Trade-off between energy budget, thermogenesis and behavior in Swiss mice under stochastic food deprivation

Cao, Jing; Zhang, Lina; Zhao, Zhanzheng

doi:10.1016/j.jtherbio.2009.03.006

Cited by 19 publications

(18 citation statements)

References 71 publications

(115 reference statements)

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“…Nevertheless, three previous studies have concerned the responses of domestic strains of mice to stochastic food deprivation. Swiss mice increased their food intake dramatically, and decreased their energy expenditure, on days between 24 h starvation events [50]. However, overall after 4 weeks, similar to the findings here, their overall body weight was decreased.…”

Section: Starvation Risksupporting

confidence: 86%

Behavioural and physiological responses of wood mice (Apodemus sylvaticus) to experimental manipulations of predation and starvation risk

Monarca

Mathias

Speakman

2015

Physiology & Behavior

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Section: Starvation Risksupporting

confidence: 86%

Behavioural and physiological responses of wood mice (Apodemus sylvaticus) to experimental manipulations of predation and starvation risk

Monarca

Mathias

Speakman

2015

Physiology & Behavior

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“…In the present study, we observed significant reductions in body mass, carcass mass, and body fat content in striped hamsters restricted to 85% of initial food intake. Weight losses were also observed in food-restricted C57/B6 mice [42], Swiss mice [28], [40], golden spine mice ( Acomys russatus, Muridae ) [17], [43] and Mongolian gerbils [6]. Inconsistently, body mass did not decrease in MF1 mice restricted to 80% of ad libitum food intake [10], and rats restricted to 75% of initial food intake [39].…”

Section: Discussionmentioning

confidence: 99%

“…This suggests that adaptive regulation of energy expenditure is more important than energy intake in the trade-off of the energy strategy in food-restricted animals [10], [40]. The maintenance requirements include the energy exported for RMR and activity.…”

Section: Discussionmentioning

confidence: 99%

Energy Budget, Behavior and Leptin in Striped Hamsters Subjected to Food Restriction and Refeeding

et al. 2013

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Food restriction induces a loss of body mass that is often followed by rapid regaining of the lost weight when the restriction ends, consequently increasing a risk of development of obesity. To determine the physiological and behavioral mechanisms underlining the regaining, striped hamsters were restricted to 85% of initial food intake for 4 weeks and refed ad libitum for another 4 weeks. Changes in body mass, energy budget, activity, body composition and serum leptin level were measured. Body mass, body fat mass and serum leptin level significantly decreased in food-restricted hamsters, and increased when the restriction ended, showing a short “compensatory growth” rather than over-weight or obesity compared with ad libitum controls. During restriction, the time spent on activity increased significantly, which was opposite to the changes in serum leptin level. Food intake increased shortly during refeeding, which perhaps contributed to the rapid regaining of body mass. No correlation was observed between serum leptin and energy intake, while negative correlations were found in hamsters that were refed for 7 and 28 days. Exogenous leptin significantly decreased the time spent on activity during food restriction and attenuated the increase in food intake during refeeding. This suggests that low leptin in restricted animals may function as a starvation signal to induce an increase in activity behavior, and high leptin likely serves as a satiety signal to prevent activity during refeeding. Leptin may play a crucial role in controlling food intake when the restriction ends, and consequently preventing overweight.

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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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Trade-off between energy budget, thermogenesis and behavior in Swiss mice under stochastic food deprivation

Cited by 19 publications

References 71 publications

Behavioural and physiological responses of wood mice (Apodemus sylvaticus) to experimental manipulations of predation and starvation risk

Behavioural and physiological responses of wood mice (Apodemus sylvaticus) to experimental manipulations of predation and starvation risk

Energy Budget, Behavior and Leptin in Striped Hamsters Subjected to Food Restriction and Refeeding

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

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