Effect of <scp>L</scp>-alanine infusion on gluconeogenesis and ketogenesis in the rat <i>in vivo</i>

Özand, Pinar; Reed, W D; Hawkins, R. L.; Stevenson, J.H.; Tildón, J. Tyson; Cornblath, Marvin

doi:10.1042/bj1700583

Cited by 18 publications

(26 citation statements)

References 23 publications

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“…Although NEFA may suppress glucagon secretion [30], whether this was the case in the present studies cannot be established. However, the results of the present studies are concordant with earlier data indicating that the formation of ketone bodies is reduced by the elevation of plasma alanine, as shown in rats [31,32] and man [33]. These studies point towards a clear anti-ketogenic effect of alanine in the setting of a reciprocal relationship between alanine and ketone bodies (alanine-ketone body cycle) [33,34].…”

Section: Discussionsupporting

confidence: 92%

Effect of the amino acid alanine on glucagon secretion in non-diabetic and type 1 diabetic subjects during hyperinsulinaemic euglycaemia, hypoglycaemia and post-hypoglycaemic hyperglycaemia

et al. 2006

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Aims/hypothesis The aim of our study was to establish whether the well-known defective or absent secretion of glucagon in type 1 diabetes in response to hypoglycaemia is selective or includes lack of responses to other stimuli, such as amino acids. Materials and methods Responses of glucagon to hypoglycaemia were measured in eight patients with type 1 diabetes and six non-diabetic subjects during hyperinsulinaemic (insulin infusion 0.5 mU kg −1 min −1 ) and eu-, hypo-and hyperglycaemic clamp studies (sequential steps of plasma glucose 5.0, 2.9, 5.0, 10 mmol/l). Subjects were studied on three randomised occasions with infusion of low-or high-dose alanine, or saline. Results With saline, glucagon increased in hypoglycaemia in non-diabetic subjects but not in diabetic subjects. Glucagon increased further with low-dose (181±16 ng l −1 min −1 ) and high-dose alanine (238±20 ng l −1 min −1 ) in non-diabetic subjects, but only with high-dose alanine in diabetic subjects (area under curve 112±5 ng l −1 min −1 ). The alanine-induced glucagon increase in diabetic subjects paralleled the spontaneous glucagon response to hypoglycaemia in non-diabetic subjects not receiving alanine. The greater responses of glucagon to hypoglycaemia with alanine infusion were offset by recovery of eu-or hyperglycaemia.

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Section: Discussionsupporting

confidence: 92%

Effect of the amino acid alanine on glucagon secretion in non-diabetic and type 1 diabetic subjects during hyperinsulinaemic euglycaemia, hypoglycaemia and post-hypoglycaemic hyperglycaemia

et al. 2006

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“…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: 99%

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

Nosadini

Datta

Hodson

et al. 1980

Biochemical Journal

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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.

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“…Glucose, lactate, pyruvate, alanine, acetoacetate and 3-hydroxybutyrate were analysed by a microautoanalytic procedure previously described (Ozand et al, 1976a). L-Alanine was assayed by using alanine dehydrogenase in experiments involving dichloroacetate (Yoshida & Freese, 1970;Ozand et al, 1976a). Unesterified fatty acids were measured colorimetrically (Lauwreys, 1969).…”

Section: Analysesmentioning

confidence: 99%

“…At the indicated intervals, 50,pl of arterial blood was quickly withdrawn and mixed with 600,1l of 1M-HCl04 at 0°C. The supernatant fluids were removed and kept at -95°C until analysed (Ozand et al, 1976a). Since the volume in the arterial catheter was approx.…”

Section: Perfusion Proceduresmentioning

confidence: 99%

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

Özand¹,

Reed²,

Girard³

et al. 1977

Biochemical Journal

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1. The injection of L-alanine (50-100 mg/kg) into 35-day-old rats that had been starveed for 48 h increased blood L-alanine concentration to values observed in fed animals and lowered the blood concentration of 3-hydroxybutyrate within 2 min. 2. This hypoketon aemic action of L-alanine was specific for 3-hydroxybutyrate, since the acetoacetate concentrations did not change significantly. 3. The decrease in 3-hydroxybutyrate elicited by L-alanine was not related to changes in the blood concentrations of insulin, glucagon, growth hormone, glucose, unesterified fatty acids, lactate or pyruvate. 4. The injection of L-alanine resulted in a decrease in total ketones that was apparently unrelated to their increased peripheral utilization. These results are interpreted as an anti-ketogenic action of L-alanine. 5. The data suggest that L-alamine lowers ketone-body formation in starved rats, possibly via an alteration in hepatic redox equilibrium.

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

Cited by 18 publications

References 23 publications

Effect of the amino acid alanine on glucagon secretion in non-diabetic and type 1 diabetic subjects during hyperinsulinaemic euglycaemia, hypoglycaemia and post-hypoglycaemic hyperglycaemia

Effect of the amino acid alanine on glucagon secretion in non-diabetic and type 1 diabetic subjects during hyperinsulinaemic euglycaemia, hypoglycaemia and post-hypoglycaemic hyperglycaemia

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

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

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