Under the influence of light: How light pollution disrupts personality and metabolism in hermit crabs.

Anthropogenic disturbances are known to cause significant physiological and behavioural changes in animals and, thus, are the critical focus of numerous studies. Light pollution is an increasingly recognised source of disturbance that has the potential to impact animal physiology and behaviour. Here, we investigate the effect of constant light on a personality trait and metabolic rate in the European hermit crab Pagurus bernhardus. We used Bayesian mixed models to estimate average behavioural change (i.e. sample mean level behavioural plasticity) and between- and within-individual variation in boldness in response to laboratory light. Hermit crabs experiencing constant light were consistently less bold and had a higher metabolic rate than those kept under a standard laboratory light regime (12:12 h light/dark). However, there was no effect of light on individual consistency in behaviour. As boldness is associated with coping with risk, hermit crabs exposed to light pollution at night may experience increased perceived predation risk, adjusting their behaviour to compensate for the increased conspicuousness. However, reduced boldness could lead to lower rates of foraging and this, in combination with elevated metabolic rate, has the potential for a reduction in energy balance.

Leptin and its relation to obesity and insulin in the SHR/N-corpulent rat, a model of type II diabetes mellitus.

The spontaneously hypertensive/NIH-corpulent (SHR/N-cp) rat is a genetic animal model that exhibits obesity, metabolic features of hyperinsulinemia, hyperglycemia, and hyperlipidemia, which are characteristic of type II diabetes and mild hypertension. To determine the role of leptin, the protein product of the ob gene, in the development of obesity and diabetes in this model, we measured steady-state circulating levels of leptin in obese and lean SHR/N-cp rats and examined the relation between plasma leptin levels and metabolic variables at the stage of established obesity in these animals. Mean fasting plasma leptin concentration was 8-fold higher in obese than in lean rats (p < 0.01). This was associated with a 6-fold elevation in plasma insulin in the obese group. Fasting levels of plasma glucose, cholesterol, and triglyceride were all significantly higher in obese rats than in lean controls. Spearman correlation analysis showed a significant positive correlation between plasma leptin concentration and body weight among the animals (r = 0.73, p < 0.01). Similarly, plasma insulin concentration was significantly correlated with BW in all animals (r = 0.54, p < 0.05). There was also a significant positive correlation between plasma leptin and plasma insulin in the entire group (r = 0.70, p < 0.01). However, this relationship was significant only for lean rats but not for obese rats (r = 10.59, p < 0.05 for lean rats, and r = 0.23, p = NS, for obese rats). Plasma leptin also correlated positively with fasting plasma glucose (r = 0.75, p < 0.05), total cholesterol (r = 0.63, p < 0.05), and triglyceride (r = 0.67, p < 0.05). The marked elevation of plasma leptin in obese SHR/N-cp rats suggests that obesity in this animal model is related to up-regulation of the ob gene. Circulating leptin appears to be one of the best biological markers of obesity and that hyperleptinemia is closely associated with several metabolic risk factors related to insulin resistance in the diabesity syndrome.