scholarly journals Chitosan Oligosaccharide Ameliorates Nonalcoholic Fatty Liver Disease (NAFLD) in Diet-Induced Obese Mice

Marine Drugs ◽  
2019 ◽  
Vol 17 (7) ◽  
pp. 391 ◽  
Author(s):  
Minyi Qian ◽  
Qianqian Lyu ◽  
Yujie Liu ◽  
Haiyang Hu ◽  
Shilei Wang ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Biological Effects ◽  
Intestinal Barrier ◽  
Integrated Analysis ◽  
Chitosan Oligosaccharide ◽  
Obese Mice ◽  
Nonalcoholic Fatty Liver

Nonalcoholic fatty liver disease (NAFLD) is a global epidemic, and there is no standard and efficient therapy for it. Chitosan oligosaccharide (COS) is widely known to have various biological effects, and in this study we aimed to evaluate the liver-protective effect in diet-induced obese mice for an enzymatically digested product of COS called COS23 which is mainly composed of dimers and trimers. An integrated analysis of the lipidome and gut microbiome were performed to assess the effects of COS23 on lipids in plasma and the liver as well as on intestinal microbiota. Our results revealed that COS23 obviously attenuated hepatic steatosis and ameliorated liver injury in diet-induced obese mice. The hepatic toxic lipids—especially triglycerides (TGs) and free fatty acids (FFAs)—were decreased dramatically after COS23 treatment. COS23 regulated lipid-related pathways, especially inhibiting the expressions of FFA-synthesis-related genes and inflammation-related genes. Furthermore, COS23 could alter lipid profiles in plasma. More importantly, COS23 also decreased the abundance of Mucispirillum and increased the abundance of Coprococcus in gut microbiota and protected the intestinal barrier by up-regulating the expression of tight-junction-related genes. In conclusion, COS23, an enzymatically digested product of COS, might serve as a promising candidate in the clinical treatment of NAFLD.

scholarly journals Impact of SchisandraChinensis Bee Pollen on Nonalcoholic Fatty Liver Disease and Gut Microbiota in HighFat Diet Induced Obese Mice

Nutrients ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 346 ◽  
Author(s):  
Ni Cheng ◽  
Sinan Chen ◽  
Xinyan Liu ◽  
Haoan Zhao ◽  
Wei Cao
Keyword(s):  
Liver Disease ◽  
Phenolic Compounds ◽  
Gut Microbiota ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Total Phenolic ◽  
Human Beings ◽  
Obese Mice ◽  
Nonalcoholic Fatty Liver

Schisandrachinensisbee pollen has been used as a health food in China for centuries; however, its bioactive constituents and functions are not very clear. In this study, we investigated the phenolic compounds of Schisandrachinensisbee pollen extract (SCPE) by UHPLC-Q-Orbitrap-HRMS/HPLC-DAD-ECD and its prevention from nonalcoholic fatty liver disease (NAFLD) and modulation of gut microbiota in high fat diet induced obese C57BL/6 mice. The results showed that 12 phenolic compounds were identified in SCPE, and naringenin, rutin and chrysin were the main constituents. The content of naringenin reached 1.89 mg/g, and total phenolic content (TPC) of SCPE were 101.83 mg GA/g. After obese mice were administrated with SCPE at 7.86 and 15.72 g/kg BW for 8 weeks, body weight gains were reduced by 18.23% and 19.37%. SCPE could decrease fasting blood glucose, cut down the lipid accumulation in serum and liver, lessen oxidative injury and inflammation in obesity mice. Moreover, SCPE could effectively inhibit the formation of NAFLD by inhibition of LXR-α, SREBP-1c and FAS genes expression, and modulate the structural alteration of gut microbiota in obesity mice. These findings suggested that SCPE could attenuate the features of the metabolism syndrome in obesity mice, which can be used to prevent obesity and NAFLD of human beings.

scholarly journals Curcumin Improved Glucose Intolerance, Renal Injury, and Nonalcoholic Fatty Liver Disease and Decreased Chromium Loss through Urine in Obese Mice

Processes ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 1132
Author(s):  
Geng-Ruei Chang ◽  
Wen-Tsong Hsieh ◽  
Lan-Szu Chou ◽  
Chen-Si Lin ◽  
Ching-Fen Wu ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Glucose Intolerance ◽  
Renal Injury ◽  
Fatty Liver Disease ◽  
Renal Damage ◽  
Control Group ◽  
Obese Mice ◽  
Nonalcoholic Fatty Liver

Obesity-associated hyperglycemia underlies insulin resistance, glucose intolerance, and related metabolic disorders including type 2 diabetes, renal damage, and nonalcoholic fatty liver disease. Turmeric root is commonly used in Asia, and curcumin, one of its pharmacological components, can play a role in preventing and treating certain chronic physiological disorders. Accordingly, this study examined how high-fat diet (HFD)-induced hyperglycemia and hyperlipidemia are reduced by curcumin through changes in fatty liver scores, chromium distribution, and renal injury in mice. Relative to the control group, also fed an HFD, the curcumin group weighed less and had smaller adipocytes; it also had lower daily food efficiency, blood urea nitrogen and creatinine levels, serum alanine aminotransferase and aspartate aminotransferase levels, serum and hepatic triglyceride levels, and hepatic lipid regulation marker expression. The curcumin-treated obese group exhibited significantly lower fasting blood glucose, was less glucose intolerant, had higher Akt phosphorylation and glucose transporter 4 (GLUT4) expression, and had greater serum insulin levels. Moreover, the group showed renal damage with lower TNF-α expression along with more numerous renal antioxidative enzymes that included superoxide dismutase, glutathione peroxidase, and catalase. The liver histology of the curcumin-treated obese mice showed superior lipid infiltration and fewer FASN and PNPLA3 proteins in comparison with the control mice. Curcumin contributed to creating a positive chromium balance by decreasing the amount of chromium lost through urine, leading to the chromium mobilization needed to mitigate hyperglycemia. Thus, the results suggest that curcumin prevents HFD-induced glucose intolerance, kidney injury, and nonalcoholic fatty liver disease.

Metformin improves nonalcoholic fatty liver disease in obese mice

2000 ◽  
Vol 118 (4) ◽  
pp. A919
Author(s):  
Christine Chuckaree ◽  
Shi Qi Yang ◽  
HuiZhi Lin ◽  
Anna Mae Diehl
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Obese Mice ◽  
Nonalcoholic Fatty Liver

scholarly journals Imipramine Accelerates Nonalcoholic Fatty Liver Disease, Renal Impairment, Diabetic Retinopathy, Insulin Resistance, and Urinary Chromium Loss in Obese Mice

2021 ◽  
Vol 8 (9) ◽  
pp. 189
Author(s):  
Geng-Ruei Chang ◽  
Po-Hsun Hou ◽  
Chao-Min Wang ◽  
Jen-Wei Lin ◽  
Wei-Li Lin ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Diabetic Retinopathy ◽  
Fatty Acid ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Binding Protein ◽  
Obese Mice ◽  
Nonalcoholic Fatty Liver

Imipramine is a tricyclic antidepressant that has been approved for treating depression and anxiety in patients and animals and that has relatively mild side effects. However, the mechanisms of imipramine-associated disruption to metabolism and negative hepatic, renal, and retinal effects are not well defined. In this study, we evaluated C57BL6/J mice subjected to a high-fat diet (HFD) to study imipramine’s influences on obesity, fatty liver scores, glucose homeostasis, hepatic damage, distribution of chromium, and retinal/renal impairments. Obese mice receiving imipramine treatment had higher body, epididymal fat pad, and liver weights; higher serum triglyceride, aspartate and alanine aminotransferase, creatinine, blood urea nitrogen, renal antioxidant enzyme, and hepatic triglyceride levels; higher daily food efficiency; and higher expression levels of a marker of fatty acid regulation in the liver compared with the controls also fed an HFD. Furthermore, the obese mice that received imipramine treatment exhibited insulin resistance, worse glucose intolerance, decreased glucose transporter 4 expression and Akt phosphorylation levels, and increased chromium loss through urine. In addition, the treatment group exhibited considerably greater liver damage and higher fatty liver scores, paralleling the increases in patatin-like phospholipid domain containing protein 3 and the mRNA levels of sterol regulatory element-binding protein 1 and fatty acid-binding protein 4. Retinal injury worsened in imipramine-treated mice; decreases in retinal cell layer organization and retinal thickness and increases in nuclear factor κB and inducible nitric oxide synthase levels were observed. We conclude that administration of imipramine may result in the exacerbation of nonalcoholic fatty liver disease, diabetes, diabetic retinopathy, and kidney injury.

Salicornia Extract Ameliorates Salt-Induced Aggravation of Nonalcoholic Fatty Liver Disease in Obese Mice Fed a High-Fat Diet

2017 ◽  
Vol 82 (7) ◽  
pp. 1765-1774 ◽  
Author(s):  
Jae Hwan Kim ◽  
Sujin Suk ◽  
Woo Jung Jang ◽  
Chang Hyung Lee ◽  
Jong-Eun Kim ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Obese Mice ◽  
High Fat ◽  
Nonalcoholic Fatty Liver

Obese mice weight loss role on nonalcoholic fatty liver disease and endoplasmic reticulum stress treated by a GLP-1 receptor agonist

2021 ◽  
Author(s):  
Rayane Miranda Pontes-da-Silva ◽  
Thatiany de Souza Marinho ◽  
Luiz Eduardo de Macedo Cardoso ◽  
Carlos Alberto Mandarim-de-Lacerda ◽  
Marcia Barbosa Aguila
Keyword(s):  
Weight Loss ◽  
Endoplasmic Reticulum ◽  
Liver Disease ◽  
Endoplasmic Reticulum Stress ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Receptor Agonist ◽  
Obese Mice ◽  
Nonalcoholic Fatty Liver
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