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Physiol. Genomics 1: 11-19, 1999. First published July 15, 1999;
1094-8341/99 $5.00
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Received 25 November 1998; accepted in final form 23 April 1999.
Physiological Genomics 1:11-19 (1999)
1094-8341/99 $5.00 © 1999 American Physiological Society

The agouti gene product stimulates pancreatic ß-cell Ca2+ signaling and insulin release

B. Z. XUE1, W. O. WILKISON2, R. L. MYNATT3, N. MOUSTAID1, M. GOLDMAN4 and M. B. ZEMEL1

1 Departments of Nutrition
4 Surgery, University of Tennessee, Knoxville, Tennessee 37996
2 Zen-Bio, Inc., Research Triangle Park, North Carolina 27709
3 Pennington Biomedical Research Center, Baton Rouge, Louisiana 70808

Xue, B. Z., W. O. Wilkison, R. L. Mynatt, N. Moustaid, M. Goldman, and M. B. Zemel. The agouti gene product stimulates pancreatic ß-cell Ca2+ signaling and insulin release. Physiol. Genomics 1: 11-19, 1999.—Ubiquitous expression of the mouse agouti gene results in obesity and hyperinsulinemia. Human agouti is expressed in adipose tissue, and we found recombinant agouti protein to stimulate lipogenesis in adipocytes in a Ca2+-dependent fashion. However, adipocyte-specific agouti transgenic mice only became obese in the presence of hyperinsulinemia. Because intracellular Ca2+ concentration ([Ca2+]i) is a primary signal for insulin release, and we have shown agouti protein to increase [Ca2+]i in several cell types, we examined the effects of agouti on [Ca2+]i and insulin release. We demonstrated the expression of agouti in human pancreas and generated recombinant agouti to study its effects on Ca2+ signaling and insulin release. Agouti (100 nM) stimulated Ca2+ influx, [Ca2+]i increase, and a marked stimulation of insulin release in two ß-cell lines (RIN-5F and HIT-T15; P < 0.05). Agouti exerted comparable effects in isolated human pancreatic islets and ß-cells, with a 5-fold increase in Ca2+ influx (P < 0.001) and a 2.2-fold increase in insulin release (P < 0.01). These data suggest a potential role for agouti in the development of hyperinsulinemia in humans.

calcium; obesity; pancreas




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