Effect of alcohol on gluconeogenesis using the isolated rat liver perfusion technique

Kaden, Melvin; Nw, Oakley; Jb, Field

doi:10.1152/ajplegacy.1969.216.4.756

Cited by 17 publications

(2 citation statements)

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“…With respect to the other major gluconeogenic substrates, alcohol acutely impairs the de novo synthesis of glucose from glycerol both in vivo [ 34 , 35 ] and in vitro [ 32 , 36 ] and from alanine in a dose-dependent manner [ 32 , 37 ]. In contrast, gluconeogenesis from pyruvate is unaltered or even elevated by acute alcohol [ 38 , 39 ].…”

Section: Alcohol and Basal Glucose Homeostasismentioning

confidence: 99%

Impact of Alcohol on Glycemic Control and Insulin Action

2015

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Alcohol has profound effects on tissue and whole-body fuel metabolism which contribute to the increased morbidity and mortality in individuals with alcohol use disorder. This review focuses on the glucose metabolic effects of alcohol, primarily in the muscle, liver and adipose tissue, under basal postabsorptive conditions and in response to insulin stimulation. While there is a relatively extensive literature in this area, results are often discordant and extrapolating between models and tissues is fraught with uncertainty. Comparisons between data generated in experimental cell and animals systems will be contrasted with that obtained from human subjects as often times results differ. Further, the nutritional status is also an important component of the sometimes divergent findings pertaining to the effects of alcohol on the regulation of insulin and glucose metabolism. This work is relevant as the contribution of alcohol intake to the development or exacerbation of type 2 diabetes remains ill-defined and a multi-systems approach is likely needed as both alcohol and diabetes affect multiple targets within the body.

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Section: Alcohol and Basal Glucose Homeostasismentioning

confidence: 99%

Impact of Alcohol on Glycemic Control and Insulin Action

2015

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“…The effects of ethanol on carbohydrate metabolism vary, depending on species, dose, route of administration, and whether it is given in the fasting or nonfasting state or whether it is administered acutely or chronically (12,13). In vitro, animal, and human studies indicate that ethanol inhibits gluconeogenesis (4,(14)(15)(16). The inhibition of gluconeogenesis would also inhibit glycogen formation (17), but the rise in blood glucose after glucagon injection that we found at the end of the study indicated that glycogen stores were still present in the liver.…”

Section: Resultsmentioning

confidence: 99%

Interaction of Ethanol and Glipizide in Humans

Hartling¹,

Faber²,

Wegmann³

et al. 1987

Diabetes Care

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The hypoglycemic effect of 2.5 mg glipizide and the potentiation of this effect by ethanol were studied in 10 normal-weight nondiabetic subjects. The reductions in blood glucose concentrations were similar in time of onset and extent (2 mM) whether glipizide was taken alone or in combination with ethanol. However, the return of blood glucose toward fasting level was delayed by ethanol. Beta-Cell secretory activity, evaluated from the concentrations of insulin and C-peptide, was unchanged by ethanol. The serum glipizide concentrations were reproducible within subjects, whereas there was a considerable interindividual variation. This heterogeneity in the rise in glipizide concentration was strongly correlated with blood glucose fall and insulin secretion. Thus, ethanol can prolong but does not augment the hypoglycemia induced by glipizide. The heterogeneity in glipizide concentration seems to be caused by an interindividual variation in kinetics.

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