Changes in plasma and urinary amino acid levels during diabetic ketoacidosis in children

Szabó, Antal; Kenesei, Éva; Körner, Anna; Miltényi, M; Szücs, L; Nagy, Iván

doi:10.1016/0168-8227(91)90085-r

Cited by 32 publications

(25 citation statements)

References 14 publications

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“…In diabetes mellitus there is a marked increase in the plasma concentration of BCAAs compared with healthy individuals, particularly in patients with deficient control of the disease (Elia and Livesey 1983;Felig et al 1969a, b;Wahren et al 1972;Berger et al 1978;Vannini et al 1982;Szabó et al 1991;Manders et al 2006). The striking elevation in the plasma level of BCAAs present during diabetic ketoacidosis promptly improves after initiation of insulin therapy and the adequate control of the disease results in normalization of the plasma BCAAs level (Vannini et al 1982;Szabó et al 1991). 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).…”

Section: Diabetes Mellitus and The Metabolism Of Bcaasmentioning

confidence: 98%

“…The striking elevation in the plasma level of BCAAs present during diabetic ketoacidosis promptly improves after initiation of insulin therapy and the adequate control of the disease results in normalization of the plasma BCAAs level (Vannini et al 1982;Szabó et al 1991). 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: 99%

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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: 98%

Section: Diabetes Mellitus and The Metabolism Of Bcaasmentioning

confidence: 99%

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

Adeva¹,

et al. 2011

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“…When studying diabetic patients it has been found that poorly controlled diabetes or ketoacidosis is associated with high urinary taurine excretion [167][168][169].…”

Section: Taurine Hyperglycemia and Diabetesmentioning

confidence: 99%

The role of taurine in diabetes and the development of diabetic complications

Hansen

2001

Diabetes Metabolism Res

243

157

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The ubiquitously found beta-amino acid taurine has several physiological functions, e.g. in bile acid formation, as an osmolyte by cell volume regulation, in the heart, in the retina, in the formation of N-chlorotaurine by reaction with hypochlorous acid in leucocytes, and possibly for intracellular scavenging of carbonyl groups. Some animals, such as the cat and the C57BL/6 mouse, have disturbances in taurine homeostasis. The C57BL/6 mouse strain is widely used in diabetic and atherosclerotic animal models. In diabetes, the high extracellular levels of glucose disturb the cellular osmoregulation and sorbitol is formed intracellularly due to the intracellular polyol pathway, which is suspected to be one of the key processes in the development of diabetic late complications and associated cellular dysfunctions. Intracellular accumulation of sorbitol is most likely to cause depletion of other intracellular compounds including osmolytes such as myo-inositol and taurine. When considering the clinical complications in diabetes, several links can be established between altered taurine metabolism and the development of cellular dysfunctions in diabetes which cause the clinical complications observed in diabetes, e.g. retinopathy, neuropathy, nephropathy, cardiomyopathy, platelet aggregation, endothelial dysfunction and atherosclerosis. Possible therapeutic perspectives could be a supplementation with taurine and other osmolytes and low-molecular compounds, perhaps in a combinational therapy with aldose reductase inhibitors.

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“…Besides glucose, amino acids (AAs) represent other osmotically active solutes that are disturbed in DM [19, 20, 21, 22]. This disturbance is due to the role exerted by insulin in AA transport through cell membranes [23, 24, 25, 26].…”

Section: Vasopressin Elevation In Diabetes Mellitusmentioning

confidence: 99%

Vasopressin and Diabetes mellitus

Bankir¹,

Bardoux²,

Ahloulay³

2001

Nephron

100

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In diabetes mellitus (DM), the urine flow rate is increased, and the fluid turnover in the body is accelerated because of the glucose-induced osmotic diuresis. On the other hand, plasma vasopressin (VP) is elevated in both type 1 and type 2 DM. This elevation seems to be due to a resetting of the osmostat. A high VP level is beneficial in the short term because it limits to some extent the amount of water required for the excretion of a markedly enhanced load of osmoles (mainly glucose). However, in the long run, it may have adverse effects by favoring the developement of diabetic nephropathy. VP has been shown in normal rats to induce kidney hypertrophy, glomerular hyperfiltration, and an increase in urinary albumin excretion (features also occurring in association in the period preceding diabetic nephropathy). Moreover, VP has been shown to participate in the progression of renal failure in rats with five-sixths reduction in renal mass. In recent studies, we have shown (1) that creatinine clearance, albuminuria and renal mass increased much less during experimental DM in Brattleboro rats unable to secrete VP than in their VP-replete Long-Evans controls, and (2) that albuminuria was prevented during experimental DM in Wistar rats when a VP nonpeptidic, highly selective V2 receptor antagonist was administered chronically for 9 weeks. Taken together, these results strongly suggest that VP plays a crucial role in the onset and aggravation of the renal complications of DM. The mechanisms by which VP exerts these adverse V2-dependent effects are not yet elucidated. They are most likely indirect and may involve several intermediate steps comprising VP-induced changes in the composition of the tubular fluid in the loop of Henle (due to solute recycling in the renal medulla associated with improved concentrating activity of the kidney), inhibition of the tubuloglomerular feedback control of glomerular function, and alterations in glomerular hemodynamics by the intrarenal renin-angiotensin system.

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Changes in plasma and urinary amino acid levels during diabetic ketoacidosis in children

Cited by 32 publications

References 14 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

The role of taurine in diabetes and the development of diabetic complications

Vasopressin and Diabetes mellitus

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