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Biomedical subjects

B Zumoff

Publications and source records attributed to B Zumoff.

At least 163 records · Page 9Linked to original sources
PubMed1967

Conversion of cholesterol injected into man to cholestanol via a 3-ketonic intermediate.

Cholesterol-3-(3)H,4-(14)C was injected intravenously in man and its transformation to cholestanol was studied. From the (3)H: (14)C ratios in cholestanol isolated from blood, evidence for the participation of a ketonic intermediate in the conversion was obtained. In a second subject given cholestanol-3-(3)H,4-(14)C the (3)H: (14)C ratios in blood sterols remained unchanged for as long as 1 wk after the injection, which showed that cholestanol did not lose tritium by interconversion with cholestanone.

Adult↗
PubMedDate not supplied

Acidic metabolites. VI. 20 alpha-isosteroids as intermediates in 20 alpha-dihydrosteroid formation.

We have previously shown that human subjects metabolize the 20 beta-epimer of isocortisol (11 beta, 17,20 beta-trihydroxy-3-oxo-pregn-4-en-21-al) to both 20 alpha- and 20 beta-hydroxy steroid end products. In this paper we describe the synthesis of tritium labeled 20 alpha-epimers of isocortisol and isoTHF (3 alpha, 11 beta, 17,20 alpha-tetrahydroxy-5 beta-pregnan-21-al) and their metabolic fate in humans. Both steroids yielded 20 alpha-hydroxy urinary neutral end-products (cortols and cortolones) and no 20 beta-hydroxy epimers. Regeneration of 17-ketols from aldols occurred to a small extent with isoTHF, but not with isocortisol. Isocortisol and isoTHF yielded less cortoic acids than did the corresponding ketols. The results provide further evidence that in man the stereochemistry at C-20 of the end-products of corticosteroid metabolism is determined by the configuration of the aldol at C-20 prior to subsequent metabolic events.

Adult↗
PubMedDate not supplied

Norethandrolone produces temporary loss of the ability to escape from salt-retaining steroids.

Patients with diseases characterized by salt retention manifest a loss of the normal ability of healthy persons to escape from repeat injections of aldosterone or other salt-retaining steroids. This phenomenon may be a clue to the pathophysiological mechanisms of salt retention. Administration of norethandrolone to a subject who had demonstrated the ability to escape from the salt-retaining effect of corticosteroid administration temporarily and reversibly deleted his ability to escape. Thus norethandrolone administration provides the basis for a model system for exploring the mechanisms of escape (and therefore of salt retention).

Body Weight↗
PubMedDate not supplied

The hypouricemic effect of o,p'-DDD.

o,p'-DDD, administered by mouth in doses of 1 to 7 grams daily for 5 to 42 days, was found to lower serum uric acid concentration in each of eight normouricemic patients (one with Cushing's disease and seven with metastatic cancer). The decrease ranged from 21 to 53% (average 39%) and the maximum effect was apparent in five to ten days. Urinary uric acid excretion showed no change, indicating that uric acid production was unaffected and that the hypouricemic effect resulted from an increase in the renal clearance of uric acid. The present findings introduce a new type of chemical compound to the group of known hypouricemic agents.

Adolescent↗
PubMedDate not supplied

Elevated daytime urinary excretion of testosterone glucuronide in men with the type A behavior pattern.

Urinary excretion of testosterone glucuronide was compared in 13 men with typical Type A behavior pattern (as determined by structured interviews) and 10 age-matched men with typical Type B behavior pattern. Twenty-four hour urine collections were divided into three periods: 9AM - 6PM , 6PM to bedtime, and bedtime to 9AM . Type A men showed a significantly higher excretion than Type B men in the daytime ( 9AM - 6PM ); the geometric mean value was 24 micrograms in Type A and 15 micrograms in Type B (P less than 0.05). There were no significant differences between Type A and Type B men for the other two time periods. Indicating an elevated daytime testosterone secretion in Type A men, this finding is consistent with a recent report that exposure to laboratory tests of reaction time causes an increase in plasma testosterone levels in Type A but not Type B men. Since a role for testosterone in the genesis of coronary heart disease (CHD) is suggested by the much higher incidence of CHD in men and the acceleration of murine atherogenesis by testosterone, the findings of this and the previous report may represent a mechanism for the elevated incidence of CHD in Type A men.

Adult↗
PubMedDate not supplied

Abnormal hormone levels in men with coronary artery disease.

Plasma concentrations and urinary excretions of various hormones and hormone metabolites were measured in four groups. Group 1 was composed of 13 men with prior myocardial infarction; Group 2 contained 35 clinically normal men; Group 3 consisted of 44 men with normal coronary arteriograms; and Group 4 was composed of 25 men with severe coronary artery disease shown on arteriogram but no infarction. There were four major findings: Group 1 had significantly higher 24-hour mean plasma concentrations of estrone (E1), dehydroisoandrosterone (DHA), and dehydroisoandrosterone sulfate (DHAS) than Group 2, while Group 3 had the same levels as Group 4; Group 4 had significantly lower urinary excretion of androsterone glucuronide (AG) than Group 3, while Group 1 excreted normal amounts. There are three possible explanations for these findings: 1) myocardial infarction occurring in men with coronary artery disease may elevate the plasma levels of E1, DHA, and DHAS and eliminate the preinfarction depression of urinary AG levels; 2) higher than average levels of E1, DHA, DHAS, and AG may favor the development of infarction in men with coronary artery disease; 3) higher than average levels of E1, DHA, DHAS, and AG may favor survival from any infarction that occurs in men with coronary artery disease. Experimental and epidemiological evidence seems to favor the third possibility.

Adult↗
PubMedDate not supplied

Inpatient intervention in an indigent, minority population with uncontrolled diabetes.

OBJECTIVE: To study whether a program of brief, intensive, inpatient intervention could improve glycemic control in an indigent, minority population with uncontrolled diabetes unresponsive to outpatient treatment. METHODS: Patients with uncontrolled diabetes unresponsive to treatment in our outpatient Diabetes Clinic were admitted to our inpatient Diabetes Unit, where their care was directed by the Diabetes Team (an attending diabetologist, an endocrinology fellow, two nurses, and two nutritionists). Of 108 patients admitted, data were available for 96. Patients from minority populations constituted 91.7% of the group. All patients were indigent. The mean duration of stay was 4.3 days. After dismissal, patients underwent follow-up again in our Diabetes Clinic. During the 540-day follow-up period, 25 patients were electively readmitted when satisfactory improvement in glycemic control was not achieved. Hemoglobin A1c levels were averaged and plotted for the group at defined time points up to 360 days before admission and up to 540 days after admission. RESULTS: During the year before admission, hemoglobin A1c increased slowly from 10.1 +/- 0.3% (mean +/- standard error) at day -360 to 10.3 +/- 0.2% at day -210 (F5 = 29; P<0.01) and then rapidly to 11.4 +/- 0.2% at admission (F7 = 1,541; P<0.001). After admission, hemoglobin A1c declined rapidly to 9.5 +/- 0.2% at day 90 (F4 = 121; P<0.005), plateaued at that level until day 240, and then declined again slowly to 9.0 +/- 0.3% at day 540, the end of the follow-up period (F10 = 70; P<0.01). All hemoglobin A1c levels 30 days or more after admission were significantly lower than the mean level at admission (P<0.05 at day 30 and P<0.001 from day 45 to day 540). CONCLUSION: Brief, intensive, inpatient intervention in an indigent, minority population with uncontrolled diabetes unresponsive to outpatient treatment produced and sustained a significant improvement in glycemic control. This mode of treatment is a practical approach to achieving the improvement in glycemic control that the Diabetes Control and Complications Trial demonstrated to be effective in delaying the onset and slowing the progression of diabetic retinopathy, nephropathy, and neuropathy.

Journal Article↗