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Hepatic glycogen metabolism in the db/db mouse
W J Roesler1, S Pugazhenthi, R L Khandelwal
1Department of Biochemistry, Case Western Reserve University, Cleveland, OH 44106.
Molecular and Cellular Biochemistry
|February 9, 1990
Summary
Type 2 diabetes in C57BL/KsJ-db/db mice shows altered hepatic glycogen structure and enzyme activity. These metabolic changes highlight the db/db mouse as a valuable model for studying insulin resistance.
Area of Science:
- Biochemistry
- Metabolic Diseases
- Animal Models
Background:
- Metabolic changes in insulin-resistant type 2 diabetes are less understood than in type 1 diabetes.
- The C57BL/KsJ-db/db mouse is a key model for type 2 diabetes research.
Purpose of the Study:
- To investigate the impact of insulin-deficient and insulin-resistant states on hepatic glycogen metabolism in db/db mice.
- To characterize longitudinal changes in liver glycogen metabolism during the development of type 2 diabetes.
Main Methods:
- Longitudinal study of db/db mice from 2 to 15 weeks of age.
- Analysis of hepatic glycogen levels, particle structure, and enzyme activities (glycogen synthase, phosphorylase).
Main Results:
- Db/db mice exhibited smaller glycogen particles with shorter chain lengths compared to controls.
- Elevated total phosphorylase and phosphorylase a activities were observed, linked to increased enzyme protein.
- Changes in kinetic properties of glycogen synthase and phosphorylase, including decreased Vmax, were noted.
Conclusions:
- Altered glycogen structure in db/db mice correlates with modified enzyme activities and properties.
- The db/db mouse serves as a relevant model for type 2 diabetes, reflecting insulin resistance and hormonal fluctuations.
- Further research is needed to clarify the roles of insulin and glucagon in these metabolic alterations.