Cafeteria diet-fed mice is a pertinent model of obesity-induced organ damage
Objective This study is aimed at evaluating the effects of a cafeteria diet (obesity) mouse model on early multi-organ functional, structural, endocrine and biochemical alterations. Materials and methods Multi-organ damage is assessed using clinical, biochemical, pathological, and inflammatory param...
Saved in:
| Main Author: | |
|---|---|
| Other Authors: | , , |
| Format: | article |
| Published: |
2015
|
| Online Access: | http://hdl.handle.net/10725/5290 http://dx.doi.org/10.1007/s00011-015-0831-z http://libraries.lau.edu.lb/research/laur/terms-of-use/articles.php https://link.springer.com/article/10.1007/s00011-015-0831-z |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| Summary: | Objective This study is aimed at evaluating the effects of a cafeteria diet (obesity) mouse model on early multi-organ functional, structural, endocrine and biochemical alterations. Materials and methods Multi-organ damage is assessed using clinical, biochemical, pathological, and inflammatory parameters in 30 mice fed one of the three diets for 15 weeks: standard chow diet (SC), high fat (HF), or “Cafeteria diet” (CAF) (standard SC and a choice of highly palatable human cafeteria foods: chocolate, biscuits, and peanut butter). Results CAF diet was associated with an increase in body weight, energy intake, and serum cholesterol levels compared to the other diets, as well as higher insulin levels and lower glucose tolerance. Additionally, consumption of the CAF diet was associated with significantly higher weight gain, abdominal fat, and serum IL-6 levels, as well as more damage in the heart (coronary perivascular fibrosis and steatosis), kidney (chronic interstitial inflammation and glomerular sclerosis), and liver (liver weight, portal fibrosis, apoptosis, and steatosis) compared to the HF diet. Conclusion Functional and structural damage in CAF were higher than HF of similar macronutrient composition. This study provides a novel dietary model in mice that mimics multi-organ physiologic alterations in humans secondary to obesity. |
|---|