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Nutrient Requirements

Vitamin A Deficiency Impairs Fetal Islet Development and Causes Subsequent Glucose Intolerance in Adult Rats^1,2

Kimberly A. Matthews^*,**, William B. Rhoten, Henry K. Driscoll^*, and Bruce S. Chertow^*,,3

^* Departments of Medicine and Anatomy, Cell and Neurobiology, Joan C. Edwards School of Medicine, Marshall University and ^** Research and Medical Services, Huntington VA Medical Center, Huntington, WV

³To whom correspondence should be addressed. E-mail: chertow{at}marshall.edu.

To determine the role of vitamin A in fetal islet development, ß- and -cell mass, apoptosis, and - and ß-cell replication were measured in rats using a model of marginal vitamin A deficiency. Female rats before and during pregnancy and their offspring postweaning were fed a diet containing retinol as retinyl palmitate at a low marginal (LM, 0.25 mg/kg diet) or a sufficient (SUFF, 4.0 mg/kg diet) level. Fetal islet size, replication, apoptosis, and offspring glucose tolerance were examined. Both ß-cell area and number per islet were reduced 50% in fetuses from dams fed an LM vitamin A diet compared with those from dams fed the SUFF vitamin A diet. The -cell area and number per fetal islet were not affected by vitamin A deficiency. Apoptosis was not increased. The percentage of newly replicated ß-cells in the LM fetal pancreas was 42% less than that of SUFF offspring, but -cell replication was not affected. To determine whether this decrease in ß-cell area affected adult glucose tolerance and insulin secretion, 65-d-old offspring were subject to glucose tolerance tests. LM rats had a 55% lower plasma insulin level and a 76% higher serum glucose than SUFF rats. The same pattern could be seen in 35-d-old rats. These findings show that vitamin A deficiency decreases ß-cell mass and this reduction can be attributed to a reduced rate of fetal ß-cell replication in LM offspring. This may contribute to impaired glucose tolerance later in adult life.

KEY WORDS: • retinoids • pancreatic ß-cells • insulin secretion • diabetes • ß-cell replication

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