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Developmental changes in thymidine kinase, DNA, and fat cellularity in Zucker rats
The American Journal of Physiology
|May 1, 1979
Summary
Genetically obese Zucker rats exhibit distinct DNA accretion and thymidine kinase activity patterns compared to lean rats, with early fat cell enlargement and later hyperplasia contributing to obesity development.
Area of Science:
- Biochemistry
- Genetics
- Physiology
Background:
- The genetically obese Zucker rat (fafa) serves as a model for studying obesity.
- Understanding DNA accretion and thymidine kinase activity is crucial for comprehending adipose tissue development.
Purpose of the Study:
- To investigate the distinct patterns of DNA accretion and thymidine kinase activity in genetically obese Zucker rats compared to lean Zucker rats.
- To characterize the temporal changes in fat cell size, number, and DNA content during obesity development in Zucker rats.
Main Methods:
- Comparative analysis of thymidine kinase activity and DNA accretion in epididymal fat depots of lean and obese Zucker rats at various ages.
- Measurement of fat cell size and number to assess hyperplasia and hypertrophy.
Main Results:
- Obese Zucker rats show significantly different DNA accretion and thymidine kinase activity compared to lean rats.
- Early stages of obesity are marked by increased fat cell size and elevated thymidine kinase activity.
- Fat cell hyperplasia becomes evident after an initial peak in cell size (around 98 days) in obese rats, with increased DNA accretion up to 182 days.
Conclusions:
- The development of genetic obesity in Zucker rats involves distinct cellular mechanisms of adipose tissue expansion, differing from normal growth patterns.
- Thymidine kinase activity and DNA accretion dynamics are key indicators of the hypertrophic and hyperplastic processes driving obesity in this model.