Zinc metabolism was studied in 32 normal volunteers after oral (n = 25) or intravenous (n = 7) administration of 65Zn. Data were collected from the blood, urine, feces, whole body, and over the liver and thigh regions for 9 mo while the subjects consumed their regular diets (containing 10 mg Zn ion/day) and for an additional 9 mo while the subjects received an exogenous oral supplement of 100 mg Zn ion/day. Data from each subject were fitted by a compartmental model for zinc metabolism that was developed previously for patients with taste and smell dysfunction. These data from normal subjects were used to determine the absorption, distribution, and excretion of zinc and the mass of zinc in erythrocytes, liver, thigh, and whole body. By use of additional data obtained from the present study, the model was refined further such that a large compartment, which was previously determined to contain 90% of the body zinc, was subdivided into two compartments to represent zinc in muscle and bone. When oral zinc intake was increased 11-fold three new sites of regulation of zinc metabolism were identified in addition to the two sites previously defined in patients with taste and smell dysfunction (absorption of zinc from gut and excretion of zinc in urine). The three new sites are exchange of zinc with erythrocytes, release of zinc by muscle, and secretion of zinc into gut. Regulation at these five sites appears to maintain some tissue concentrations of zinc when dietary zinc increases.

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Patients with adrenal cortical insufficiency exhibit an increased taste sensitivity for sodium chloride (NaCl) (1). Treatment with carbohydrate-active steroids returns the abnormal threshold to normal levels (1). In a variety of acute and chronic debilitating diseases, a number of them exhibiting major abnormalities of water and electrolyte metabolism, taste threshold for NaCi is comparable to that observed in healthy subjects (1). Taste thresholds for all modalities are decreased in cystic fibrosis, but they do not change after treatment with steroids (2).The present study was designed to examine in detail taste thresholds in adrenal insufficiency and to explore the effect of adrenal cortical hormones on taste. METHODSThe subjects of this study were 13 normal volunteers, aged 6 to 35, two patients with anterior pituitary insufficiency, aged 21 and 36, and seven patients with Addison's disease, aged 25 to 65. All patients with Addison's disease had clinical features of this disease, urinary 17-hydroxycorticosteroids that were below 2 mg per 24 hours and did not increase with adrenocorticotropin (ACTH), 40 U given intravenously over 8 hours, each day for 5 days. Both patients with anterior pituitary insufficiency had hypothyroidism, hypogonadism, and adrenal insufficiency, with urinary 1 7-hydroxycorticosteroids in J.M. and S.P. of 1.1 and 2.2 mg per day, respectively, rising to 27 and 10.9 mg per day, respectively, with ACTH. All patients remained on an air-conditioned metabolic ward and ate a normal diet, which was well tolerated even when they were not receiving treatment. Sodium intake was 100 to 200 mEq per day. Body weight, determined with metabolic scales daily on arising, was used to provide a gross estimate of changes in the volume of body fluids. The patients were studied under each of three conditions: a) untreated for 4 or more days, b) treated with desoxycorticosterone acetate (DOCA), 20 mg per day for 1 to 7 days, and c) treated with prednisolone (A1F), 20 mg per day for 2 to 5 days.In addition, detection thresholds for the taste of NaCl were measured between 7 and 8 a.m. in three normal Caucasian males, aged 18 to 20, before and during treatment with Pitressin. The two levels of sodium intake during Pitressin were 9 mEq and 150 mEq per day. Taste was evaluated by measuring the detection threshold. A detection threshold is defined as the lowest concentration of test solution that can be consistently distinguished from distilled water. Thresholds were measured by one observer in the early morning hours in the normal subjects and in the morning or evening hours, or both, in the patients with adrenal insufficiency. Occasional retesting of the patient by another observer gave comparable results on each occasion. At the time of testing, the patients had not smoked or eaten for at least 1 hour. After the mouth was rinsed with distilled water, the solutions of test substance or glass-distilled water were administered as single drops and placed on alternate sides of the anterior one-third of the tongue.Each...

Viruses have been implicated in the development of neurodegenerative diseases, such as Alzheimer's, Parkinson’s, and multiple sclerosis. Human herpesvirus-6 (HHV-6) is a neurotropic virus that has been associated with a wide variety of neurologic disorders, including encephalitis, mesial temporal lobe epilepsy, and multiple sclerosis. Currently, the route of HHV-6 entry into the CNS is unknown. Using autopsy specimens, we found that the frequency of HHV-6 DNA in the olfactory bulb/tract region was among the highest in the brain regions examined. Given this finding, we investigated whether HHV-6 may infect the CNS via the olfactory pathway. HHV-6 DNA was detected in a total of 52 of 126 (41.3%) nasal mucous samples, showing the nasal cavity is a reservoir for HHV-6. Furthermore, specialized olfactory-ensheathing glial cells located in the nasal cavity were demonstrated to support HHV-6 replication in vitro. Collectively, these results support HHV-6 utilization of the olfactory pathway as a route of entry into the CNS.

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