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Journal of Nutrition Vol. 109 No. 8 August 1979, pp. 1483-1491
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myo-Inositol Deficiency: Studies on the Mechanism of Lactation-Dependent Fatty Liver Formation in the Rat1

Louis E. Burton2 and William W. Wells3

Department of Biochemistry, Michigan State University, East Lansing, Michigan 48824

Intravenous administration of [1-14C]palmitate to 8-day lactating rats fed a myo-inositol supplemented or deficient diet resulted in rapid labeling of liver triglycerides and phospholipids. Compared with myo-inositol deficient rats, those supplemented with myo-inositol showed a greater loss of isotope from liver triglycerides with a more rapid appearance of isotope in serum triglyceride. Loss of 14C from liver phospholipids was similar for both groups, whereas the appearance of labeled phospholipids in serum was slightly greater for myo-inositol supplemented controls compared with myo-inositol deficient rats. The labeling pattern of liver microsomal triglycerides and phospholipids of the two dietary groups was similar; however, liver microsomal protein was significantly reduced in myo-inositol deficient rats relative to the control group. Concurrent administration of Triton WR-1339 with [1-14C]palmitate resulted in significantly less label accumulation in serum triglycerides of myo-inositol deficient rats compared with myo-inositol supplemented rats. Labeled triglycerides in whole liver and in liver microsomes of myo-inositol supplemented rats turned over more rapidly than those of myo-inositol deficient rats while no significant difference was noted for the [14C]palmitate labeled phospholipid of either source. The incorporation of [guanido-14C]arginine into total liver and serum protein 1 hour after injection of the precursor was similar whether the 14-day lactating dams were myo-inositol supplemented or deficient, but total serum protein specific radioactivity of myo-inositol deficient rats was 66% that of myo-inositol supplemented rats. Thus, the significantly reduced release of hepatic triglycerides appears to be the cause of the fatty liver observed during lactation-dependent myo-inositol deficiency.


KEY WORDS: myo-inositol deficiency • rat • fatty liver • triglyceride • phospholipid • Triton • palmitate • microsomes • serum • liver • intestine

1 This work was supported by Grant HD06007, U.S. Public Health Service, Michigan Agricultural Experiment Station Journal Article No. 8901.

2 Present address: Department of Neurobiology, Stanford Medical School, Stanford, California (CA) 94305.

3 To whom inquiries should be addressed.

Manuscript received 12 February 1979.





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