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Changes in Hepatic Parenchymal and Nonparenchymal Cell Vitamin A Content During Vitamin A Depletion in the Rat^1,2,

Institute for Nutrition Research, School of Medicine, University of Oslo, 0316 Oslo 3, Norway

Levels of total, unesterified and esterified retinol were determined in liver, liver parenchymal cells (PC) and liver nonparenchymal cells (NPC) during vitamin A depletion in rats. Liver vitamin A levels decreased from 113 to 4 µg over a 97-d experimental period; plasma retinol concentrations did not change significantly during this time. Initially, >90% of hepatic vitamin A was in the esterified form and most (93%) was localized in NPC. During vitamin A depletion, there were significant declines in retinyl ester content of both PC and NPC, but unesterified retinol levels were not significantly affected. Plasma retinol concentrations were significantly correlated with unesterified retinol mass in PC and NPC, but not with retinyl ester mass. Although 94% of the liver's negative vitamin A balance was due to changes in NPC retinyl ester levels, the fractional rate of retinyl ester loss from PC and NPC was almost identical. Since unesterified retinol levels in plasma, PC and NPC appeared to be conserved even when liver retinyl ester stores were virtually depleted, and since the retinol utilization rate was apparently not decreasing during this stage of vitamin A depletion, these data support the hypotheses that homeostatic mechanisms controlling the three pools of unesterified retinol are linked, and that vitamin A utilization rate is maintained as long as unesterified retinol levels in plasma, PC and NPC are normal.

KEY WORDS: • liver retinol • perisinusoidal stellate cells • retinol utilization • plasma retinol

¹ This research was supported by grants from Anders Jahres Fond, Nansenfondet, the Norwegian Cancer Society and the Nordic Insulin Foundation. Research visits by M. H. G. and J. B. G. to Oslo were supported by a Fulbright Research Scholar Award to M. H. G., by a grant from the National Science Foundation (INT-8419955) and by a NATO Grant for International Collaboration.

² Data were presented in part at the June 1986 FASEB Summer Research Conference on Retinoids, Saxtons River, VT.

³ Address of author to whom correspondence should be sent: The Pennsylvania State University, Nutrition Department, 126 South Henderson Building, University Park, PA 16802.

⁴ Permanent address: Nutrition Department, The Pennsylvania State University, University Park, PA 16802.

Manuscript received 8 March 1988. Revision accepted 6 July 1988.

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