The Effect of Predation Risk on Body Weight in the Field Vole, Microtus agrestis

Carlsen, Michael; Lodal, J.; Leirs, Herwig; Jensen, Tommy R.

doi:10.2307/3546742

Cited by 42 publications

(35 citation statements)

References 24 publications

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“…From an experiment where mammalian and avian predators were excluded, we know that the field voles generally lost less or gained more weight in autumn and winter than voles from corresponding control grids (Carlsen et al 1999). Also, predators can strongly influence the microhabitat use and foraging behavior of prey.…”

Section: A Rodent Disease Modelmentioning

confidence: 99%

Rodent-borne diseases and their risks for public health

Meerburg¹,

Singleton²,

Kijlstra³

2009

Critical Reviews in Microbiology

804

722

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Rodents are the most abundant and diversified order of living mammals in the world. Already since the Middle Ages we know that they can contribute to human disease, as black rats were associated with distribution of plague. However, also in modern times rodents form a threat for public health. In this review article a large number of pathogens that are directly or indirectly transmitted by rodents are described. Moreover, a simplified rodent disease model is discussed.

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Section: A Rodent Disease Modelmentioning

confidence: 99%

Rodent-borne diseases and their risks for public health

Meerburg¹,

Singleton²,

Kijlstra³

2009

Critical Reviews in Microbiology

804

722

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“…One idea is that fat storage not only brings advantages but also disadvantages, the most conspicuous of which is the risk of predation (9,10,24,29,43,45). This might come about in several ways.…”

Section: Long-term Regulation Of Energy Balance and Fat Storagementioning

confidence: 99%

If Body Fatness is Under Physiological Regulation, Then How Come We Have an Obesity Epidemic?

Speakman

2014

Physiology

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Life involves a continuous use of energy, but food intake, which supplies that energy, is episodic. Feeding is switched on and off by a complex array of predominantly gut-derived peptides (and potentially nutrients) that initiate and terminate feeding bouts. Energy is stored as glucose and glycogen to overcome the problem of the episodic nature of intake compared with the continuous demand. Intake is also adjusted to meet immediate changes in demands. Most animals also store energy as fat. In some cases, this serves the purpose of storing energy in anticipation of a known future shortfall (e.g., hibernation, migration, or reproduction). Other animals, however, store fat in the absence of such anticipated needs, and in this case the fat appears to be stored in preparation for unpredictable catastrophic shortfalls in supply. Fat storage, however, brings disadvantages as well as advantages, in particular an increased risk of predation. Hence, many animals seem to have evolved a dual intervention point system preventing them from storing too little or too much fat. The physiological basis of the lower intervention point is well established, but the upper intervention point is much less studied. Human obesity can potentially be understood in an evolutionary context as due to drift in the upper intervention point following release from predation 2 million years ago (the drifty gene hypothesis) combined with a stimulus in modern society to overconsume calories, possibly attempting to satisfy intake of a limiting microor macro-nutrient like protein (the protein leverage hypothesis).

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“…Nevertheless, there have been several experimental studies indicating that actual (or perceived) increases in predation risk have a suppressive impact on body weight/fatness, particularly in small mammals such as mice and voles (Heikkila et al, 1993;Tidhar et al, 2007;Macleod et al, 2007;Monarca et al, 2015a,b;Sundell and Norrdahl, 2002;Carlsen et al, 1999Carlsen et al, , 2000. This effect may come about not because greater fatness reduces the quality of escape responses, but because predation risk depends on time spent moving, and the greater energy demands of fatter/heavier animals, such as voles, will increase their exposure to predation (Daly et al, 1990;Korpimäki, 1998, 2000).…”

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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The Effect of Predation Risk on Body Weight in the Field Vole, Microtus agrestis

Cited by 42 publications

References 24 publications

Rodent-borne diseases and their risks for public health

Rodent-borne diseases and their risks for public health

If Body Fatness is Under Physiological Regulation, Then How Come We Have an Obesity Epidemic?

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

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