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Glucocorticoid receptor number in ob/ob mice and streptozotocin-treated rats

Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme
|August 1, 1985
PubMed

Insights

Glucocorticoid receptor number and affinity remain normal in two diabetes models. This study found no abnormalities in glucocorticoid receptors in liver, kidney, or pancreas tissues from diabetic mice and rats compared to normal controls.

Area of Science:

  • Endocrinology
  • Metabolic Research
  • Molecular Pharmacology

Background:

  • Glucocorticoid hormones play a crucial role in regulating carbohydrate metabolism.
  • Abnormalities in carbohydrate metabolism, such as diabetes, may involve altered glucocorticoid hormone signaling.
  • Understanding glucocorticoid receptor (GR) function is key to characterizing these metabolic states.

Purpose of the Study:

  • To investigate the number and affinity of glucocorticoid receptors in specific tissues of animal models with abnormal carbohydrate metabolism.
  • To compare glucocorticoid receptor characteristics in diabetic models to those in normal controls.

Main Methods:

  • Utilized ob/ob mice and streptozotocin-treated rats as models for abnormal carbohydrate metabolism.
  • Prepared cytosolic extracts from liver, kidney, and pancreatic tissues.
  • Employed Scatchard analysis to determine the number and affinity of glucocorticoid receptors for dexamethasone.

Main Results:

  • Scatchard analysis indicated that the number of glucocorticoid receptors per milligram of cytosolic protein was unchanged in the diabetic models compared to controls.
  • The affinity of these glucocorticoid receptors for dexamethasone remained consistent across all tested tissues and conditions.
  • No significant differences in glucocorticoid receptor number were observed between diabetic and normal control groups.

Conclusions:

  • The study concludes that the characterized forms of diabetes in mice (ob/ob) and rats (streptozotocin-induced) are not associated with abnormalities in glucocorticoid receptor number.
  • These findings suggest that potential dysregulation of glucocorticoid hormone action in these models does not stem from altered glucocorticoid receptor quantity.

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