Insulin increases distinct species of 1,2-diacylglycerol in isolated perfused rat heart

Kenji Okumura, Hideo Matsui, Kichiro Murase, Akemi Shimauchi, Kiyokazu Shimizu, Yukio Toki, Takayuki Ito, Tetsuo Hayakawa

Research output: Contribution to journalArticlepeer-review

8 Citations (Scopus)

Abstract

Insulin and glucose increase the synthesis of 1,2-diacylglycerol (1,2- DAG), the physiological activator of protein kinase C (PKC) in a variety of tissues and cells. The effects of insulin and glucose on the abundance and fatty acid composition of 1,2-DAG were investigated in isolated perfused rat hearts with the use of capillary gas chromatography and 1,2-dipentadecanoin as an internal standard. A high concentration of insulin (25 mU/mL) significantly increased cardiac contractility and reduced coronary flow. In addition, perfusion with 25 mU/mL insulin induced significant increases of 18.2% and 26.4% in 1,2-DAG mass after 5 and 30 minutes, respectively, in the presence of 8.6 mmol/L glucose, whereas there was no increase in 1,2-DAG with 2.5 mU/mL insulin. Analysis of the fatty acid composition of 1,2-DAG showed that only species containing specific fatty acids (16:0, 18:1, and 18:2) were increased in response to insulin. In contrast, an increase in glucose concentration in the perfusion medium from 3 to 17 mmol/L had no effect on the total mass or fatty acid composition of 1,2-DAG, cardiac contractility, or coronary flow. Addition of a high insulin concentration to the high- glucose medium increased the abundance of 1,2-DAG containing 16:0, 18:1, and 18:2 fatty acids, as well as cardiac contractility. It is concluded that the effect of insulin on cardiac contractility may be related to the associated increase in 1,2-DAG abundance.

Original languageEnglish
Pages (from-to)774-781
Number of pages8
JournalMetabolism: Clinical and Experimental
Volume45
Issue number6
DOIs
Publication statusPublished - 1996
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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