Obesogens in a naturally obese animal: An experimental approach to assess the impact of marine pollutants on fat tissue function in seals

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The ability of organisms to survive and thrive in a changing and increasingly exploited and polluted environment depends on appropriate regulation of energy balance. Growing evidence suggests that exposure to pollutants can alter how fat is stored and used in humans and in other animals. Recent research in humans suggests that many marine pollutants can interfere with the way fat tissue responds to hormonal signals. In particular, pollutants make it difficult to lose weight by switching on pathways that increase fat storage, and this could contribute to problems like diabetes and obesity. Large amounts of persistent organic pollutants (POPs) were made in the early part of the 20th century for use in high capacity electrical conductors and inks, insulators and plastics. Although many POPs are not made anymore because they are very toxic, they are extremely stable and remain in the environment for a long time, ending up in the sea from transport in air and water. Other pollutants, such as phthalates, which are important plasticisers, easily make their way into the sea in run off from urban areas and from marine litter. In particular, POPs do not break down very easily, accumulate in fat and become more concentrated as they are passed up the food chain, ending up in liver and fat. Seals are important top marine predators that have to build up a thick blubber layer while feeding at sea, and then use the fat as a metabolic fuel to keep them alive when they come ashore to breed, moult and rest. They have metabolic similarities to obese and diabetic patients. Their need to rely on fat for fuel and insulation makes them vulnerable to the effects of marine pollutants on the way fat tissue works. The higher the level of POPs in the blubber of seal pups, the lower their chance of survival. Fat tissue like blubber is important for storing fat, releasing it into the bloodstream for use by other parts of the body and producing fat-regulating hormones that control how much fat is stored or used. Recently, the genes of some fat-regulating hormones were shown to be switched on more in blubber of seals from polluted areas in the Baltic Sea than in clean areas in the Arctic, suggesting marine pollutants alter energy balance in seals. However, the mechanisms that control how fat tissue works in seals, and the way marine contaminants interfere with this control, are not well understood. If contaminants can prevent seals from releasing fat from blubber to give them fuel when they are fasting on land, they may have to use more of their protein from muscle tissue instead. This could put them at risk of starvation during moulting, breeding and development, even when they are fat. We will investigate whether pollutants alter fat storage and mobilisation in young grey seals, which are most at risk. We will take small blubber samples from live feeding and fasting seals, without harming them, and treat the blubber with pollutants and fat regulating hormones. We will measure levels of genes and hormones involved in energy balance, the ability of blubber to release fat, and its metabolic rate. By comparing these measures between treatments we will begin to find out how energy balance is normally regulated in seals, how it is altered by marine contaminants, and whether seals are more vulnerable during feeding or fasting. This will help predict the effects of pollutants on seal population size, by contributing a better understanding of how contaminants affect survival of young seals and change their energetic requirements. Because seals naturally experience extreme changes in fat mass, have metabolic similarities to diabetes and obesity, and eat fish, like people do, this work will also inform the likely impacts of POPs and phthalates on human fat regulation. This work has far reaching consequences for health and survivorship in seals and other animals, but also for the management of obesity, diabetes and related metabolic abnormalities in humans.