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Genetic obesity and dietary sucrose decrease hepatic glucagon and insulin receptors in LA/N-corpulent rats.
Summary
Genetically obese rats show impaired glucagon activity, with lower glucagon binding contributing to hyperlipemia. Sucrose may worsen this effect, impacting obesity and lipid levels.
Area of Science:
- Metabolic Research
- Endocrinology
- Obesity Studies
Background:
- Glucagon normally has catabolic and hypolipemic effects.
- Genetically obese rats (LA/N-cp/cp) exhibit hyperlipemia.
- The role of glucagon in genetic obesity requires further investigation.
Purpose of the Study:
- To investigate the role of glucagon in genetically obese, hyperlipemic rats.
- To assess the impact of diet (starch vs. sucrose) on glucagon and insulin dynamics.
- To determine the relationship between hormone levels, receptor binding, and lipogenic enzymes.
Main Methods:
- Fed genetically obese (corpulent) and lean rats starch or sucrose for 12 weeks.
- Measured plasma glucagon and insulin levels.
- Assessed glucagon and insulin binding to liver membranes and correlated with lipogenic enzymes.
Main Results:
- Corpulent rats had significantly higher plasma insulin and lower insulin and glucagon binding compared to lean rats.
- Sucrose feeding marginally affected insulin but decreased glucagon binding in corpulent rats.
- Negative correlations were found between glucagon and lipogenic enzymes, and glucagon binding and these enzymes.
Conclusions:
- Impaired glucagon activity, indicated by decreased glucagon binding, contributes to hyperlipemia and obesity in these rats.
- Hyperinsulinemia is also a significant factor in the corpulent phenotype.
- Sucrose may exacerbate obesity and hyperlipemia by further reducing glucagon binding.