『味覚機能への亜鉛酵素「炭酸脱水酵素」の寄与』

抄録

Zinc deficiency induces growth retardation, reduced reproductive function, dermatitis, taste abnormality, immune dysfunction, and so on. In the present paper we summarize the effects of dietary zinc deficiency and carbonic anhydrase (CA) on the taste function were studied in SD rats. At an early stage of zinc deficiency after 3 to 7 days of the feeding, it was shown that abnormal increase of taste preference for NaCl solution were observed, though this occurred before any change in the chorda tympani (taste) nerve sensitivity to NaCl. This suggested the contribution of the central nervous system might be involved in this behavioral change. Actually, we observed the decreased oxytocin secretion through the hypophysis, which was paralleled well with the increase of salt preference. After 7 to 14 days feeding of zinc-deficient diet, the rats showed the decreased chorda tympani and lingual trigeminal nerves sensitivity to carbonated water, in addition to the decreased CA activity in the submandibular gland. At a severe stage, i.e., after 3 weeks or much longer-term of the zinc deficiency, it was shown the decrease in the chorda tympani nerve sensitivity to most of the basic tastes except for sweet taste (sucrose), the degenerative histological changes in the lingual trigeminal nerve fibers, the decreased CA II protein expression in the submandibular gland, and the decreased salivary secretion (28 days or later). We have also undertaken the tongue surface CA inhibition studies, and found out that the CA activity is indispensable factor to maintain the taste perception normally. Finally, we investigated the role of zinc in food intake regulation using rats during earlystage zinc deficiency without decreased zinc concentrations in plasma and tissues. The results showed that orally administered zinc may stimulate food intake via orexigenic peptides coupled to the afferent vagal stimulation through the gastrointestinal tract in rats after short-term treatment with a zinc-deficient diet.