In humans and animals the liver is a complex metabolic organ that is fundamental for keeping up the entire body’s homeostasis. Age-related changes in the liver capacity adds to systemic vulnerability to age-related diseases. The liver hepatocytes have been shown to undergo genomic instability with aging. The stability of the hepatocytes depends on its nuclear architecture and the nuclear architecture in eukaryotic cells is maintained by the nuclear membrane lamin scaffold, and chromatin organization.Calorie restriction (CR) has been shown to favorably extend lifespan and this maybe through the reorganization of the nuclear structure.
Therefore in order to find the effect of cyclic feeding regime on the chromatin assembly anchored to the nuclear membrane scaffold of old and young rats hepatocytes nuclei. We investigated the chromatin decondensation and nuclear membrane disintegration of the hepatocytes using fluorescence imaging methods.
It took 60 seconds for protease to decondense the chromatin and disintergrate the nuclear membrane of controls. After the first fasting the time increased to 145 seconds in 3 months old rats, the first refeeding increased the time to 156 seconds with further rise to 340 seconds following the second fasting then dropped to 116 seconds by the second refeeding. 20 months old rats showed 186 seconds increase in time of chromatin decondensation and nuclear membrane disintegration after the first fasting with a decrease to 140 seconds observed after first refeeding. The second fasting increased the time to 165 seconds, which then slightly decreased to 163 second after the second refeeding.
This enabled us to show that intermittent fasting may have acted on chromatin histone interactions and the structural lamin networks of the nuclear membranes in bringing about nuclear stability, which is essential for normal cellular function.
In humans and animals the liver is a complex metabolic organ that is fundamental for keeping up the entire body’s homeostasis. Age-related changes in the liver capacity adds to systemic vulnerability to age-related diseases. The liver hepatocytes have been shown to undergo genomic instability with aging. The stability of the hepatocytes depends on its nuclear architecture and the nuclear architecture in eukaryotic cells is maintained by the nuclear membrane lamin scaffold, and chromatin organization.Calorie restriction (CR) has been shown to favorably extend lifespan and this maybe through the reorganization of the nuclear structure.
Therefore in order to find the effect of cyclic feeding regime on the chromatin assembly anchored to the nuclear membrane scaffold of old and young rats hepatocytes nuclei. We investigated the chromatin decondensation and nuclear membrane disintegration of the hepatocytes using fluorescence imaging methods.
It took 60 seconds for protease to decondense the chromatin and disintergrate the nuclear membrane of controls. After the first fasting the time increased to 145 seconds in 3 months old rats, the first refeeding increased the time to 156 seconds with further rise to 340 seconds following the second fasting then dropped to 116 seconds by the second refeeding. 20 months old rats showed 186 seconds increase in time of chromatin decondensation and nuclear membrane disintegration after the first fasting with a decrease to 140 seconds observed after first refeeding. The second fasting increased the time to 165 seconds, which then slightly decreased to 163 second after the second refeeding.
This enabled us to show that intermittent fasting may have acted on chromatin histone interactions and the structural lamin networks of the nuclear membranes in bringing about nuclear stability, which is essential for normal cellular function.
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