Little is known about the sites of production and uptake of acetate in nonruminants. We placed blood sampling catheters in the femoral artery and in the femoral, portal, hepatic, and renal veins of mongrel dogs (n = 11). The animals were studied in the conscious state 2 wk later during a primed continuous infusion of [1-14C]acetate. Systemic acetate turnover, oxidation, and clearance were determined, as well as regional uptake and release, by measuring 14CO2 excretion as well as plasma concentration and specific activity at the five sampling sites. Results showed systemic acetate turnover was 8.8 +/- 1.9 mumol.kg-1.min-1, approximating 5% of energy expenditure in dogs. Simultaneous uptake and release of acetate was demonstrated in intestine, liver, kidney, and hindlimb. The intestine was the greatest contributor to acetate production, whereas the liver was the most important site of uptake. Plasma acetate oxidation was 77 +/- 4% of turnover. Both systemic clearance (129 +/- 22 ml.kg-1.min-1) and tissue fractional extraction (68-85%) were many times greater than values reported for glucose, free fatty acids, lactate, or amino acids. In conclusion, most tissues simultaneously take up and release acetate in dogs. This may represent a mechanism for interorgan transport of energy, especially under conditions of caloric deprivation.
Triacetin is a water-soluble triglyceride that may have a role as a parenteral nutrient. In the present study triacetin was administered intravenously to mongrel dogs (n = 10) 2 wk after surgical placement of blood-sampling catheters in the aorta and in the portal, hepatic, renal, and femoral veins. [1-14C]Acetate was infused to allow quantification of organ uptake of acetate as well as systemic turnover and oxidation. Systemic acetate turnover accounted for approximately 70% of triacetin-derived acetate, assuming complete hydrolysis of the triglyceride. Approximately 80% of systemic acetate uptake was rapidly oxidized. Significant acetate uptake was demonstrated in all tissues (liver, 559 +/- 68; intestine, 342 +/- 23; hindlimb, 89 +/- 7; and kidney, 330 +/- 37 mumol/min). In conclusion, during intravenous administration in dogs, the majority of infused triacetin undergoes intravascular hydrolysis, and the majority of the resulting acetate is oxidized. Thus, energy in the form of short-chain fatty acids can be delivered to a resting gut via intravenous infusion of a short-chain triglyceride.
Systemic and lower limb skeletal muscle lactate metabolism was studied in 10 men with congestive heart failure by use of a primed continuous intravenous infusion of L-(+)-[U-14C]lactate. Arterial and deep femoral venous blood samples were obtained at rest and during 30 min of submaximal exercise. Systemic lactate metabolic turnover rate (Rd) was determined using Steele's isotopic steady-state equation (Rd = isotopic infusion rate/arterial specific activity). Plasma lactate concentrations in the artery and deep femoral vein did not change significantly from resting values during exercise (1.11 +/- 0.13 vs. 1.26 +/- 0.12 and 1.27 +/- 0.12 vs. 1.30 +/- 0.12 mM, respectively), whereas Rd increased from 22.5 +/- 1.8 to 41.6 +/- 4.8 mumol.kg-1.min-1 (P < 0.005). Rd did not significantly correlate with arterial lactate concentration during rest or exercise. Because of simultaneous uptake and release of lactate in skeletal muscle, arterial and deep femoral venous lactate concentrations are not closely related to either systemic or lower limb skeletal muscle lactate metabolism in patients with congestive heart failure.
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