Acknowledgements The authors are funded by the Scottish Government, Rural and Environment Science and Analytical Services Division, Strategic Research Programme, ‘Food, Health and Wellbeing’ Theme. P.B. also acknowledges funding from Biotechnology and Biological Sciences Research Council (BBSRC; BB/M001504/1), J.G.M. from the European Union (EU)-funded Full4Health project (grant agreement no. 266408; Seventh Framework Programme [FP7/2007-2013]), and P.J.M. from BBSRC (BB/G014272/1).Peer reviewedPublisher PD

Barrett, Perry

Mercer, Julian G

Morgan, Peter J

Disease Models & Mechanisms

PubMed

Acknowledgements The authors are funded by the Scottish Government, Rural and Environment Science and Analytical Services Division, Strategic Research Programme, ‘Food, Health and Wellbeing’ Theme. P.B. also acknowledges funding from Biotechnology and Biological Sciences Research Council (BBSRC; BB/M001504/1), J.G.M. from the European Union (EU)-funded Full4Health project (grant agreement no. 266408; Seventh Framework Programme [FP7/2007-2013]), and P.J.M. from BBSRC (BB/G014272/1).Peer reviewe

Aberdeen University Research

English

Preclinical models for obesity research

ABSTRACT
               A multi-dimensional strategy to tackle the global obesity epidemic requires an in-depth understanding of the mechanisms that underlie this complex condition. Much of the current mechanistic knowledge has arisen from preclinical research performed mostly, but not exclusively, in laboratory mouse and rat strains. These experimental models mimic certain aspects of the human condition and its root causes, particularly the over-consumption of calories and unbalanced diets. As with human obesity, obesity in rodents is the result of complex gene–environment interactions. Here, we review the traditional monogenic models of obesity, their contemporary optogenetic and chemogenetic successors, and the use of dietary manipulations and meal-feeding regimes to recapitulate the complexity of human obesity. We critically appraise the strengths and weaknesses of these different models to explore the underlying mechanisms, including the neural circuits that drive behaviours such as appetite control. We also discuss the use of these models for testing and screening anti-obesity drugs, beneficial bio-actives, and nutritional strategies, with the goal of ultimately translating these findings for the treatment of human obesity.</jats:p

Perry Barrett

Julian G. Mercer

Peter J. Morgan

Crossref

A multi-dimensional strategy to tackle the global obesity epidemic requires an in-depth understanding of the mechanisms that underlie this complex condition. Much of the current mechanistic knowledge has arisen from preclinical research performed mostly, but not exclusively, in laboratory mouse and rat strains. These experimental models mimic certain aspects of the human condition and its root causes, particularly the over-consumption of calories and unbalanced diets. As with human obesity, obesity in rodents is the result of complex gene–environment interactions. Here, we review the traditional monogenic models of obesity, their contemporary optogenetic and chemogenetic successors, and the use of dietary manipulations and meal-feeding regimes to recapitulate the complexity of human obesity. We critically appraise the strengths and weaknesses of these different models to explore the underlying mechanisms, including the neural circuits that drive behaviours such as appetite control. We also discuss the use of these models for testing and screening anti-obesity drugs, beneficial bio-actives, and nutritional strategies, with the goal of ultimately translating these findings for the treatment of human obesity

Preclinical models for obesity research

Abstract

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Aberdeen University Research

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