Influence of Acetate on Glucose Metabolism in the Perfused Hind‐Quarter of the Rat

Karlsson, N.; Fellenius, E.; Kiesslin, K.-H.

doi:10.1111/j.1748-1716.1976.tb10319.x

Cited by 7 publications

(6 citation statements)

References 21 publications

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“…As reported recently (Karlsson et al 1976) the addition of exogenous substrates to the perfusion medium will cause a net production of lactate by the perfused hind-quarter (Table IV). This effect is discussed in the cited paper (op.…”

Section: Discussionsupporting

confidence: 62%

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Influence of Acetate on the Metabolism of Palmitate in the Perfused Hind‐Quarter of the Rat

Karlsson

Fellenius

Kiessling

1977

Acta Physiologica Scandinavica

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The metabolism of 1-14C-palmitate and its metabolic interaction with U-14C-acetate were studied in the perfused hind-quarter of the rat. 9% of 1-14C-palmitate taken up was oxidized to 14CO2 accounting for 7% of total oxygen consumption by the perfused tissue. Most label from 1-14C-palmitate was found in the lipid fraction of the muscle tissue. In spite of a 40% inhibition of palmitate oxidation, acetate only caused minor changes in the overall metabolism of palmitate. U-14C-acetate was mainly oxidized to 14CO2 and the oxygen consumption due to oxidation of acetate accounted for 20-30% of the total oxygen uptake. Minor amounts of 14C-acetate were found in muscle lipids. The addition of palmitate did not alter the metabolism of acetate. It is concluded that the presence of palmitate did not affect 14C-acetate metabolism, while the presence of acetate inhibited 14C-palmitate oxidation. The possible sites of interaction are discussed. The found interaction will probably not contribute to any major extent to the disturbed lipid metabolism found in animals and man during ethanol intake. No major changes in the tissue content of high-energy phosphate compounds were found in the presence of palmitate or acetate or both.

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Section: Discussionsupporting

confidence: 62%

“…Previous studies on acetate metabolism in skeletal muscle have included investigation of the effect of acetate on the metabolism of exogenous glucose (Karlsson et al 1976). The present report deals with the effect of acetate on the metabolism of palmitate, a long-chain fatty acid, in the perfused hind-quarter of the rat.…”

mentioning

confidence: 99%

Influence of Acetate on the Metabolism of Palmitate in the Perfused Hind‐Quarter of the Rat

Karlsson

Fellenius

Kiessling

1977

Acta Physiologica Scandinavica

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“…After correction for the 3H retention in lactate, less than 10% of the utilized glucose was oxidized to CO2, and thus it appears that most of the metabolic fuel of the resting leg was provided by tissue lipids. Berger et al (1976) recovered in the presence of insulin 7%, and Karlsson et al (1976) 5%, of the utilized glucose in CO2. The glucose-uptake and glycogen-synthesis rates in our preparation are somewhat higher than those reported for perfused hindleg preparations (Karlsson et al, 1976;Berger et al, 1976) and in the range of rates reported in vivo (Conlee et al, 1978;Terjung et al, 1974).…”

Section: Glucose Utilizationmentioning

confidence: 99%

“…Berger et al (1976) recovered in the presence of insulin 7%, and Karlsson et al (1976) 5%, of the utilized glucose in CO2. The glucose-uptake and glycogen-synthesis rates in our preparation are somewhat higher than those reported for perfused hindleg preparations (Karlsson et al, 1976;Berger et al, 1976) and in the range of rates reported in vivo (Conlee et al, 1978;Terjung et al, 1974). There was very little 3H from position 2 retained in glycogen, and it appears thus that the activity of hexose-6-phosphate isomerase is very high relative to glucose flux (Katz & Rognstad, 1976).…”

Section: Glucose Utilizationmentioning

confidence: 99%

Lactate metabolism in the perfused rat hindlimb

Shiota¹,

Golden²,

Katz³

1984

Biochemical Journal

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A preparation of isolated rat hindleg was perfused with a medium consisting of bicarbonate buffer containing Ficoll and fluorocarbon, containing glucose and/or lactate. The leg was electrically prestimulated to deplete partially muscle glycogen. The glucose was labelled uniformly with 14C and with 3H in positions 2, 5 or 6, and lactate uniformly with 14C and with 3H in positions 2 or 3. Glucose carbon was predominantly recovered in glycogen, and to a lesser extent in lactate. The 3H/14C ration in glycogen from [5-3H,U-14C]- and [6-3H,U-14C]-glucose was the same as in glucose. Nearly all the utilized 3H from [2-3H]glucose was recovered as water. Insulin increased glucose uptake and glycogen synthesis 3-fold. When the muscle was perfused with a medium containing 10 mM-glucose and 2 mM-lactate, there was little change in lactate concentration. 14C from lactate was incorporated into glycogen. There was a marked exponential decrease in lactate specific radioactivity, much greater with [3H]- than with [14C]-lactate. The 'apparent turnover' of [U-14C]lactate was 0.28 mumol/min per g of muscle, and those of [2-3H]- and [3-3H]-lactate were both about 0.7 mumol/min per g. With 10 mM-lactate as sole substrate, there was a net uptake of lactate, at a rate of about 0.15 mumol/min per g, and the apparent turnover of [U-14C]lactate was 0.3 mumol/min per g. The apparent turnover of [3H]lactate was 3-5 times greater. When glycogen synthesis was low (no prestimulation, no insulin), the incorporation of lactate carbon into glycogen exceeded that from glucose, but at high rates of glycogen deposition the incorporation of lactate carbon was much less than that of glucose. Lactate incorporation into glycogen was similar in fast-twitch white and fast-twitch red muscle, but was very low in slow-twitch red fibres. We find that (a) pyruvate in muscle is incorporated into glycogen without randomization of carbon, and synthesis is not inhibited by mercaptopicolinate or cycloserine; (b) there is extensive lactate turnover in the absence of net lactate uptake, and there is a large dilution of 14C-labelled lactate from endogenous supply; (c) there is extensive detritiation of [2-3H]- and [3-3H]-lactate in excess of 14C utilization.

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“…I. Data taken from Karlsson et al (1976 a). a Significantly different from perfusion with acetate without @-hydroxybutyrate, pi0.01.…”

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confidence: 99%

Influence of Acetate on the Metabolism of β‐Hydroxybutyrate in the Perfused Hind‐Quarter of the Rat

Karlsson

Fellenius

Kiessling

1977

Acta Physiologica Scandinavica

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The effect of acetate, at concentrations normally found during ethanol combustion in intact animals and man in vivo, on the uptake and oxidation of beta-hydroxybutyrate by the perfused rat hind-quarter was studied. The addition of acetate did not significantly affect the total uptake of beta-hydroxybutyrate, but caused a 40% decrease in the oxidation of beta-hydroxybutyrate to CO2. The oxidation of 14C-beta-hydroxybutyrate to 14CO2 accounted for about 10% of the total oxygen consumption by the perfused muscle in the absence of acetate. In the presence of acetate this figure was reduced to about 5%. The addition of beta-hydroxybutyrate did not significantly affect the metabolic fate of 14C-acetate. It is concluded that acetate is preferred as oxidative substrate to beta-hydroxybutyrate. The inhibited oxidation of beta-hydroxybutyrate by acetate did not affect the concentration ratio between beta-hydroxybutyrate and acetoacetate in the medium at the end of the perfusion, indicating that the ability of the muscle tissue to restore an increased redoxlevel, "exported" from the liver during ethanol combustion to extrahepatic tissues, was not impaired by acetate.

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Influence of Acetate on Glucose Metabolism in the Perfused Hind‐Quarter of the Rat

Cited by 7 publications

References 21 publications

Influence of Acetate on the Metabolism of Palmitate in the Perfused Hind‐Quarter of the Rat

Influence of Acetate on the Metabolism of Palmitate in the Perfused Hind‐Quarter of the Rat

Lactate metabolism in the perfused rat hindlimb

Influence of Acetate on the Metabolism of β‐Hydroxybutyrate in the Perfused Hind‐Quarter of the Rat

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