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Response of hepatic proteins to 3,5,3'-tri-iodo-L-thyronine in diabetic rats
T Takeda1, K Ichikawa, M Kobayashi
1Department of Geriatrics, Shinshu University School of Medicine, Japan.
Abstract:
In order to study whether peripheral action of thyroid hormones is altered in insulin deficiency and to elucidate the biological consequences of alteration of the cytosolic 3,5,3'-tri-iodo-L-thyronine (T3) binding protein (CTBP), we measured malic enzyme, T3-responsive nuclear n protein, CTBP and nuclear thyroid hormone receptor in the liver and kidney of streptozotocin (STZ)-induced diabetic rats that were treated with or without insulin and/or a receptor-saturating dose of T3. The following results were obtained. 1. Induction of malic enzyme by T3 was apparently diminished in diabetic rats. However, supplementary injection of insulin enabled previously given T3 to take effect in diabetic rats. 2. T3-responsiveness of other hepatic proteins (n protein and CTBP) was not altered by insulin in diabetic rats. 3. The level of n protein was increased by insulin in diabetic rats in vivo and in perfused rat liver, indicating that the hepatic n protein is a novel insulin-responsive protein. T3 and insulin increased the level of n protein non-synergistically in diabetic rat liver. 4. Hepatic nuclear receptor levels were not altered in diabetic rats. 5. Hepatic CTBP levels were decreased in diabetic rats. This was not due to the toxic effect of STZ. Low CTBP level was only partially increased by insulin after 30 days of diabetic period. Renal CTBP levels were not altered in diabetic rats with or without insulin treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Insights
Insulin deficiency impairs thyroid hormone action on malic enzyme in diabetic rats. Insulin therapy partially restores this effect and influences hepatic n protein levels.
Area of Science:
- Endocrinology
- Metabolic Research
- Molecular Biology
Background:
- Insulin deficiency in diabetes mellitus can alter peripheral thyroid hormone metabolism.
- Cytosolic 3,5,3'-tri-iodo-L-thyronine (T3) binding protein (CTBP) plays a role in thyroid hormone action.
- Understanding these interactions is crucial for managing diabetic complications.
Purpose of the Study:
- To investigate if insulin deficiency alters peripheral thyroid hormone action.
- To elucidate the biological consequences of altered cytosolic T3 binding protein (CTBP) in diabetes.
- To examine the effects of insulin and T3 on specific proteins in diabetic rat liver and kidney.
Main Methods:
- Streptozotocin (STZ)-induced diabetic rat model.
- Measurement of malic enzyme, nuclear n protein, CTBP, and thyroid hormone receptors in liver and kidney.
- Treatment with insulin and/or T3.
Main Results:
- T3-induced malic enzyme induction was diminished in diabetic rats but restored with insulin.
- Hepatic n protein levels increased with insulin in diabetic rats, indicating it's an insulin-responsive protein.
- Hepatic CTBP levels decreased in diabetic rats, with only partial recovery upon insulin treatment.
Conclusions:
- Insulin is essential for the peripheral action of thyroid hormones on malic enzyme in diabetes.
- Hepatic n protein is a novel insulin-responsive protein.
- Decreased hepatic CTBP in diabetes may contribute to altered thyroid hormone signaling, requiring insulin therapy for partial restoration.