Inhibitory Effect of Betanin From Hylocereus ocamponis Against Steatohepatitis in Mice Fed a High-Fat Diet

Betanin is a phytocompound whose effect in steatohepatitis has not yet been tested. Betanin was extracted from the fruits of Hylocereus ocamponis, and its effects were evaluated in a mice model for non-alcoholic fatty liver disease. Six-week-old male BALB/c mice fed with a high-fat diet received 9.6 mg of betanin per day during 40 days. Body, liver, and epididymal fat pad weights and the levels of blood serum total cholesterol, triglycerides, high-density lipoproteins, alanine aminotransferase, blood nitrogen urea, creatinine, and total antioxidant capacity were measured. Hepatosteatosis and inflammatory infiltration were categorized, and the relative cell area of hepatocytes was determined. Betanin inhibited the inflammatory infiltration of the liver ( P = 4.000 × 10−6) and the necrosis of hepatocytes ( P = 9.634 × 10−7); it also produced a predominance of microvesicular steatosis ( P = 9.634 × 10−7), decreased epididymal fat pad weight ( P = 8.250 × 10−4), and increased blood serum total cholesterol ( P = 0.011). Betanin is a promising compound for fatty liver, steatohepatitis, and chronic liver disease.

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Effects of the Perilla frutescens Britton var. acuta Kudo Ethanol Extract (PFE) on the Improvement of Metabolic Syndrome and Non-Alcoholic Fatty Liver Disease Induced by High-Fat Diet

Journal of the Korean Society of Food Science and Nutrition ◽

10.3746/jkfn.2020.49.10.1045 ◽

2020 ◽

Vol 49 (10) ◽

pp. 1045-1053

Author(s):

Ji-Young Choi ◽

Ji-Won Kim ◽

Eun-Young Kwon

Keyword(s):

Metabolic Syndrome ◽

Liver Disease ◽

Fatty Liver ◽

High Fat Diet ◽

Fatty Liver Disease ◽

Ethanol Extract ◽

Perilla Frutescens ◽

High Fat ◽

Alcoholic Fatty Liver ◽

Alcoholic Fatty Liver Disease

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Maternal tadalafil therapy for fetal growth restriction prevents non-alcoholic fatty liver disease and adipocyte hypertrophy in the offspring

Scientific Reports ◽

10.1038/s41598-020-80643-0 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Takuya Kawamura ◽

Hiroaki Tanaka ◽

Ryota Tachibana ◽

Kento Yoshikawa ◽

Shintaro Maki ◽

...

Keyword(s):

Liver Disease ◽

Fatty Liver ◽

Fetal Growth ◽

Fetal Programming ◽

High Fat Diet ◽

Fatty Liver Disease ◽

Control Group ◽

High Fat ◽

Alcoholic Fatty Liver ◽

Alcoholic Fatty Liver Disease

AbstractWe aimed to investigate the effects of maternal tadalafil therapy on fetal programming of metabolic function in a mouse model of fetal growth restriction (FGR). Pregnant C57BL6 mice were divided into the control, L-NG-nitroarginine methyl ester (L-NAME), and tadalafil + L-NAME groups. Six weeks after birth, the male pups in each group were given a high-fat diet. A glucose tolerance test (GTT) was performed at 15 weeks and the pups were euthanized at 20 weeks. We then assessed the histological changes in the liver and adipose tissue, and the adipocytokine production. We found that the non-alcoholic fatty liver disease activity score was higher in the L-NAME group than in the control group (p < 0.05). Although the M1 macrophage numbers were significantly higher in the L-NAME/high-fat diet group (p < 0.001), maternal tadalafil administration prevented this change. Moreover, the epididymal adipocyte size was significantly larger in the L-NAME group than in the control group. This was also improved by maternal tadalafil administration (p < 0.05). Further, we found that resistin levels were significantly lower in the L-NAME group compared to the control group (p < 0.05). The combination of exposure to maternal L-NAME and a high-fat diet induced glucose impairment and non-alcoholic fatty liver disease. However, maternal tadalafil administration prevented these complications. Thus, deleterious fetal programming caused by FGR might be modified by in utero intervention with tadalafil.

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