Modification of Metabolic Effects of Ethanol by Fructose

Abstract

Abstract. Present knowledge of the metabolic interactions between fructose and ethanol in man and laboratory animals is reviewed. The possible biochemical mechanisms of these interactions are considered. Some new data on the effects of fructose and ethanol on carbohydrate and lipid metabolism are included. Fructose increases the effects of ethanol on the hepatic lactate/pyruvate and a‐glycerophosphate/dihydroxyacetone phosphate ratios. Thus it augments the basic metabolic effect of ethanol, i.e. reduction of the hepatic redox state. The ethanol‐induced increase in hepatic a‐glycerophosphate concentration has been regarded as an important factor in the pathogenesis of the acute alcoholic fatty liver. But although fructose causes hypertriglyceridaemia and augments the effect of ethanol on hepatic a‐glycerophosphate concentration, it was found to diminish the ethanol‐induced accumulation of triglycerides in the liver. Glucose had a similar effect. The reason for this is uncertain, but the inhibition of peripheral lipolysis by fructose and glucose might be partly responsible. The most important effect of ethanol on carbohydrate metabolism is to inhibit hepatic gluconeogenesis by producing NADH in excess. Although the production of glucose from fructose is not directly dependent on the redox state of the liver, it is slightly inhibited by ethanol in vitro. However, in vivo fructose is effectively converted to glucose even during ethanol oxidation, and in ethanol‐induced hypoglycaemia it rapidly restores the blood glucose level.

Alcohol‑induced attenuation of post‑traumatic inflammation is�not necessarily liver‑protective following trauma/hemorrhage

“…depending on the group assignment, the animals either received a single dose of alcohol (5 g/kg, 30% ethanol, EtOH) or control solution (sodium chloride, Nacl 0.9%, ctrl) via oral gavage either 2 h (acute) or 12 h (sub-acute) before experimentation. Previous studies using the same dose of EtOH clearly demonstrated alcohol-dependent changes in the liver, including decreased graft survival, disturbance of hepatic microcirculation and increased triglyceride content (19)(20)(21). This is consistent with our previous studies, in which fatty liver was induced by this dose and concentration of alcohol (2,22).…”

Effects of Hangover on Psychomotor Skills Related to Driving: Modification by Fructose and Glucose

“…Several studies indicate that ethanol and carbohydrates modify the metabolisms of each other ( OGATA et al 1966;FORSANDER et al 1958;YLIKAHRI et al 1972). We found no clear hypoglycaemia, as KELLY et al (1970) did, even though hypoglycaemia has usually been observed during hangover ( VARTIA et al 1960;OGATA et al 1966;YLIKAHRI et al 1974).…”

“…We found no clear hypoglycaemia, as KELLY et al (1970) did, even though hypoglycaemia has usually been observed during hangover ( VARTIA et al 1960;OGATA et al 1966;YLIKAHRI et al 1974). We were also unable to find any decreased blood ethanol level in subjects receiving sugars, even though glucose and fructose have been found to accelerate the ethanol elimination rate ( DAMGAARD et al 1972;THIEDEN et al 1972;YLIKAHRI et al 1972). The administration of monosaccharides had subjectively no effect on hangover.…”

“…Blood glucose peak of the A-SM group at 8 a.m. had no essential influence on psychomotor skills. It is not surprising that no differences in performance between glucose and fructose subjects were found, since the metabolic effects of glucose and fructose are very similar ( YLIKAHRI et al 1972), and since fruc-tose is converted to glucose in vivo, especially when ethyl alcohol is present (YLIKAHRI et al 1972).…”

Acute alcohol intoxication reduces mortality, inflammatory responses and hepatic injury after haemorrhage and resuscitationin vivo

“…In the present study, we evaluated the effect of a binge‐like ethanol treatment, 12 h before the onset of H/R. Previous studies using doses of 5 g·kg −1 of ethanol clearly demonstrated ethanol‐dependent changes in the liver, that is, decreased graft survival and disturbance of hepatic microcirculation as well as increased triglyceride content (Ylikahri et al ., 1972; Zhong et al ., 1996; Enomoto et al ., 2000) This is consistent with our study where a fatty liver was induced by this dose of ethanol (Figure 1). Taken together, these data provide a valid basis for using ethanol at a dose of 5 g·kg −1 to study the effects of an acute fatty liver in inflammatory conditions, that is, with the H/R procedure.…”