Hypoketonaemic effect of <scp>L</scp>-alamine. Specific decrease in blood concentrations of 3-hydroxybutyrate in the rat

Özand, Pinar; Reed, W D; Girard, Jean; Hawkins, R. L.; Collins, Roger M.; Tildón, J. Tyson; Cornblath, Marvin

doi:10.1042/bj1640557

Cited by 20 publications

(19 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our finding that the anti-ketogenic effect involved acetoacetate as much as 3-hydroxybutyrate in the rat as well as in man is in direct contrast with the reports of Ozand et al (1977Ozand et al ( , 1978. The only major differences in experimental protocol were that our rats were older and, perhaps more importantly, we used a simultaneous infusion of somatostatin.…”

Section: Discussionmentioning

confidence: 73%

“…It was deduced that this was independent of an effect on insulin. The decrease in blood ketone-body concentration caused by alanine was confirmed in the rat by Ozand et al (1977), who showed that the effect was unchanged by the presence of anti-insulin serum, suggesting more directly that insulin was not involved in the phenomenon. A notable finding of Ozand et al (1977Ozand et al ( , 1978 was that the antiketogenic effect was restricted to 3-hydroxybutyrate with blood acetoacetate concentrations remaining unchanged or even increasing.…”

Section: Discussionmentioning

confidence: 91%

“…The failure to observe a change in ketone-body ratio is important in that Ozand et al (1977Ozand et al ( , 1978 have based their explanation of the anti-ketogenic effect of alanine on this change. In the starved state the reducing equivalents needed for gluconeogenesis are generated in the mitochondria and transported to the cytosol by the malate-aspartate shuttle (D. H.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

A possible mechanism for the anti-ketogenic action of alanine in the rat

Nosadini

Datta

Hodson

et al. 1980

Biochemical Journal

View full text Add to dashboard Cite

1. The anti-ketogenic effect of alanine has been studied in normal starved and diabetic rats by infusing l-alanine for 90min in the presence of somatostatin (10mug/kg body wt. per h) to suppress endogenous insulin and glucagon secretion. 2. Infusion of alanine at 3mmol/kg body wt. per h caused a 70+/-11% decrease in [3-hydroxybutyrate] and a 58+/-9% decrease in [acetoacetate] in 48h-starved rats. [Glucose] and [lactate] increased, but [non-esterified fatty acid], [glycerol] and [3-hydroxybutyrate]/[acetoacetate] were unchanged. 3. Infusion of alanine at 1mmol/kg body wt. per h caused similar decreases in [ketone body] (3-hydroxybutyrate plus acetoacetate) in 24h-starved normal and diabetic rats, but no change in other blood metabolites. 4. Alanine [3mmol/kg body wt. per h] caused a 72+/-9% decrease in the rate of production of ketone bodies and a 57+/-8% decrease in disappearance rate as assessed by [3-(14)C]acetoacetate infusion. Metabolic clearance was unchanged, indicating that the primary effect of alanine was inhibition of hepatic ketogenesis. 5. Aspartate infusion at 6mmol/kg body wt. per h had similar effects on blood ketone-body concentrations in 48h-starved rats. 6. Alanine (3mmol/kg body wt. per h) caused marked increases in hepatic glutamate, aspartate, malate, lactate and citrate, phosphoenolpyruvate, 2-phosphoglycerate and glucose concentrations and highly significant decreases in [3-hydroxybutyrate] and [acetoacetate]. Calculated [oxaloacetate] was increased 75%. 7. Similar changes in hepatic [malate], [aspartate] and [ketone bodies] were found after infusion of 6mmol of aspartate/kg body wt. per h. 8. It is suggested that the anti-ketogenic effect of alanine is secondary to an increase in hepatic oxaloacetate and hence citrate formation with decreased availability of acetyl-CoA for ketogenesis. The reciprocal negative-feedback cycle of alanine and ketone bodies forms an important non-hormonal regulatory system.

show abstract

Section: Discussionmentioning

confidence: 73%

Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

A possible mechanism for the anti-ketogenic action of alanine in the rat

Nosadini

Datta

Hodson

et al. 1980

Biochemical Journal

View full text Add to dashboard Cite

show abstract

“…Alanine, one of the primary gluconeogenic substrates (Ross et al, 1967;Felig, 1975;Garber et al, 1976), is released in substantial amounts from skeletal muscle (Blackshear et al, 1975;Felig, 1975;Garber et al, 1976). In addition, the elevation of this arnino acid in blood above 0.6mm causes a marked decrease in the blood [3-hydroxybutyrate] and alters the overall production of ketone bodies (Ozand et al, 1977). These findings suggest that this amino acid may have a regulatory role in both gluconeogenesis and ketogenesis.…”

mentioning

confidence: 90%

Effect of L-alanine infusion on gluconeogenesis and ketogenesis in the rat in vivo

Özand¹,

Reed²,

Hawkins³

et al. 1978

Biochemical Journal

Self Cite

View full text Add to dashboard Cite

1. In 48 h-starved 6-week-old rats the 14C incorporation in vivo into blood glucose from a constant-specific-radioactivity pool of circulating [14c]actateconfirmed that lactate is the preferred gluconeogenic substrate. 2. Increasing the blood [alanine] to that occurrring in the fed state increased 14C incorporation into blood glucose 2.3-fold from [14c]alanine and 1.7-fold from [14c]lactate. 3. When the blood [alanine] was increased to that in the fed state, the 14C incorporation into liver glycogen from circulating [14c]alanine or [14c]lactate increased 13.5- and 1.7-fold respectively. 4. The incorporation of 14C into blood acetoacetate and 3-hydroxybutyrate from a constant-specific-radioactivity pool of circulating [14c]oleate was virtually abolished by increasing the blood [alanine] to that existing in the fed state. However, the [acetoacetate] remained unchanged, whereas [3-hydroxybutyrate] decreased, although less rapidly than did its radiochemical concentration. 5. It is concluded that during starvation in 6-week-old rats, the blood [alanine] appears to influence ketogenesis for circulating unesterfied fatty acids and inversely affects gluconeogenesis from either lactate or alanine. A different pattern of gluconeogenesis may exist for alanine and lactate as evidenced by comparative 14C incorporation into liver glycogen and blood glucose.

show abstract

“…Enhanced hepatic fatty acid oxidation results in the increased production of acetoacetic acid which is in turn converted to D-3-hydroxybutyric acid by a reaction catalyzed by 3-hydroxybutyrate dehydrogenase. D-3-Hydroxybutyrate represents a major form of ketone bodies, especially in such metabolic situations as starvation 1,2) and diabetes mellitus, 2) by which hepatic fatty acid oxidation is enhanced. Enzymatic methods, [3][4][5][6] which have been widely employed for the determination of this compound, involve the conversion of D-3-hydroxybutyric acid to acetoacetic acid through a reaction catalyzed by 3-hydroxybutyrate dehydrogenase, and subsequent spectrophotometric determination of the NADH produced.…”

mentioning

confidence: 99%

Enzymatic-HPLC Method to AnalyzeD-3-Hydroxybutyric Acid in Rat Serum

Ishii

2010

Bioscience, Biotechnology, and Biochemistry

View full text Add to dashboard Cite

Hypoketonaemic effect of L-alamine. Specific decrease in blood concentrations of 3-hydroxybutyrate in the rat

Cited by 20 publications

References 44 publications

A possible mechanism for the anti-ketogenic action of alanine in the rat

A possible mechanism for the anti-ketogenic action of alanine in the rat

Effect of L-alanine infusion on gluconeogenesis and ketogenesis in the rat in vivo

Enzymatic-HPLC Method to AnalyzeD-3-Hydroxybutyric Acid in Rat Serum

Contact Info

Product

Resources

About