Quality control in the MRFIT local screening and clinic laboratory.

Quality control was emphasized in the screening and clinic laboratory during the early stages of the trial to cover all aspects of screening, and in the later stages to cover local testing used to monitor the participant in the clinic and to guarantee collection of valid specimens to be shipped to the Central Laboratory. Special attention throughout the trial was focused on techniques for collection of specimens, since it was recognized that analytical results could not be better than the quality of the specimens. Training courses, on-site visits, and newsletters were used to sensitize the staff of the clinic laboratory about the necessity to follow protocol. Any monitoring evidence of carelessness, use of deteriorated supplies, failure to follow safety rules, and deviation from directions in the MRFIT Manual of Operations resulted in memoranda from the Coordinating Center or the Central Laboratory.

Acid-base balance in continuous ambulatory peritoneal dialysis.

Metabolic acidosis was demonstrated in a group of anuric CAPD patients. Dialysate HCO3- loss was the major determinant of a negative base balance of 26.4 +/- 23.5 mMol/day. Bicarbonate supplementation corrected the acidosis. A primary respiratory alkalosis was also present in several patients.

Plasma acetone metabolism in the fasting human.

The metabolism of acetone was studied in lean and obese humans during starvation ketosis. Acetone concentrations in plasma, urine, and breath; and rates of endogenous production, elimination in breath and urine, and in vivo metabolism were determined. There was a direct relationship between plasma acetone turnover (20-77 mumol/m(2) per min) and concentration (0.19-1.68 mM). Breath and urinary excretion of acetone accounted for a 2-30% of the endogenous production rate, and in vivo metabolism accounted for the remainder. Plasma acetone oxidation accounted for congruent with60% of the production rate in 3-d fasted subjects and about 25% of the production rate in 21-d fasted subjects. About 1-2% of the total CO(2) production was derived from plasma acetone oxidation and was not related to the plasma concentration or production rate. Radioactivity from [(14)C]acetone was not detected in plasma free fatty acids, acetoacetate, beta-hydroxybutyrate, or other anionic compounds, but was present in plasma glucose, lipids, and proteins. If glucose synthesis from acetone is possible in humans, this process could account for 11% of the glucose production rate and 59% of the acetone production rate in 21-d fasted subjects. During maximum acetonemia, acetone production from acetoacetate could account for 37% of the anticipated acetoacetate production, which implies that a significant fraction of the latter compound does not undergo immediate terminal oxidation.

Mechanized micro-scale determination of protein in platelet pellet sonicates.

With the method described here, samples can be assayed at the rate of 40/h, with increased reproducibility. As described, the method covers an analytical range of 1 to 7 g/liter, but it can be readily adapted to measure different ranges of concentration in other protein preparations.

Ketone-body production and oxidation in fasting obese humans.

Rates of plasma acetoacetate and total ketone-body production and oxidation to CO2 were determined by an isotope tracer technique in eight obese subjects undergoing progressive starvation. After a brief fast and under conditions of mild ketonemia and minimal ketonuria, rates of acetoacetate and total ketone-body production and oxidation were directly related to the increasing plasma concentration. After a longer fast and with severer ketonemia, acetoacetate and total ketone-body production and oxidation rates were higher but became constant and unrelated to the plasma concentrations. The maximum rates of total ketone-body production and oxidation were about 150 g/24 h and 129 g/24 h, respectively. Although an increased ketone-body production was the primary factor responsible for the hyperketonemia, an imbalance between production and removal of the ketone bodies cannot be excluded. Such an imbalance could account, at least in part, for the developing hyperketonemia and for the lack of relationship between production rates and plasma concentrations.

Glycerol turnover and oxidation in man.

The oxidation and turnover of plasma glycerol has been studied in lean and obese, fed and starving man by means of a long-term infusion of glycerol-(14)C, and the participation of glycerol in gluconeogenesis has been determined. Under none of the experimental conditions did glycerol contribute more than 10% of the total respiratory CO(2). Glycerol turnover in fed lean subjects was 106 mmoles/min. Glycerol levels and turnover were higher in the obese subjects and with all subjects after starvation. There was a direct correlation between plasma levels and turnover values for which a regression equation was derived: y = 1556 x + 33.1, when y = turnover in micromoles per minute and x = glycerol level in micromoles per milliliter. Whereas a direct relation was established between glycerol and FFA levels, the FFA/glycerol turnover ratio was 4.7:1 in the lean group indicating incomplete hydrolysis of adipose tissue triglycerides.During starvation plasma glycerol is nearly or completely converted to glucose in the lean and obese groups, respectively. Of the new glucose formed from protein and glycerol 38% is derived from glycerol in the lean and 79% in the obese. Protein and glycerol have been shown to be adequate as precursors to supply at least as much glucose as is being oxidized per day.