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AJP - Regulatory, Integrative and Comparative Physiology, Vol 269, Issue 4 930-R937, Copyright © 1995 by American Physiological Society
ARTICLES |
Y. Ninomiya, N. Sako and Y. Imai
Department of Oral Physiology, Asahi University School of Dentistry, Gifu, Japan.
Sweet taste sensitivity in a genetic model of diabetes, the db/db mouse, in which a single major gene defect leads to the expression of diabetes and obesity, was studied by examining chorda tympani nerve responses to various taste stimuli, including sugars. The chorda tympani responses to four sugars, sucrose, fructose, glucose, and maltose, in adult db/db mice showed greater relative magnitudes and lower thresholds than those in adult lean mice, but responses to other basic taste stimuli, such as NaCl, HCl, and quinine HCl, were not different in the two groups. Behavioral experiments using a two-bottle preference test demonstrated that taste preference scores for the four sugars at suprathreshold concentrations, except 1.0 M, were higher in db/db than in control mice. Infant mice of 7-9 days of age possessing the genotype db/db also exhibited greater neural responses and lower thresholds for sugars than infant control mice, whereas streptozotocin-induced adult diabetic mice possessing the genotype +/+ did not exhibit larger sugar responses. These findings suggest that the enhanced sugar sensitivities observed in db/db mice are probably determined by a single major gene, db. The db gene may act on a common factor(s) involved in the stimulus-secretion coupling in the pancreatic B cell and the taste cell of db/db mice.
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