Insulin receptor exon 11+/- isoform mRNA in spontaneously hypertensive and adrenocorticotropin-hypertensive rats

J Hypertens. 1998 Jul;16(7):1009-14. doi: 10.1097/00004872-199816070-00015.

Abstract

Objective: To test the hypothesis that insulin resistance of the spontaneously hypertensive rat (SHR) and adrenocorticotropin-hypertensive rat is related to a difference in the proportion of the functionally different, alternatively spliced exon 11 isoforms of the insulin receptor.

Design: We determined the proportions of mRNA for the exon 11+ and exon 11- isoforms in various tissues of SHR and Wistar-Kyoto rats aged 3, 6, 9 and 12 weeks, which span the pre-hypertensive phase through to established hypertension, as well as in Sprague-Dawley rats with adrenocorticotropin-induced hypertension and Sprague-Dawley controls.

Methods: Detection of mRNA involved a reverse-transcriptase polymerase chain reaction technique specific for each isoform and quantification was by slot and dot blot hybridization.

Results: Mean proportions of exon 11+ mRNA in SHR, Wistar-Kyoto rats, adrenocorticotropin-hypertensive rats and Sprague-Dawley control rats at each age were 95% for liver, 82% for adipose tissue, 77% for kidney, 66% for adrenal, 53% for heart, 26% for cerebral cortex, 23% for hypothalamus, and 3% for skeletal muscle. There was also no difference in concentration of total insulin receptor mRNA.

Conclusions: The absence of any difference in proportions of insulin receptor mRNA isoforms argues against the hypothesis that an alteration of differential splicing plays a role in the models of hypertension studied.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenocorticotropic Hormone
  • Alternative Splicing
  • Animals
  • Base Sequence
  • DNA, Complementary / genetics
  • Exons
  • Hypertension / chemically induced
  • Hypertension / genetics*
  • Hypertension / metabolism*
  • Insulin Resistance / genetics
  • Male
  • RNA, Messenger / genetics*
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Inbred SHR
  • Rats, Inbred WKY
  • Receptor, Insulin / genetics*

Substances

  • DNA, Complementary
  • RNA, Messenger
  • Adrenocorticotropic Hormone
  • Receptor, Insulin