Article Summary

The research team from North Carolina University identified an interesting scientific finding. They purportedly identified a genetic switch in fruit flies. This genetic switch is said to play a key role that chiefly makes the flies alcohol-tolerant.

The team was headed by Dr. Tatiana Morozova, a post-doctoral researcher in biology. Other members of the team were Dr. Trudy Mackay, a genetics professor of the William Neal Reynolds Distinguished University, Dr. Eric Stone, a statistics expert, Julien Ayroles, and researchers from Boston University School of Medicine.

The team is highly interested on the impact of polymorphisms on phenotypic variations. Thus, this led to this study that chiefly aims to characterize the system of genes in response to the exposure of the flies to alcohol. The team measured the time in which the flies stagger following alcohol intake while concurrently identifying the differences in the expression of their genes.  A statistical method was employed to determine if the genes have worked collectively to help foster in flies tolerance and adaptability to alcohol. They look closely to the counterpart gene they referred to as ME1. This gene is presumed to indicate the genetic propensity of an individual to drink strong alcoholic beverages.

The results of their study seemed to indicate that the team has identified the metabolic pathways that drive a person to excessive alcoholism. Although the results were derived from experimental models, such as flies, the authors are convinced that their results can be applicable to humans.

The implication of their study is linked to its possible therapeutic use in human alcoholism. Their discovery of the genetic switch may be applied to regulate the metabolic pathways in an alcoholic individual. Although the details have not been provided in this article their findings may be used as proof and basis for therapeutic management inpatients with deadly liver diseases, such as cirrhosis. Cirrhosis is a clear manifestation of chronic alcoholism formed when a counterpart human gene cause the shift from alcohol metabolism to fat formation, especially in heavy drinkers.


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