Adipose tissue compensates for defect of phosphatidylinositol 3′-kinase induced in liver and muscle by dietary fish oil in fed rats

Dec 13, 2005American journal of physiology. Endocrinology and metabolism

Fat tissue compensates for enzyme defects in liver and muscle caused by fish oil in fed rats

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Abstract

In liver, fish oil decreased phosphatidylinositol 3'-kinase activity by 54% compared with a control diet.

Fish oil substitution in a low-fat diet had different effects on insulin signaling in liver and muscle compared to adipose tissue.
In liver and muscle, fish oil inhibited phosphatidylinositol 3'-kinase activity while amplifying the effects of dexamethasone.
Adipose tissue showed an increase in phosphatidylinositol 3'-kinase activity by 74%, countering the 65% decrease caused by dexamethasone.
Dexamethasone did not alter phosphatidylinositol 3'-kinase activity differently between the fish oil and control diet groups.
GLUT4 protein content remained unchanged in muscle but increased by 61% in adipose tissue with fish oil consumption.
Overall, fish oil may play a significant role in maintaining whole body glucose homeostasis through its effects on adipose tissue.

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The present work aimed to study in rats whether substitution of a low level of fish oil (FO; 2.2% of calories) into a low-fat diet (6.6% of calories from fat as peanut-rape oil or control diet) 1) has a tissue-specific effect on insulin signaling pathway and 2) prevents dexamethasone-induced alteration of insulin signaling in liver, muscle, and adipose tissue. Sixteen rats were used for study of insulin signaling, and sixteen rats received an oral glucose load (3 g/kg). Eight rats/group consumed control diet or diet containing FO over 5 wk. Four rats from each group received a daily intraperitoneal injection of saline or dexamethasone (1 mg.kg(-1).day(-1)) for the last 5 days of feeding. In liver, FO decreased phosphatidylinositol 3'-kinase (PI 3'-kinase) activity by 54% compared with control diet. A similar result was obtained in muscle. In both liver and muscle, FO clearly amplified the effect of dexamethasone. FO did not alter early steps of insulin signaling, and in muscle GLUT4 protein content remained unaltered. In adipose tissue, FO increased PI 3'-kinase activity by 74%, whereas dexamethasone decreased it by 65%; inhibition of PI 3'-kinase activity by dexamethasone was similar in rats fed FO or control diet, and GLUT4 protein content was increased by 61% by FO. Glycemic and insulinemic responses to oral glucose were not modified by FO. In conclusion, FO increased PI 3'-kinase activity in adipose tissue while inhibiting it in liver and muscle. The maintenance of whole body glucose homeostasis suggests an important role of adipose tissue for control of glucose homeostasis.

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Adipose tissue compensates for defect of phosphatidylinositol 3′-kinase induced in liver and muscle by dietary fish oil in fed rats

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