NDLI: Cafeteria diet-fed mice is a pertinent model of obesity-induced organ damage: a potential role of inflammation

Content Provider	Springer Nature Link
Author	Zeeni, Nadine Dagher Hamalian, Carole Dimassi, Hani Faour, Wissam H.
Copyright Year	2015
Abstract	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.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).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.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.
Starting Page	501
Ending Page	512
Page Count	12
File Format	PDF
ISSN	10233830
Journal	Inflammation Research
Volume Number	64
Issue Number	7
e-ISSN	1420908X
Language	English
Publisher	Springer Basel
Publisher Date	2015-05-13
Publisher Place	Basel
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Obesity model Cafeteria diet Food intake Palatability Pathological damage Immunology Pharmacology/Toxicology Rheumatology Allergology Dermatology Neurology
Content Type	Text
Resource Type	Article
Subject	Pharmacology Immunology

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