Crosstalk between Autophagy and Obesity: Potential Use of Avian Model

Irina Angel

Crosstalk between Autophagy and Obesity: Potential Use of Avian Model.

Human Obesity is a devastating multifactorial disease with continuous increasing prevalence and, thus, there is a need for more extensive research using several experimental models to understand its underlying molecular mechanisms. Emerging evidence indicates a key role of autophagy in the
development of obesity and has been a focus of research interest in recent years. This review
will briefly describe the autophagy processes and provide insight into metabolic characteristics
of avian species that make birds a model of choice for investigation of autophagy particularly
with respect to obesity.

Recent studies found that hepatic autophagy is defective and its up-regulation improves insulin sensitivity in common rodent obese models. Furthermore, insulin inhibited autophagy via mTOR activation and mTOR inhibition by rapamycin lead to a hyperinsulinemic and hyperglycaemic states in rat skeletal muscle. These results indicate that insulin and autophagy might participate in a feedback mechanism of reciprocal regulation. Thus, autophagy may regulate insulin sensitivity in a tissue specific manner. For instance, HFD decreased and increased LC3-II levels in mouse liver and adipose tissue, respectively.

Brown Adipose Tissue (BAT), a specialized fat that dissipates energy to produce heat, plays an important role in the regulation of energy balance. Interestingly, chickens do not have functional
BAT. Thus, these unique metabolic characteristics make chickens an interesting model for understanding the role of autophagy in obesity development.
In conclusion, studies using avian models may provide critical information on the role of autophagy in lipogenesis and lipid metabolism because the liver is the primary site of de novo fatty acid synthesis in chickens and may help for targeting new therapeutic strategies to treat obesity and its related diseases.

Adv Food Technol Nutr Sci Open J. 2015; 1(1): 32-37.doi: 10.17140/AFTNSOJ-1-106