The elimination kinetics of acetate, the main end product of ethanol metabolism in the liver and the influence of acetate oxidation on the redox- and energy state of the isolated perfused hind-quarter of the rat were studied. The rate of acetate uptake increased with increasing initial concentration of acetate in the perfusion medium, suggesting that the plasma level of free acetate may be one factor in the regulation of acetate uptake in the skeletal muscle. Addition of acetate as a single dose did not affect the net production of lactate or the uptake of glucose. In continuous infusion experiments at a constant concentration of 2 mM of acetate in the medium, the lactate/pyruvate ratio was unaffected in the medium and in the muscle tissue. Addition of acetate did not affect the oxygen uptake. Experiments with 14-C-acetate showed that about 50% of added radioactivity was found in form of 14-CO2 accounting for 25 to 45% of the oxidative metabolism in the muscle tissue. It was calculated that about 25% of the acetate produced in the liver during ethanol oxidation can be consumed in the resting, perfused hind-quarter of the rat. The tissue content of high-energy phosphate compounds was not significantly affected by acetate.
The metabolism of U-14C-glucose and U-14C-acetate and the interaction between the two substrates in the perfused hind-quarter of the rat was studied. 5% of glucose taken up was oxidized to CO2, accounting for 15% of total oxygen consumption. Glucose was mainly incorporated into glycogen, while incorporation into lipids was negligible. Acetate did not significantly alter glucose uptake, 14C-glucose oxidation or the incorporation of 14C-glucose into glycogen and lipids. 45% of acetate taken up was oxidized to CO2, accounting for 20-25% of total oxygen consumption. Insulin did not affect acetate uptake but increased 14C-acetate oxidation. Oxygen consumption was slightly increased by simultaneous oxidation of glucose and acetate and in this situation the tissue content.of high-energy phosphate compounds was slightly elevated. It is concluded that only minor effects by acetate on glucose metabolism in the perfused skeletal muscle were found. The insignificant effects compared to previously reported studies on heart tissue (Neely and Morgan 1974) can be explained by differences in acetate metabolism between the two tissues.
The metabolic changes in blood, red (m. soleus) and white (m. vastus lateralis) skeletal muscle fibres were investigated after short-term (3 min) infusion of adrenaline with or without prior treatment with propranolol or metoprolol. The adrenaline-induced increase in plasma lactate levels was totally prevented by prior treatment with metoprolol or propranolol, whilst the beta-blockers had no effect on blood glucose levels. Similar effects on lactate levels were found in the m. soleus, while metoprolol was less effective than propranolol in m. vastus lateralis. Adrenaline decreased the level of muscle creatinine phosphate and ADP, causing the equilibrium of the creatinine kinase reaction to change in the direction of ATP synthesis, although the level of ATP usually decreased. This effect was more pronounced in m. vastus lateralis compared with m. soleus. The [ATP]/[ADP] [Pi]-ratio tended to increase during infusion of adrenaline. This effect was counteracted by metroprolol but not by propranolol. The effects on the "phosphate potential" ([ATP]/[ADP] [Pi]) and the equilibrium within the creatine kinase were more pronounced in m. vastus lateralis than in m. soleus. The results demonstrate the possible role of receptors other than beta-receptors, i.e. alpha-receptors, in mediating changes in plasma glucose levels, while plasma lactate levels are regulated by the beta-adrenergic system. The role of beta-receptors in mediating changes in muscle lactate levels may differ in m. soleus and m. vastus lateralis, with a relative predominance of beta 2-receptors in m. vastus lateralis. Quantitative and qualitative differences in the adrenergic control of the energy state in the two types of muscle fibre were obvious, although it was not possible to distinguish clearly between the relative importance of alpha, beta 1 and beta 2-receptors.
1. The effects of chronic ethanol administration on the metabolism of ethanol and acetaldehyde were studied in rats fed on a commercial diet containing an aldehyde dehydrogenase inhibitor, calcium cyanamide (calcium carbimide), as a contaminant in the calcinated bone-meal fraction of the diet. 2. Rats given an ethanol solution (150 ml/l) for 3 months and fed on a diet containing calcinated bone meal showed two times higher activity of the low-Km acetaldehyde dehydrogenase in the liver, 26% higher rate of ethanol elimination, and two to three times lower acetaldehyde levels in blood during ethanol elimination compared with control rats pair-fed on the same diet. 3. The results obtained from the ethanol-treated rats were similar to those obtained in experiments on control rats fed on diets not containing calcinated bone meal. 4. Experiments performed in vitro and in vivo on the inhibition of the acetaldehyde metabolism by cyanamide suggested that the apparent effects of chronic ethanol intake were really caused by calcium cyanamide in the diet.
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