Acetate metabolism in humans is not well known. Kinetic aspects of acetate were investigated in the postabsorptive state on healthy subjects. In a first study, six subjects were infused with a primed constant infusion of [1-13C]acetate for 3 h and a prime of NaH13CO3. No difference was found between arterialized and venous tracer enrichments from the arm, although arterialized acetate concentrations were higher (74 +/- 12 vs. 59 +/- 14 mumol/l, P < 0.05), suggesting that the hand muscles used but did not produce acetate in the postabsorptive state. Total body flux of acetate was 8.4 +/- 0.6 mumol.kg-1.min-1, of which 69 +/- 5% was oxidized. Acetate contributed to 6.5 +/- 0.4% of the basal energy expenditure. In a second study, five volunteers were submitted to a gastric infusion for 3 h followed by an intravenous infusion of [1-13C]acetate for 3 h. Higher fluxes were observed with the tracer gastric infusion, and the first-pass removal of acetate within the splanchnic bed was 60 +/- 7%. Acetate contributes significantly to the energy supply of the body. It is mainly used by the liver when produced in the gut.

Colonic fermentation of dietary fibres produces short-chain fatty acids (e.g. acetate, propionate). Measurements of whole body acetate turnover was used in order to estimate the production of colonic short-chain fatty acids in human subjects. However, higher flux rates for acetate have been reported in human studies with stable isotopes as compared to radioactive tracers. The reasons for this discrepancy are unclear. In this study, the stable isotope (1-13C)acetate was used and a method was developed to measure its enrichment in plasma. Variations between and within assays were less than 5%. The standard curve was linear from 0.5% to 10% enrichment. When this tracer was infused for 160 min in six healthy volunteers, acetate turnover was found to be 7.5 +/- 1 mumol kg-1 min-1, which is similar to data reported with radioactive tracers. We assumed that the higher flux rate previously observed with stable isotope tracers was related to differences in the physiological status of the subjects involved in these studies.

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In vitro data suggested that albumin is a key factor controlling apolipoprotein (apo) synthesis by hepatocytes. Studies in analbuminemic rats have shown an increase in secretion of apoB-containing lipoprotein from the liver. We studied the kinetic aspects of apoB- and apoAI-containing lipoprotein metabolism in two sisters with analbuminemia using a constant 14-hour infusion of leucine labeled with stable isotopes. Compared with control subjects, total cholesterol was higher in the two patients (432 and 461 versus 155 +/- 14 mg/dL), as was apoB (257 and 230 versus 72 +/- 7 mg/dL). Triglycerides were slightly increased (134 and 105 versus 89 +/- 9 mg/dL), whereas apoAI was lower (109 and 105 versus 124 +/- 6 mg/dL). VLDL-apoB production was higher, as was the production of IDL-apoB and LDL-apoB (32.8 and 36.0 versus 24.8 +/- 5.9, 32.1 and 27.2 versus 16.4 +/- 2.3, and 14.1 and 17.6 versus 10.3 +/- 1.2 mg.kg-1.d-1, respectively). The fractional catabolic rate of all the apoB-containing lipoproteins was decreased (0.23 and 0.37 versus 0.48 +/- 0.05, 0.27 and 0.28 versus 0.62 +/- 0.08, and 0.012 and 0.009 versus 0.022 +/- 0.002.h-1, respectively). A similar mechanism could explain the dyslipidemia observed in other conditions associated with low albumin levels, such as nephrotic syndrome.

Incorporation of amino acids labeled with stable isotopes in apoliproproteins is