scholarly journals A Mouse Model of Metabolic Syndrome: Insulin Resistance, Fatty Liver and Non-Alcoholic Fatty Pancreas Disease (NAFPD) in C57BL/6 Mice Fed a High Fat Diet

2010 ◽  
Vol 46 (3) ◽  
pp. 212-223 ◽  
Author(s):  
Julio C. Fraulob ◽  
Rebeca Ogg-Diamantino ◽  
Caroline Fernandes-Santos ◽  
Marcia Barbosa Aguila ◽  
Carlos A. Mandarim-de-Lacerda
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Mouse Model ◽  
Fatty Liver ◽  
High Fat Diet ◽  
High Fat ◽  
Pancreas Disease ◽  
Fatty Pancreas

PBI-4547 Improves Glucose Metabolism and Insulin Resistance, and Reduces Liver Damage in a High-Fat Diet Mouse Model of Obesity and Metabolic Syndrome

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1858-P
Author(s):  
MARTIN LEDUC ◽  
BRIGITTE GROUIX ◽  
MIKAËL TREMBLAY ◽  
LIETTE GERVAIS ◽  
FRANÇOIS SARRA-BOURNET ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Glucose Metabolism ◽  
Mouse Model ◽  
Liver Damage ◽  
High Fat Diet ◽  
High Fat

scholarly journals α,β-Amyrin prevents steatosis and insulin resistance in a high-fat diet-induced mouse model of NAFLD via the AMPK-mTORC1-SREBP1 signaling mechanism

2021 ◽  
Vol 54 (10) ◽  
Author(s):  
R.P. de Lima ◽  
P.I.G. Nunes ◽  
A.F.S.C. Viana ◽  
F.T.B. de Oliveira ◽  
R.A.C. Silva ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Mouse Model ◽  
High Fat Diet ◽  
High Fat ◽  
Signaling Mechanism

scholarly journals Combined effect of canagliflozin and exercise training on high-fat diet-fed mice

2020 ◽  
Vol 318 (4) ◽  
pp. E492-E503
Author(s):  
Kenichi Tanaka ◽  
Hirokazu Takahashi ◽  
Sayaka Katagiri ◽  
Kazuyo Sasaki ◽  
Yujin Ohsugi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Exercise Training ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Characteristic Change ◽  
High Fat ◽  
Nonalcoholic Fatty Liver ◽  
Sodium Glucose Cotransporter

Sodium-glucose cotransporter 2 inhibitors (SGLT2is) have been reported to improve obesity, diabetes, and nonalcoholic fatty liver disease (NAFLD) in addition to exercise training, whereas the combined effects remain to be elucidated fully. We investigated the effect of the combination of the SGLT2i canagliflozin (CAN) and exercise training in high-fat diet-induced obese mice. High-fat diet-fed mice were housed in normal cages (sedentary; Sed) or wheel cages (WCR) with or without CAN (0.03% of diet) for 4 wk. The effects on obesity, glucose metabolism, and hepatic steatosis were evaluated in four groups (Control/Sed, Control/WCR, CAN/Sed, and CAN/WCR). Numerically additive improvements were found in body weight, body fat mass, blood glucose, glucose intolerance, insulin resistance, and the fatty liver of the CAN/WCR group, whereas CAN increased food intake and reduced running distance. Exercise training alone, CAN alone, or both did not change the weight of skeletal muscle, but microarray analysis showed that each resulted in a characteristic change of gene expression in gastrocnemius muscle. In particular, in the CAN/WCR group, there was acceleration of the angiogenesis pathway and suppression of the adipogenesis pathway compared with the CAN/Sed group. In conclusion, the combination of an SGLT2i and exercise training improves obesity, insulin resistance, and NAFLD in an additive manner. Changes of gene expression in skeletal muscle may contribute, at least in part, to the improvement of obesity and insulin sensitivity.

scholarly journals Ethyl Acetate Fraction of Amomum xanthioides Ameliorates Nonalcoholic Fatty Liver Disease in a High-Fat Diet Mouse Model

Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2433
Author(s):  
Hwi-Jin Im ◽  
Seung-Ju Hwang ◽  
Jin-Seok Lee ◽  
Sung-Bae Lee ◽  
Ji-Yun Kang ◽  
...  
Keyword(s):  
Liver Disease ◽  
Mouse Model ◽  
Fatty Liver ◽  
Ethyl Acetate ◽  
Nonalcoholic Fatty Liver Disease ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Ethyl Acetate Fraction ◽  
High Fat ◽  
Nonalcoholic Fatty Liver

The global prevalence of nonalcoholic fatty liver disease (NAFLD) is estimated to be 25% and has continued to increase; however, no drugs have yet been approved for NAFLD treatments. The ethyl acetate fraction of Amomum xanthioides (EFAX) was previously reported to have an anti-hepatic fibrosis effect, but its effects on steatosis or steatohepatitis remain unclear. This study investigated the anti-fatty liver of EFAX using a high-fat diet mouse model. High-fat diet intake for 8 weeks induced hepatic steatosis with mild inflammation and oxidative damage and increased the adipose tissue weight along with the development of dyslipidemia. EFAX treatment significantly ameliorated the steatohepatic changes, the increased weight of adipose tissues, and the altered serum lipid profiles. These observed effects were possibly due to the lipolysis-dominant activity of EFAX on multiple hepatic proteins including sterol regulatory element-binding protein (mSREBP)-1c, peroxisome proliferator-activated receptor (PPAR)-α, AMP-activated protein kinase, and diglyceride acyltransferases (DGATs). Taken together, these results show that EFAX might be a potential therapeutic agent for regulating a wide spectrum of NAFLDs from steatosis to fibrosis via multiple actions on lipid metabolism-related proteins. Further studies investigating clear mechanisms and their active compounds are needed.

scholarly journals Characterization of the variability in the extent of nonalcoholic fatty liver induced by a high‐fat diet in the genetically diverse Collaborative Cross mouse model

2020 ◽  
Vol 34 (6) ◽  
pp. 7773-7785
Author(s):  
Aline Conti ◽  
Volodymyr Tryndyak ◽  
Rose A. Willett ◽  
Barbara Borowa‐Mazgaj ◽  
Anna Watson ◽  
...  
Keyword(s):  
Mouse Model ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Collaborative Cross ◽  
High Fat ◽  
Nonalcoholic Fatty Liver

Salidroside and Curcumin Formula Prevents Liver Injury in Nonalcoholic Fatty Liver Disease in Rats

2018 ◽  
Vol 17 (5) ◽  
pp. 0-10
Author(s):  
Hong-Shan Li ◽  
Hao Ying ◽  
Zhe-Yun He
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Lipid Deposition ◽  
Model Group ◽  
High Fat ◽  
Nonalcoholic Fatty Liver

Introduction and aim. Salidroside and curcumin (SC) formula could alleviate lipid deposition in high fat diet-induced nonalcoholic fatty liver disease (NAFLD). However, the mechanisms are still unknown, and the magnitude of potential therapeutic benefit remains understudied. Material and methods. The rats were treated with high fat diet for 14 weeks to induce NAFLD. The experiment was divided into control, model (NAFLD), SC formula and rosiglitazone groups (n = 7 in each group). Hematoxylin-eosin (H&E) staining was applied to detect liver morphological changes. Biochemical, metabolic indices and inflammation factors in liver tissue and serum were detected. Additionally, the activities of related enzymes were detected by enzyme-linked immunosorbent assay. Results. In the established rat model, typical lipid deposition and liver steatosis were observed. Liver triglyceride, free fatty acids, sera alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase, fasting insulin, fasting blood glucose and homeostasis model assessment of insulin resistance were elevated in model group. Liver malondialdehyde was significantly elevated, while superoxide dismutase was significantly decreased in model group, compared with control. Moreover, tumor necrosis factor-α and Interleukin-1 were significantly produced in model group, compared with control. As a mechanism, high fat diet decreased tissue AMP-activated protein kinase (AMPK), phosphorylated AMPK, carnitine palmitoyltransferase 1 and increased inacetyl-CoA carboxylase (ACCase), phosphorylated ACCase. Importantly, these abnormal changes caused by high fat diet were reduced by SC formula administration. Conclusion. SC formula could ameliorate the injury caused by high fat diet. The effect was likely mediated via its influence on insulin resistance, lipid peroxidation injury and AMPK signaling pathway.

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