 regulation in non-alcoholic fatty liver disease

2019 ◽  
Vol 10 (3) ◽  
pp. 1540-1551 ◽  
Author(s):  
Tingting Ren ◽  
Lili Zhu ◽  
Yanyan Shen ◽  
Qiuju Mou ◽  
Tao Lin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
Mitochondrial Function ◽  
Fatty Liver Disease ◽  
Alcoholic Fatty Liver ◽  
Nonalcoholic Fatty Liver ◽  
Blueberry Juice ◽  
And Oxidative Stress ◽  
Alcoholic Fatty Liver Disease

Blueberry juice and probiotics improves mitochondrial dysfunction and oxidative stress induced by nonalcoholic fatty liver disease (NAFLD), by modulating the SIRT1 pathway.

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