Characterization of inflammation and insulin resistance in high‐fat diet‐induced male C57BL/6J mouse model of obesity

• Published in: Animal models and experimental medicine Vol. 2; no. 4; pp. 252 - 258
• Main Authors: Avtanski, Dimiter, Pavlov, Valentin A., Tracey, Kevin J., Poretsky, Leonid
• Format: Journal Article
• Language: English
• Published: United States John Wiley & Sons, Inc 01-12-2019; John Wiley and Sons Inc; Wiley
• Subjects: Abdomen; Adipocytes; Adipose tissue; Animal models; Blood glucose; Body weight; Diabetes; Diet; Energy; Fasting; High fat diet; high‐fat; Inflammation; Insulin; Insulin resistance; Leptin; Lipids; Liver; Medical research; Mimicry; mouse model; Obesity; Original; Plasma levels; Tumor necrosis factor; New York; United States > US; high‐fat; diet; mouse model; insulin resistance
• ISSN: 2576-2095; 2096-5451; 2576-2095
• DOI: 10.1002/ame2.12084

Background
Animal models of diet‐induced obesity (DIO) are commonly used in medical research for mimicking human diseases. There is no universal animal model, and careful evaluation of variety of factors needs to be considered when designing new experiments. Here, we investigated the effect of 9 weeks high‐fat diet (HFD) intervention, providing 60% energy from fat, on parameters of inflammation and insulin resistance in male C57BL/6J mice.
Methods
Six weeks old mice were initiated on regular diet (RD) or HFD providing 60 kcal energy from fat for 9 weeks. Fasting blood glucose levels were measured by glucometer, and fasting plasma levels of insulin and proinflammatory cytokines by Luminex assay. Insulin sensitivity was evaluated by using QUICKI and HOMA2 indexes.
Results
HFD mice showed ~ 40% higher body weight and ~ 20% larger abdominal circumference, due to an increase in the white adipose tissue mass. Liver examination revealed increased size and higher hepatic lipid accumulation in livers from HFD mice compared to their RD counterparts. Animals from the HFD group were characterized with significantly higher presence of crown‐like structures (CLS) in WAT and higher plasma levels of proinflammatory cytokines (TNF‐α, IL‐6, leptin, MCP‐1, PAI‐1, and resistin). HFD‐fed mice also demonstrated impaired insulin sensitivity (lower QUICKI, higher HOMA‐insulin resistance (HOMA‐IR), and lower HOMA‐percent sensitivity (HOMA‐%S)) index values.
Conclusion
Male C57BL/6J mice on 9 weeks HFD providing 60 kcal energy from fat display impaired insulin sensitivity and chronic inflammation, thus making this DIO mouse model appropriate for studies of early stages of obesity‐related pathology.