Abstract
Alcohol is one of the most commonly abused intoxicants with 1 in 6 adults at risk for alcohol use disorder (AUD) in the United States. As such, animal models have been extensively investigated with rodent AUD models being the most widely studied. However, inherent anatomical and physiological differences between rodents and humans pose a number of limitations in studying the complex nature of human AUD. For example, rodents differ from humans in that rodents metabolize alcohol rapidly and do not innately demonstrate voluntary alcohol consumption. Comparatively, pigs exhibit similar patterns observed in human AUD including voluntary alcohol consumption and intoxication behaviors, which are instrumental in establishing a more representative AUD model that could in turn delineate the risk factors involved in the development of this disorder. Pigs and humans also share anatomical similarities in the two major target organs of alcohol- the brain and liver. Pigs possess gyrencephalic brains with comparable cerebral white matter volumes to humans, thus enabling more representative evaluations of susceptibility and neural tissue damage in response to AUD. Furthermore, similarities in the liver result in a comparable rate of alcohol elimination as humans, thus enabling a more accurate extrapolation of dosage and intoxication level to humans. A porcine model of AUD possesses great translational potential that can significantly advance our current understanding of the complex development and continuance of AUD in humans.
Highlights
Alcohol is one of the most preventable causes of death in the United States, it causes 88,000 deaths each year and claims the life of 1 in 10 working age adults (Mokdad et al, 2004; Gonzales et al, 2014)
While rodent models are useful in understanding the mechanisms of alcohol induced damage, it is challenging for them to replicate the complex physiological, behavioral, and psychological nature of alcohol use disorder (AUD) in humans
We have highlighted some of the advantages of the pig model in studying the pathology and progression of AUD by examining alcohol-induced damage to the brain and liver
Summary
Alcohol is one of the most preventable causes of death in the United States, it causes 88,000 deaths each year and claims the life of 1 in 10 working age adults (Mokdad et al, 2004; Gonzales et al, 2014). A defining characteristic of AUD is continued alcohol usage despite negative consequences, which cannot be studied in forced consumption paradigms (American Psychiatric Association, 2013) To overcome this challenge, researchers have implemented several tactics to encourage voluntary consumption in rodents, including selective breeding and food and water deprivation (Crabbe et al, 2011). After animals were no longer allowed to have access to alcohol, withdrawal symptoms such as static and volitional tremor, dilated pupils, and muscle fasciculation were observed These studies showed that pigs displayed continued voluntary alcohol consumption despite experiencing the negative effects of alcohol intoxication. We discuss the limitations of current rodent models in studying AUD mechanisms in the brain and liver and examine the porcine model as a potentially more representative animal model due to intrinsic behavioral, anatomical, and physiological attributes (Figure 1)
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