| Budget Amount *help |
¥6,900,000 (Direct Cost: ¥6,900,000)
Fiscal Year 1995: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1994: ¥5,300,000 (Direct Cost: ¥5,300,000)
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| Research Abstract |
The goals of this work are to modulate sarcoplasmic reticulum (SR) functions in rainbow trout skeltal muscle by dietary oils and to control qualities, such as freshness, of cultured fish muscle.
・ Two-months feeding test after 1 month feeding with essential fatty acids (EFA) deficient diet cause alteration in fatty acid compositions of muscles and the SRs. Phosphatidylcholine fractions from each muscle and the SR were more easily altered by feeding diets than phosphatidylethanolamine fractions.
・ Ca^<2+>-ATPase activities of the SR from fish fed n-3 rich diet were lower than those of the SRs from n-6 rich and EFA deficient groups.
・ Apparent ATP and creatine phosphate (CP) degradations were slightly accelerated by n-6 rich and EFA deficient diet feedings. Accumulation of lactic acid in muscles was slightly retarded by n-6 rich and EFA deficient diet feedings. However, ATP breakdown rate of n-3 group, which was calculated from CP degradation and lactic acid accumulation rates, was higher than that of n-6 group.
These results suggest that fatty acid compositions of SR membrane can be controled by dietary lipids, that we can control physiological SR functions, reducing cytosolic Ca^<2+> concentration, and that n-6 feeding would decrease cytosolic Ca^<2+> concentration and ATP breakdown rate. It is, therefore, reminescent to us that n-6 rich diet feeding for 1 or 2 months would make fish muscle in resting stage. However, because these diet feedings would influence fish body weight, energy consumption efficiency, and other signal transduction mechanisms, further investigations are required to evaluate effects of n-6 fatty acid feeding on fish muscle.
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