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Ca(2+)-channels and adrenoceptors in diabetic skeletal muscle
1Division of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, University of Manitoba, Winnipeg, Canada.
Abstract:
The status of Ca(2+)-channels and adrenoceptors in the hind leg skeletal muscle was examined in rats 8 weeks after inducing diabetes by an intravenous injection of streptozotocin (65 mg/kg). Scatchard plot analysis of the data on specific binding of 3H-nitrendipine with crude membranes from diabetic muscle revealed an increase in the density of Ca(2+)-channels without any significant change in their affinity for the ligand. An increase in the density of beta-adrenoceptors without any alteration in their affinity, as measured by 3H-dihydroalprenolol binding, was also evident in the diabetic muscle. The observed increase in the number of Ca2+ channels or beta-adrenoceptors seems specific since no change in the alpha-adrenoceptor density or affinity, as measured by 3H-prazosin binding, was seen in the diabetic membranes. These results support the view that higher activities of Ca2+ transport systems or regulatory mechanisms may be associated with hyperfunction of the diabetic skeletal muscle.
Insights
Diabetic rat muscle shows increased calcium (Ca2+) channels and beta-adrenoceptors, but not alpha-adrenoceptors. This suggests altered ion channel and receptor activity contributes to diabetic muscle hyperfunction.
Area of Science:
- Biochemistry
- Physiology
- Endocrinology
Background:
- Diabetes mellitus is a metabolic disorder with significant complications affecting various tissues.
- Skeletal muscle function is crucial for overall health and can be impaired in diabetic conditions.
- Understanding molecular changes in diabetic muscle is key to addressing associated complications.
Purpose of the Study:
- To investigate alterations in calcium (Ca2+) channels and adrenoceptors in skeletal muscle of diabetic rats.
- To determine if changes in receptor density or affinity occur in response to diabetes.
- To explore the potential link between these molecular changes and muscle hyperfunction in diabetes.
Main Methods:
- Induction of diabetes in rats using streptozotocin injection.
- Scatchard plot analysis to quantify receptor binding.
- Radioligand binding assays using 3H-nitrendipine (for Ca2+ channels), 3H-dihydroalprenolol (for beta-adrenoceptors), and 3H-prazosin (for alpha-adrenoceptors).
Main Results:
- Diabetic rat skeletal muscle exhibited a significant increase in the density of Ca2+ channels.
- A notable increase in beta-adrenoceptor density was observed in diabetic muscle.
- No significant changes in the density or affinity of alpha-adrenoceptors were detected.
Conclusions:
- Diabetes induces specific increases in Ca2+ channel and beta-adrenoceptor density in skeletal muscle.
- These molecular alterations may contribute to the observed hyperfunction of diabetic skeletal muscle.
- The findings highlight potential targets for managing diabetic muscle complications.