Does activation of p53 enhance apoptosis and insulin resistance in a rat model of alcoholic liver disease?
p53 activation correlates with the susceptibility to ethanol-induced liver damage in different rat strains. p53 not only orchestrates apoptosis and suppresses cell survival, but by activating TIGAR and decreasing hepatic Fru-2,6-P₂) levels it promotes insulin resistance and therefore, contributes to the metabolic abnormalities associated with hepatic steatosis.
Both in clinical practice and in epidemiological studies, it is important to consider that the origin of chronic productive cough could be frequently outside the lower respiratory tract; a consistent percentage of young adults with persistent productive cough has indeed chronic rhino-sinusitis.