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The Molecular Basis of Taste and Its Disorders

ROBERT I. HENKIN, M.D., PH.D.; P. P. G. GRAZIADEI, PH.D.; and DAN F. BRADLEY, PH.D.
Ann Intern Med. 1969;71(4):791-821. doi:10.7326/0003-4819-71-4-791
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SUMMARY:

Changes in taste acuity accompany various disease processes and are useful in diagnosis. Lingual lesions may decrease acuity for salt and sweet, maxillary dentures decrease acuity for sour and bitter. Patients with gonadal dysgenesis and pseudohypoparathyroidism also exhibit decreased acuity for sour and bitter. Patients with type I familial dysautonomia (Riley-Day syndrome) and many patients treated with D-penicillamine exhibit decreased acuity for each quality, whereas those with untreated adrenal cortical insufficiency exhibit increased detection acuity for each quality. These abnormalities have provided clues for physiological definition of taste localization in man and for reevaluation of the role of taste buds. From these data the taste process was separated into two sets of events, preneural and neural. Mechanisms controlling the preneural or initial events are assumed to regulate the flux of sapid substances (tastants) across the taste bud membrane by changes in the conformation of an hypothesized protein (gatekeeper protein) that lines the holes of the taste bud pore membrane. This control is partly exerted by an equilibrium between thiols and metal ions. Shifting this equilibrium alters the conformation of the gatekeeper protein causing it to open or close, thereby altering taste acuity by altering tastant flux.

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