Behavioral susceptibility to obesity: Gene–environment interplay in the development of weight

Llewellyn, Clare H.; Wardle, Jane

doi:10.1016/j.physbeh.2015.07.006

Cited by 192 publications

(168 citation statements)

References 53 publications

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“…However, the resistance to diet-induced obesity observed in the current Fto -KO mice indicate an improved ability of adipose tissue to respond to environmental changes such as HFD. This is important with regards to human genetics of obesity, since environmental factors have been shown to alter the effects of genetic variants in individual’s risk of obesity and assessment of these factors may help in choosing the most suitable interventions in the prevention and management of obesity (reviewed in [7]).…”

Section: Discussionmentioning

confidence: 99%

“…While genetic factors are estimated to account for 40%–70% of BMI variation, only a fraction of it is explained by presently known genetic variants [6]. This may in part be due to the limited amount of genetic variants yet identified, but there is also growing evidence of a gene-environment interaction, which needs to be fully established when the genetics of obesity is under investigation (reviewed in [7]). For example, individuals homozygous for the obesity-risk allele of Fto variant rs9939609 showed improved weight loss and metabolic markers after low-fat, but not low-carbohydrate, hypocaloric dietary intervention, while the improvement was evident on both diets in the group of the protective allele carriers [8].…”

Section: Introductionmentioning

confidence: 99%

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Fto-Deficiency Affects the Gene and MicroRNA Expression Involved in Brown Adipogenesis and Browning of White Adipose Tissue in Mice

Ronkainen

Mondini

Cinti

et al. 2016

IJMS

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Genetic variants in the fat mass- and obesity-associated gene Fto are linked to the onset of obesity in humans. The causal role of the FTO protein in obesity is supported by evidence obtained from transgenic mice; however, the underlying molecular pathways pertaining to the role of FTO in obesity have yet to be established. In this study, we investigate the Fto gene in mouse brown adipose tissue and in the browning process of white adipose tissue. We analyze distinct structural and molecular factors in brown and white fat depots of Fto-deficient mice under normal and obesogenic conditions. We report significant alterations in the morphology of adipose tissue depots and the expression of mRNA and microRNA related to brown adipogenesis and metabolism in Fto-deficient mice. Furthermore, we show that high-fat feeding does not attenuate the browning process of Fto-deficient white adipose tissue as observed in wild-type tissue, suggesting a triggering effect of the FTO pathways by the dietary environment.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Fto-Deficiency Affects the Gene and MicroRNA Expression Involved in Brown Adipogenesis and Browning of White Adipose Tissue in Mice

Ronkainen

Mondini

Cinti

et al. 2016

IJMS

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“…She developed the BST in which she hypothesised that genes influence weight at least partly via biological mechanisms that control appetite regulation [26]. The BST explains how human body weight can have both genetic and environmental drivers at the same time and why genetic expression on weight is likely to be stronger in more ‘obesogenic’ environments (see Fig.…”

Section: Behavioural Susceptibility Theory: Appetite Mediates Geneticmentioning

confidence: 99%

Behavioural Susceptibility Theory: Professor Jane Wardle and the Role of Appetite in Genetic Risk of Obesity

Llewellyn

Fildes

2017

Curr Obes Rep

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Purpose of ReviewThere is considerable variability in human body weight, despite the ubiquity of the ‘obesogenic’ environment. Human body weight has a strong genetic basis and it has been hypothesised that genetic susceptibility to the environment explains variation in human body weight, with differences in appetite being implicated as the mediating mechanism; so-called ‘behavioural susceptibility theory’ (BST), first described by Professor Jane Wardle. This review summarises the evidence for the role of appetite as a mediator of genetic risk of obesity.Recent FindingsVariation in appetitive traits is observable from infancy, drives early weight gain and is highly heritable in infancy and childhood. Obesity-related common genetic variants identified through genome-wide association studies show associations with appetitive traits, and appetite mediates part of the observed association between genetic risk and adiposity.SummaryObesity results from an interaction between genetic susceptibility to overeating and exposure to an ‘obesogenic’ food environment.

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“…Although there is some literature about the development of OW/OB in children dating back to the early 1980s, it is mainly in the last 10 to 15 years that the topic has gained increased attention, partly as a basis for designing intervention and prevention programs . In relation to questions about the etiology of OW/OB, including in childhood, the predominant approach whether from reviews, individual research studies, or in the design of intervention strategies has been one based on correlates, predictors, or risks.…”

Section: Introductionmentioning

confidence: 99%

A biopsychosocial approach to processes and pathways in the development of overweight and obesity in childhood: Insights from developmental theory and research

Russell

2019

Obesity Reviews

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Summary Childhood obesity has reached alarming proportions in many countries. There is consensus that both biological (especially genetic) and environmental (including psychosocial) factors contribute to weight gain and obesity in childhood. Research has identified extensive risk or predictive factors for childhood obesity from both of these domains. There is less consensus about the developmental processes or pathways showing how these risk factors lead to overweigh/obesity (OW/OB) in childhood. We outline a biopsychosocial process model of the development of OW/OB in childhood. The model and associated scholarship from developmental theory and research guide an analysis of research on OW/OB in childhood. The model incorporates biological factors such as genetic predispositions or susceptibility genes, temperament, and homeostatic and allostatic processes with the psychosocial and behavioral factors of parenting, parental feeding practices, child appetitive traits, food liking, food intakes, and energy expenditure. There is an emphasis on bidirectional and transactional processes linking child biology and behavior with psychosocial processes and environment. Insights from developmental theory and research include implications for conceptualization, measurement, research design, and possible multiple pathways to OW/OB. Understanding the developmental processes and pathways involved in childhood OW/OB should contribute to more targeted prevention and intervention strategies in childhood.

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Behavioral susceptibility to obesity: Gene–environment interplay in the development of weight

Cited by 192 publications

References 53 publications

Fto-Deficiency Affects the Gene and MicroRNA Expression Involved in Brown Adipogenesis and Browning of White Adipose Tissue in Mice

Fto-Deficiency Affects the Gene and MicroRNA Expression Involved in Brown Adipogenesis and Browning of White Adipose Tissue in Mice

Behavioural Susceptibility Theory: Professor Jane Wardle and the Role of Appetite in Genetic Risk of Obesity

A biopsychosocial approach to processes and pathways in the development of overweight and obesity in childhood: Insights from developmental theory and research

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