Zinc deficiency enhances salt preference through altered peripheral and central taste processing mechanisms

Zinc deficiency alters salt preference, however, the underlying mechanisms remain unclear. We hypothesized that altered salt preference, during zinc deficiency, is associated with brainstem and hypothalamic nuclei modified activity which is involved in the gustatory processing and fluid balance regulation.

This study elucidated the abnormal intake of high-concentrated sodium chloride solution caused by zinc deficiency in taste reception, taste nerve, and brain. Initially, we performed taste behavioral tests including the chorda tympani (CT) nerve transection (CTx) and the sodium channel blocker. Secondly, the neural activity in the aforementioned regions was investigated by assessing the c-Fos-like protein expression, as a marker of neuronal activity, in the parabrachial nuclei (PBN) for the taste pathway, as well as in the supraoptic nucleus (SON) and the paraventricular nucleus (PVN) for fluid regulation-related areas.

Zinc-deficient Sprague-Dawley rats showed increased licking responses and preference for high salt concentrations compared to the controls. Neither the CTx nor the administration of amiloride, a sodium channel blocker, affected NaCl preference in zinc-deficient rats. High salt stimulation induced significantly fewer c-Fos-immunoreactive neurons in the PBN, SON, and PVN of zinc-deficient rats compared to controls.

These findings suggest that zinc deficiency disrupts NaCl reception and alters neuronal responses to NaCl in the gustatory pathway and fluid balance regulation, potentially leading to modified NaCl ingestive behaviors. Our results provide new insights into the neural mechanisms underlying taste dysfunction and altered salt preference in zinc deficiency.