Predation risk modulates diet‐induced obesity in male <scp>C</scp>57<scp>BL</scp>/6 mice

Monarca, Rita I.; Mathias, Maria da Luz; Wang, Dehua; Speakman, John R.

doi:10.1002/oby.21193

Cited by 14 publications

(15 citation statements)

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“…As with studies on birds, the evidence with respect to stochastic variations in food supply are less clear cut compared with the impacts of modified predation risk. There is some limited support for the idea that increased stochasticity drives elevated fat storage Cao et al, 2009;Zhang et al, 2012;Zhu et al, 2014); however, other studies suggest the reverse (Monarca et al, 2015b). In humans, this idea is generally called the 'food insecurity' hypothesis, or the 'hunger-obesity' paradigm (Nettle et al, 2017;Dhurandhar, 2016), i.e.…”

Section: Set-point Theorymentioning

confidence: 99%

The evolution of body fatness: trading off disease and predation risk

Speakman

2018

Journal of Experimental Biology

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Human obesity has a large genetic component, yet has many serious negative consequences. How this state of affairs has evolved has generated wide debate. The thrifty gene hypothesis was the first attempt to explain obesity as a consequence of adaptive responses to an ancient environment that in modern society become disadvantageous. The idea is that genes (or more precisely, alleles) predisposing to obesity may have been selected for by repeated exposure to famines. However, this idea has many flaws: for instance, selection of the supposed magnitude over the duration of human evolution would fix any thrifty alleles (famines kill the old and young, not the obese) and there is no evidence that hunter-gatherer populations become obese between famines. An alternative idea (called thrifty late) is that selection in famines has only happened since the agricultural revolution. However, this is inconsistent with the absence of strong signatures of selection at single nucleotide polymorphisms linked to obesity. In parallel to discussions about the origin of obesity, there has been much debate regarding the regulation of body weight. There are three basic models: the setpoint, settling point and dual-intervention point models. Selection might act against low and high levels of adiposity because food unpredictability and the risk of starvation selects against low adiposity whereas the risk of predation selects against high adiposity. Although evidence for the latter is quite strong, evidence for the former is relatively weak. The release from predation ∼2-million years ago is suggested to have led to the upper intervention point drifting in evolutionary time, leading to the modern distribution of obesity: the drifty gene hypothesis. Recent critiques of the dual-intervention point/ drifty gene idea are flawed and inconsistent with known aspects of energy balance physiology. Here, I present a new formulation of the dual-intervention point model. This model includes the novel suggestion that food unpredictability and starvation are insignificant factors driving fat storage, and that the main force driving up fat storage is the risk of disease and the need to survive periods of pathogen-induced anorexia. This model shows why two independent intervention points are more likely to evolve than a single set point. The molecular basis of the lower intervention point is likely based around the leptin pathway signalling. Determining the molecular basis of the upper intervention point is a crucial key target for future obesity research. A potential definitive test to separate the different models is also described.

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Section: Set-point Theorymentioning

confidence: 99%

The evolution of body fatness: trading off disease and predation risk

Speakman

2018

Journal of Experimental Biology

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“…The predation risk treatment involved the broadcasting of playback calls from nocturnal raptors (Monarca et al ., 2015b), specifically, Barn Owl ( Tyto alba ) and Eurasian Eagle‐Owl ( Bubo bubo) (European bird calls; Jean C. Roché, Kosmos Verlag, Stuttgart, Germany). The owl calls were broadcasted for 2 min, every 2 h, during night time (9 pm to 7 am ).…”

Section: Methodsmentioning

confidence: 99%

“…The ideas that adiposity and muscularity are involved in the ability to avoid predators have been refined (Higginson, McNamara & Houston, 2012), and the predation‐starvation framework has been extended to understand the adiposity regulation in several species. Empirical data have largely supported the premise that exposure and elevated perception of increased predation risk leads to reduced body mass in birds and mammals (Gosler, Greenwood & Perrins, 1995; Tidhar, Bonier & Speakman, 2007; Monarca, Mathias & Speakman, 2015b; Genné‐Bacon, Trinko & DiLeone, 2016; Walters et al ., 2017). This is potentially because larger/fatter mammals are slower and less able to outrun predators (Hodges, Cunningham & Mills, 2014), or because they are unable to exploit small refuges to avoid predation (Sundell & Norrdahl, 2002; Carlsen et al ., 2012).…”

Section: Introductionmentioning

confidence: 99%

“…In the wild, resources are unpredictable, through their life small mammals must encounter periods of shortage in food abundance. The impacts of starvation risk on regulated weight have been less impressive, the support for the thought that stochasticy drives the increase of body fat is limited (Zhang et al ., 2012; Monarca, Mathias & Speakman, 2015b). Although there have been many studies on the impacts of predation risk on development in aquatic organisms (e.g.…”

Section: Introductionmentioning

confidence: 99%

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Effects of predation risk on the body mass regulation of growing wood mice

2020

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Body mass in wild animals has been suggested to be regulated by the opposing fitness consequences of variation in body size (and fat storage) for starvation and predation risk. Many studies of adult mammals and birds have broadly confirmed the predictions of this model. However, relatively few studies have addressed the potential role of such trade-offs during early phases of development when animals are growing. Similarly, studies of the impact of high-fat diets on wild small mammals generally show a resistance to weight gain. But whether growing animals are similarly resistant is unclear. In this study, weaned wood mice (Apodemus sylvaticus) were exposed to a high risk of predation, simulated by the broadcasting of owl calls, for 66 days during which body mass and energy intake were monitored. We hypothesized that if the risk of predation plays a role in regulating body mass during this phase then animals growing under predation risk would grow less. We found female (but not male) mice exposed to the predation risk treatment had lower growth rates and ended the experiment lighter; however, variations in energy intake and resting metabolic rate did not explain the observed differences. Feeding on high-fat diet resulted in individuals with higher body mass. Females reached their adult size earlier than males and were more responsive to the predation risk treatment when feeding on high-fat diet. Our data suggest males body mass to have fitness consequences on social dominance and reproductive success not accounted for in the simple starvation-predation trade-off model.

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“…[ (Blanchard et al 1995;Carlsen et al 1999;Higginson et al 2012Higginson et al , 2016Monarca et al 2015;Ramler et al 2014;Thaler et al 2012;Tidhar et al 2007). Although this has been generally interpreted as a "stress response" (Kestemont and Baras 2007) it is likely that it is a strategic response of the system evolved to optimize foraging gains against foraging risk (Tidhar et al 2007).…”

Section: Explanatory Power Evidence and Testable Predictions Of The mentioning

confidence: 99%

Foraging theory and the propensity to be obese: an alternative to thrift

Watve

Baig

Lokhande³

et al. 2018

Preprint

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The evolutionary origin of obesity is classically believed to be genetic or developmentally induced thrift, as an adaptation to ancestral feast and famine conditions. However, recently the thrift family of hypotheses have attracted serious criticism necessitating alternative thinking. Optimization of foraging behaviour is an important aspect of behavioural evolution. For a species evolved for optimizing nutritional benefits against predation or other foraging risks, reduction in foraging risk below a threshold dramatically increases the steady-state body weight. In modern life where feeding is detached from foraging, the behavioural regulation mechanisms are likely to fail resulting into escalation of adiposity. At a proximate level the signalling pathways for foraging optimization involve fear induced signal molecules in the brain including Cocaine and Amphetamine Regulated Transcript (CART) interacting with adiposity signals such as leptin. While leptin promotes the expression of the fear peptides, the fear peptides promote anorectic action of leptin.This interaction promotes foraging drive and risk tolerance when the stored energy is low and suppresses hunger and foraging drive when the perceived risk is high.The ecological model of foraging optimization and the molecular model of interaction of these peptides converge in the outcome that the steady state adiposity is an inverse square root function of foraging risk. The foraging optimization model is independent of thrift or insurance hypotheses, but not mutually exclusive. We review existing evidence and suggest testable predictions of the model.Understanding obesity simultaneously at proximate and ultimate levels is likely to suggest effective means to curb the obesity epidemic.

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Predation risk modulates diet‐induced obesity in male C57BL/6 mice

Cited by 14 publications

References 40 publications

The evolution of body fatness: trading off disease and predation risk

The evolution of body fatness: trading off disease and predation risk

Effects of predation risk on the body mass regulation of growing wood mice

Foraging theory and the propensity to be obese: an alternative to thrift

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