Serum branched chain amino and keto acid response to fasting in humans

Schauder, P.; Herbertz, L; Langenbeck, U.

doi:10.1016/0026-0495(85)90061-7

Cited by 23 publications

(10 citation statements)

References 20 publications

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“…The 24-h urinary excretion of BCAAs is also elevated in diabetic patients before insulin treatment and normalizes after initiation of insulin (Sasaki et al 1988;Szabó et al 1991). Early starvation (within 36 h of fasting) in healthy subjects is also accompanied by elevated blood concentration of BCAAs and BCKAs, coinciding with a period of maximal fall in serum insulin (Adibi 1968;Felig et al 1969a, b;Rudolph et al 1981;Elia and Livesey 1983;Schauder et al 1985).…”

Section: Diabetes Mellitus and The Metabolism Of Bcaasmentioning

confidence: 92%

Insulin resistance and the metabolism of branched-chain amino acids in humans

Adeva¹,

et al. 2011

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Peripheral resistance to insulin action is the major mechanism causing the metabolic syndrome and eventually type 2 diabetes mellitus. The metabolic derangement associated with insulin resistance is extensive and not restricted to carbohydrates. The branched-chain amino acids (BCAAs) are particularly responsive to the inhibitory insulin action on amino acid release by skeletal muscle and their metabolism is profoundly altered in conditions featuring insulin resistance, insulin deficiency, or both. Obesity, the metabolic syndrome and diabetes mellitus display a gradual increase in the plasma concentration of BCAAs, from the obesity-related low-grade insulin-resistant state to the severe deficiency of insulin action in diabetes ketoacidosis. Obesity-associated hyperinsulinemia succeeds in maintaining near-normal or slightly elevated plasma concentration of BCAAs, despite the insulin-resistant state. The low circulating levels of insulin and/or the deeper insulin resistance occurring in diabetes mellitus are associated with more marked elevation in the plasma concentration of BCAAs. In diabetes ketoacidosis, the increase in plasma BCAAs is striking, returning to normal when adequate metabolic control is achieved. The metabolism of BCAAs is also disturbed in other situations typically featuring insulin resistance, including kidney and liver dysfunction. However, notwithstanding the insulin-resistant state, the plasma level of BCAAs in these conditions is lower than in healthy subjects, suggesting that these organs are involved in maintaining BCAAs blood concentration. The pathogenesis of the decreased BCAAs plasma level in kidney and liver dysfunction is unclear, but a decreased afflux of these amino acids into the blood stream has been observed.

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Section: Diabetes Mellitus and The Metabolism Of Bcaasmentioning

confidence: 92%

Insulin resistance and the metabolism of branched-chain amino acids in humans

Adeva¹,

et al. 2011

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“…Brief starvation uniquely increases BCAA concentrations in plasma. In humans, the increase is evident within a day, and reaches maximum by the second or third day [ 27 , 28 ].…”

Section: Effects Of Starvation and Diets With A Different Protein Conmentioning

confidence: 99%

Branched-chain amino acids in health and disease: metabolism, alterations in blood plasma, and as supplements

2018

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Branched-chain amino acids (BCAAs; valine, leucine, and isoleucine) are essential amino acids with protein anabolic properties, which have been studied in a number of muscle wasting disorders for more than 50 years. However, until today, there is no consensus regarding their therapeutic effectiveness.In the article is demonstrated that the crucial roles in BCAA metabolism play: (i) skeletal muscle as the initial site of BCAA catabolism accompanied with the release of alanine and glutamine to the blood; (ii) activity of branched-chain keto acid dehydrogenase (BCKD); and (iii) amination of branched-chain keto acids (BCKAs) to BCAAs. Enhanced consumption of BCAA for ammonia detoxification to glutamine in muscles is the cause of decreased BCAA levels in liver cirrhosis and urea cycle disorders. Increased BCKD activity is responsible for enhanced oxidation of BCAA in chronic renal failure, trauma, burn, sepsis, cancer, phenylbutyrate-treated subjects, and during exercise. Decreased BCKD activity is the main cause of increased BCAA levels and BCKAs in maple syrup urine disease, and plays a role in increased BCAA levels in diabetes type 2 and obesity. Increased BCAA concentrations during brief starvation and type 1 diabetes are explained by amination of BCKAs in visceral tissues and decreased uptake of BCAA by muscles.The studies indicate beneficial effects of BCAAs and BCKAs in therapy of chronic renal failure. New therapeutic strategies should be developed to enhance effectiveness and avoid adverse effects of BCAA on ammonia production in subjects with liver cirrhosis and urea cycle disorders. Further studies are needed to elucidate the effects of BCAA supplementation in burn, trauma, sepsis, cancer and exercise. Whether increased BCAA levels only markers are or also contribute to insulin resistance should be known before the decision is taken regarding their suitability in obese subjects and patients with type 2 diabetes.It is concluded that alterations in BCAA metabolism have been found common in a number of disease states and careful studies are needed to elucidate their therapeutic effectiveness in most indications.

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“…The consequence should be decreased flux of BCKA through BCKA dehydrogenase. Increased BCKA levels have been reported in starvation and diabetes [ 13 , 50 , 51 ]. Decreased supply of OA and PYR for conversion of GLU to α-KG due to decreased glycolysis.…”

Section: Etiopathogenesis Of Increased Bcaa Levels In Starvation mentioning

confidence: 99%

“…Among the amino acids, starvation uniquely increases the concentrations of all three BCAAs. In humans, increases are evident within a day, and the maximum is reached within 3 days [ 1 , 2 , 45 , 50 ]. The first 3 days of starvation, called the early or adjustment phase of starvation, are characterized by a decreased ratio of insulin to glucagon, decreased glycolysis, increased gluconeogenesis in the liver, preferential use of fatty acids as a source of energy, and accelerated proteolysis in muscles.…”

Section: Etiopathogenesis Of Increased Bcaa Levels In Starvation mentioning

confidence: 99%

Why Are Branched-Chain Amino Acids Increased in Starvation and Diabetes?

Holeček

2020

Nutrients

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Branched-chain amino acids (BCAAs; valine, leucine, and isoleucine) are increased in starvation and diabetes mellitus. However, the pathogenesis has not been explained. It has been shown that BCAA catabolism occurs mostly in muscles due to high activity of BCAA aminotransferase, which converts BCAA and α-ketoglutarate (α-KG) to branched-chain keto acids (BCKAs) and glutamate. The loss of α-KG from the citric cycle (cataplerosis) is attenuated by glutamate conversion to α-KG in alanine aminotransferase and aspartate aminotransferase reactions, in which glycolysis is the main source of amino group acceptors, pyruvate and oxaloacetate. Irreversible oxidation of BCKA by BCKA dehydrogenase is sensitive to BCKA supply, and ratios of NADH to NAD+ and acyl-CoA to CoA-SH. It is hypothesized that decreased glycolysis and increased fatty acid oxidation, characteristic features of starvation and diabetes, cause in muscles alterations resulting in increased BCAA levels. The main alterations include (i) impaired BCAA transamination due to decreased supply of amino groups acceptors (α-KG, pyruvate, and oxaloacetate) and (ii) inhibitory influence of NADH and acyl-CoAs produced in fatty acid oxidation on citric cycle and BCKA dehydrogenase. The studies supporting the hypothesis and pros and cons of elevated BCAA concentrations are discussed in the article.

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Serum branched chain amino and keto acid response to fasting in humans

Cited by 23 publications

References 20 publications

Insulin resistance and the metabolism of branched-chain amino acids in humans

Insulin resistance and the metabolism of branched-chain amino acids in humans

Branched-chain amino acids in health and disease: metabolism, alterations in blood plasma, and as supplements

Why Are Branched-Chain Amino Acids Increased in Starvation and Diabetes?

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