A new animal diet based on human Western diet is a robust diet-induced obesity model: comparison to high-fat and cafeteria diets in term of metabolic and gut microbiota disruption

Background/Objectives: Obesity is a metabolic disorder that predisposes patients to numerous diseases and has become a major global public-health concern. Animal models of diet-induced obesity (DIO) are frequently used to study obesity, but which DIO model most accurately reflects the pathology of h...

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Published in:International Journal of Obesity Vol. 42; no. 3; pp. 525 - 534
Main Authors: Bortolin, R C, Vargas, A R, Gasparotto, J, Chaves, P R, Schnorr, C E, Martinello, Kd B, Silveira, A K, Rabelo, T K, Gelain, D P, Moreira, J C F
Format: Journal Article
Language:English
Published: London Nature Publishing Group UK 01-03-2018
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Abstract Background/Objectives: Obesity is a metabolic disorder that predisposes patients to numerous diseases and has become a major global public-health concern. Animal models of diet-induced obesity (DIO) are frequently used to study obesity, but which DIO model most accurately reflects the pathology of human obesity remains unclear. In this study, we designed a diet based on the human Western diet (WD) and compared it with the cafeteria diet (CAF) and high-fat diet (HFD) in order to evaluate which diet most closely mirrors human obesity. Methods: Wistar rats were fed four different diets (WD, CAF, HFD and a low-fat diet) for 18 weeks. Metabolic parameters and gut microbiota changes were then characterized. Results: Rats fed the four different diets exhibited completely different phenotypes, highlighting the importance of diet selection. This study also revealed that WD most effectively induced obesity and obesity-related disorders, and thus proved to be a robust model of human obesity. Moreover, WD-fed rats developed obesity and obesity-related comorbidities independent of major alterations in gut microbiota composition (dysbiosis), whereas CAF-fed rats developed the greatest dysbiosis independent of obesity. We also characterized gut microbiota after feeding on these four different diets and identified five genera that might be involved in the pathogenesis of obesity. Conclusions: These data suggest that diet, and not the obese state, was the major driving force behind gut microbiota changes. Moreover, the marked dysbiosis observed in CAF-fed rats might have resulted from the presence of several additives present in the CAF diet, or even a lack of essential vitamins and minerals. Based on our findings, we recommend the use of the prototypic WD (designed here) in DIO models. Conversely, CAF could be used to investigate the effects of excessive consumption of industrially produced and highly processed foods, which are characteristic of Western society.
AbstractList Background/Objectives: Obesity is a metabolic disorder that predisposes patients to numerous diseases and has become a major global public-health concern. Animal models of diet-induced obesity (DIO) are frequently used to study obesity, but which DIO model most accurately reflects the pathology of human obesity remains unclear. In this study, we designed a diet based on the human Western diet (WD) and compared it with the cafeteria diet (CAF) and high-fat diet (HFD) in order to evaluate which diet most closely mirrors human obesity. Methods: Wistar rats were fed four different diets (WD, CAF, HFD and a low-fat diet) for 18 weeks. Metabolic parameters and gut microbiota changes were then characterized. Results: Rats fed the four different diets exhibited completely different phenotypes, highlighting the importance of diet selection. This study also revealed that WD most effectively induced obesity and obesity-related disorders, and thus proved to be a robust model of human obesity. Moreover, WD-fed rats developed obesity and obesity-related comorbidities independent of major alterations in gut microbiota composition (dysbiosis), whereas CAF-fed rats developed the greatest dysbiosis independent of obesity. We also characterized gut microbiota after feeding on these four different diets and identified five genera that might be involved in the pathogenesis of obesity. Conclusions: These data suggest that diet, and not the obese state, was the major driving force behind gut microbiota changes. Moreover, the marked dysbiosis observed in CAF-fed rats might have resulted from the presence of several additives present in the CAF diet, or even a lack of essential vitamins and minerals. Based on our findings, we recommend the use of the prototypic WD (designed here) in DIO models. Conversely, CAF could be used to investigate the effects of excessive consumption of industrially produced and highly processed foods, which are characteristic of Western society.
Background/Objectives:Obesity is a metabolic disorder that predisposes patients to numerous diseases and has become a major global public-health concern. Animal models of diet-induced obesity (DIO) are frequently used to study obesity, but which DIO model most accurately reflects the pathology of human obesity remains unclear. In this study, we designed a diet based on the human Western diet (WD) and compared it with the cafeteria diet (CAF) and high-fat diet (HFD) in order to evaluate which diet most closely mirrors human obesity.Methods:Wistar rats were fed four different diets (WD, CAF, HFD and a low-fat diet) for 18 weeks. Metabolic parameters and gut microbiota changes were then characterized.Results:Rats fed the four different diets exhibited completely different phenotypes, highlighting the importance of diet selection. This study also revealed that WD most effectively induced obesity and obesity-related disorders, and thus proved to be a robust model of human obesity. Moreover, WD-fed rats developed obesity and obesity-related comorbidities independent of major alterations in gut microbiota composition (dysbiosis), whereas CAF-fed rats developed the greatest dysbiosis independent of obesity. We also characterized gut microbiota after feeding on these four different diets and identified five genera that might be involved in the pathogenesis of obesity.Conclusions:These data suggest that diet, and not the obese state, was the major driving force behind gut microbiota changes. Moreover, the marked dysbiosis observed in CAF-fed rats might have resulted from the presence of several additives present in the CAF diet, or even a lack of essential vitamins and minerals. Based on our findings, we recommend the use of the prototypic WD (designed here) in DIO models. Conversely, CAF could be used to investigate the effects of excessive consumption of industrially produced and highly processed foods, which are characteristic of Western society.
Background/Objectives: Obesity is a metabolic disorder that predisposes patients to numerous diseases and has become a major global public-health concern. Animal models of diet-induced obesity (DIO) are frequently used to study obesity, but which DIO model most accurately reflects the pathology of human obesity remains unclear. In this study, we designed a diet based on the human Western diet (WD) and compared it with the cafeteria diet (CAF) and high-fat diet (HFD) in order to evaluate which diet most closely mirrors human obesity. Methods: Wistar rats were fed four different diets (WD, CAF, HFD and a low-fat diet) for 18 weeks. Metabolic parameters and gut microbiota changes were then characterized. Results: Rats fed the four different diets exhibited completely different phenotypes, highlighting the importance of diet selection. This study also revealed that WD most effectively induced obesity and obesity-related disorders, and thus proved to be a robust model of human obesity. Moreover, WD-fed rats developed obesity and obesity-related comorbidities independent of major alterations in gut microbiota composition (dysbiosis), whereas CAF-fed rats developed the greatest dysbiosis independent of obesity. We also characterized gut microbiota after feeding on these four different diets and identified five genera that might be involved in the pathogenesis of obesity. Conclusions: These data suggest that diet, and not the obese state, was the major driving force behind gut microbiota changes. Moreover, the marked dysbiosis observed in CAF-fed rats might have resulted from the presence of several additives present in the CAF diet, or even a lack of essential vitamins and minerals. Based on our findings, we recommend the use of the prototypic WD (designed here) in DIO models. Conversely, CAF could be used to investigate the effects of excessive consumption of industrially produced and highly processed foods, which are characteristic of Western society. International Journal of Obesity (2018) 42, 525-534; doi: 10.1038/ijo.2017.225; published online 3 October 2017
Obesity is a metabolic disorder that predisposes patients to numerous diseases and has become a major global public-health concern. Animal models of diet-induced obesity (DIO) are frequently used to study obesity, but which DIO model most accurately reflects the pathology of human obesity remains unclear. In this study, we designed a diet based on the human Western diet (WD) and compared it with the cafeteria diet (CAF) and high-fat diet (HFD) in order to evaluate which diet most closely mirrors human obesity. Wistar rats were fed four different diets (WD, CAF, HFD and a low-fat diet) for 18 weeks. Metabolic parameters and gut microbiota changes were then characterized. Rats fed the four different diets exhibited completely different phenotypes, highlighting the importance of diet selection. This study also revealed that WD most effectively induced obesity and obesity-related disorders, and thus proved to be a robust model of human obesity. Moreover, WD-fed rats developed obesity and obesity-related comorbidities independent of major alterations in gut microbiota composition (dysbiosis), whereas CAF-fed rats developed the greatest dysbiosis independent of obesity. We also characterized gut microbiota after feeding on these four different diets and identified five genera that might be involved in the pathogenesis of obesity. These data suggest that diet, and not the obese state, was the major driving force behind gut microbiota changes. Moreover, the marked dysbiosis observed in CAF-fed rats might have resulted from the presence of several additives present in the CAF diet, or even a lack of essential vitamins and minerals. Based on our findings, we recommend the use of the prototypic WD (designed here) in DIO models. Conversely, CAF could be used to investigate the effects of excessive consumption of industrially produced and highly processed foods, which are characteristic of Western society.
BACKGROUND/OBJECTIVESObesity is a metabolic disorder that predisposes patients to numerous diseases and has become a major global public-health concern. Animal models of diet-induced obesity (DIO) are frequently used to study obesity, but which DIO model most accurately reflects the pathology of human obesity remains unclear. In this study, we designed a diet based on the human Western diet (WD) and compared it with the cafeteria diet (CAF) and high-fat diet (HFD) in order to evaluate which diet most closely mirrors human obesity. METHODSWistar rats were fed four different diets (WD, CAF, HFD and a low-fat diet) for 18 weeks. Metabolic parameters and gut microbiota changes were then characterized. RESULTSRats fed the four different diets exhibited completely different phenotypes, highlighting the importance of diet selection. This study also revealed that WD most effectively induced obesity and obesity-related disorders, and thus proved to be a robust model of human obesity. Moreover, WD-fed rats developed obesity and obesity-related comorbidities independent of major alterations in gut microbiota composition (dysbiosis), whereas CAF-fed rats developed the greatest dysbiosis independent of obesity. We also characterized gut microbiota after feeding on these four different diets and identified five genera that might be involved in the pathogenesis of obesity. CONCLUSIONSThese data suggest that diet, and not the obese state, was the major driving force behind gut microbiota changes. Moreover, the marked dysbiosis observed in CAF-fed rats might have resulted from the presence of several additives present in the CAF diet, or even a lack of essential vitamins and minerals. Based on our findings, we recommend the use of the prototypic WD (designed here) in DIO models. Conversely, CAF could be used to investigate the effects of excessive consumption of industrially produced and highly processed foods, which are characteristic of Western society.
Obesity is a metabolic disorder that predisposes patients to numerous diseases and has become a major global public-health concern. Animal models of diet-induced obesity (DIO) are frequently used to study obesity, but which DIO model most accurately reflects the pathology of human obesity remains unclear. In this study, we designed a diet based on the human Western diet (WD) and compared it with the cafeteria diet (CAF) and high-fat diet (HFD) in order to evaluate which diet most closely mirrors human obesity. Wistar rats were fed four different diets (WD, CAF, HFD and a low-fat diet) for 18 weeks. Metabolic parameters and gut microbiota changes were then characterized. Rats fed the four different diets exhibited completely different phenotypes, highlighting the importance of diet selection. This study also revealed that WD most effectively induced obesity and obesity-related disorders, and thus proved to be a robust model of human obesity. Moreover, WD-fed rats developed obesity and obesity-related comorbidities independent of major alterations in gut microbiota composition (dysbiosis), whereas CAF-fed rats developed the greatest dysbiosis independent of obesity. We also characterized gut microbiota after feeding on these four different diets and identified five genera that might be involved in the pathogenesis of obesity. These data suggest that diet, and not the obese state, was the major driving force behind gut microbiota changes. Moreover, the marked dysbiosis observed in CAF-fed rats might have resulted from the presence of several additives present in the CAF diet, or even a lack of essential vitamins and minerals. Based on our findings, we recommend the use of the prototypic WD (designed here) in DIO models. Conversely, CAF could be used to investigate the effects of excessive consumption of industrially produced and highly processed foods, which are characteristic of Western society.
Audience Academic
Author Chaves, P R
Vargas, A R
Rabelo, T K
Silveira, A K
Bortolin, R C
Martinello, Kd B
Moreira, J C F
Gasparotto, J
Schnorr, C E
Gelain, D P
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  surname: Vargas
  fullname: Vargas, A R
  organization: Centro de Estudos em Estresse Oxidativo—Departamento de Bioquímica – Instituto de Ciências Básicas da Saúde—Universidade Federal do Rio Grande do Sul (UFRGS)
– sequence: 3
  givenname: J
  orcidid: 0000-0003-2545-7288
  surname: Gasparotto
  fullname: Gasparotto, J
  organization: Centro de Estudos em Estresse Oxidativo—Departamento de Bioquímica – Instituto de Ciências Básicas da Saúde—Universidade Federal do Rio Grande do Sul (UFRGS)
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  surname: Schnorr
  fullname: Schnorr, C E
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  surname: Martinello
  fullname: Martinello, Kd B
  organization: Departamento de Ingeniería Civil y Ambiental—Universidad de la Costa
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  givenname: A K
  surname: Silveira
  fullname: Silveira, A K
  organization: Centro de Estudos em Estresse Oxidativo—Departamento de Bioquímica – Instituto de Ciências Básicas da Saúde—Universidade Federal do Rio Grande do Sul (UFRGS)
– sequence: 8
  givenname: T K
  surname: Rabelo
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  givenname: D P
  surname: Gelain
  fullname: Gelain, D P
  organization: Centro de Estudos em Estresse Oxidativo—Departamento de Bioquímica – Instituto de Ciências Básicas da Saúde—Universidade Federal do Rio Grande do Sul (UFRGS)
– sequence: 10
  givenname: J C F
  surname: Moreira
  fullname: Moreira, J C F
  organization: Centro de Estudos em Estresse Oxidativo—Departamento de Bioquímica – Instituto de Ciências Básicas da Saúde—Universidade Federal do Rio Grande do Sul (UFRGS)
BackLink https://www.ncbi.nlm.nih.gov/pubmed/28895587$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright Macmillan Publishers Limited, part of Springer Nature. 2018
COPYRIGHT 2018 Nature Publishing Group
Copyright Nature Publishing Group Mar 2018
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Snippet Background/Objectives: Obesity is a metabolic disorder that predisposes patients to numerous diseases and has become a major global public-health concern....
Obesity is a metabolic disorder that predisposes patients to numerous diseases and has become a major global public-health concern. Animal models of...
Background/Objectives: Obesity is a metabolic disorder that predisposes patients to numerous diseases and has become a major global public-health concern....
Background/Objectives:Obesity is a metabolic disorder that predisposes patients to numerous diseases and has become a major global public-health concern....
BACKGROUND/OBJECTIVESObesity is a metabolic disorder that predisposes patients to numerous diseases and has become a major global public-health concern. Animal...
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SubjectTerms 631/326/41
631/45
692/699/2743/2037
692/699/2743/393
Additives
Analysis
Animal feeding and feeds
Animal models
Animals
Causes of
Diagnosis
Diet
Diet, High-Fat
Diet, Western
Disease Models, Animal
Dysbacteriosis
Dysbiosis - metabolism
Epidemiology
Fast Foods
Food
Food processing
Gastrointestinal Microbiome - physiology
Health Promotion and Disease Prevention
High fat diet
Internal Medicine
Intestinal microflora
Low fat diet
Male
Medicine
Medicine & Public Health
Metabolic Diseases
Metabolic Diseases - metabolism
Metabolic disorders
Metabolism
Microbiota
Microbiota (Symbiotic organisms)
Minerals
Nutrient deficiency
Obesity
Obesity - metabolism
Obesity - microbiology
Obesity - physiopathology
original-article
Pathogenesis
Processed foods
Public Health
Rats
Rats, Wistar
Risk factors
Rodents
Vitamins
Title A new animal diet based on human Western diet is a robust diet-induced obesity model: comparison to high-fat and cafeteria diets in term of metabolic and gut microbiota disruption
URI https://link.springer.com/article/10.1038/ijo.2017.225
https://www.ncbi.nlm.nih.gov/pubmed/28895587
https://www.proquest.com/docview/2019427375
https://search.proquest.com/docview/1938187436
Volume 42
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