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Neurosci Lett. 2002 Jan 25;318(2):57-60.

Increase of beta-endorphin biosynthesis in the adrenal gland of streptozotocin-induced diabetic rats.

Author information

1
Division of Neuroscience and Neuropathology, Graduate School of Medicine, China Medical College, Taichung City, 40401 Taiwan.

Abstract

Opioid plays an important role in the regulation of glucose homeostasis in diabetic rats lacking insulin. The present study investigated the changes of beta-endorphin biosynthesis in the adrenal medulla of streptozotocin-induced diabetic rats (STZ-diabetic rats) by determination of the gene expression of pro-opiomelanocortin (POMC) and the amount of beta-endorphin. Expression of the distinct mRNA that encodes proteins of POMC was studied using reverse transcription combined with polymerase chain reaction (RT-PCR). Results of RT-PCR demonstrated that the mRNA level of POMC in the adrenal gland markedly increased in STZ-diabetic rats as compared with that in normal rats. The content of beta-endorphin-like immunoreactivity (BER) in the adrenal medulla, determined by enzyme-linked immunosorbent assay, was actually higher in diabetic rats with insulin deficiency. Normalization of the plasma glucose concentration in STZ-diabetic rats with exogenous insulin or phlorizin, an inhibitor of the renal tubular glucose transport, reversed the mRNA level of POMC in the adrenal gland after 4 days of treatment. A similar decrease of BER amount also observed in the adrenal medulla of STZ-diabetic rats received the same treatment with exogenous insulin or phlorizin. Therefore, correction of hyperglycemia in STZ-diabetic rats could reverse the higher gene expression of POMC in the adrenal gland. These results suggest that hyperglycemia is responsible for the increase of POMC gene expression to enhance beta-endorphin biosynthesis in the adrenal gland of STZ-diabetic rats.

PMID:
11796185
DOI:
10.1016/s0304-3940(01)02473-9
[Indexed for MEDLINE]

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