Effect of acute acidosis and alkalosis on leucine kinetics in man

Straumann, Edwin; Keller, Ulrich; Küry, Dieter; Bloesch, D.; Thélin, A.; Arnaud, M.; Stauffacher, Werner

doi:10.1111/j.1475-097x.1992.tb00292.x

Cited by 27 publications

(15 citation statements)

References 36 publications

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“…The study of Ballmer et al [14] confirmed that induced metabolic acidosis causes a negative nitrogen balance and a significant decrease in serum albumin synthesis. Furthermore, Reaich et al [15] found a significant increase in protein breakdown and amino acid oxidation after the ingestion of NH 4 CI for 5 days, findings confirmed by Straumann et al [16] but not by Nair et al [17]. In addition, a depression in muscle protein synthesis was observed after 2 days of metabolic acidosis in humans [18] and after 1 day in rats [19, 20].…”

Section: Introductionsupporting

confidence: 62%

“…Several studies have demonstrated the substantial influence ofpH on whole body protein turnover and muscle protein degradation [14,15,16, 36, 37], but only a few studies have investigated the impact of pH on muscle protein synthesis in vivo. Garibotto et al [21] showed, using the arterio-venous difference technique and a constant infusion of L -[ 3 H]phenylalanine, that CKD patients had significantly higher rates of both synthesis and degradation of muscle protein.…”

Section: Discussionmentioning

confidence: 99%

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Does Increasing Blood pH Stimulate Protein Synthesis in Dialysis Patients?

et al. 2009

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Background: Although the mechanism of muscle wasting in end-stage renal disease is not fully understood, there is increasing evidence that acidosis induces muscle protein degradation and could therefore contribute to the loss of muscle protein stores of patients on hemodialysis, a prototypical state of chronic metabolic acidosis (CMA). Because body protein mass is controlled by the balance between synthesis and degradation, protein loss can occur as result of either increased breakdown, impaired synthesis, or both. Correction of acidosis may therefore help to maintain muscle mass and improve the health of patients with CMA. We evaluated whether alkalizing patients on hemodialysis might have a positive effect on protein synthesis and on nutritional parameters. Methods: Eight chronic hemodialysis patients were treated daily with oral sodium bicarbonate (NaHCO₃) supplementation for 10–14 days, yielding a pre-dialytic plasma bicarbonate concentration of 28.6 ±1.6 mmol/l. The fractional synthesis rates (FSR) of muscle protein and albumin were obtained by the L-[²H₅ring]phenylalanine flooding technique. Results: Oral NaHCO₃supplementation induced a significant increase in serum bicarbonate (21.5 ± 3.4 vs. 28.6 ± 1.6 mmol/l; p = 0.018) and blood pH (7.41 vs. 7.46; p = 0.041). The FSR of muscle protein and the FSR of albumin did not change significantly (muscle protein: 2.1 ± 0.2 vs. 2.0 ± 0.5% per day, p = 0.39; albumin: 8.3 ± 2.2 vs. 8.6 ± 2.5% per day, p = 0.31). Plasma concentrations of insulin-like growth factor 1 decreased significantly (33.4 ± 21.3 vs. 25.4 ± 12.3 nmol/l; p = 0.028), whereas thyroid-stimulating hormone, free thyroxin and free triiodothyronine did not change significantly and nutritional parameters showed no improvement. Conclusion: In contrast to other findings, raising the blood pH of dialysis patients was not associated with a positive effect on albumin and muscle protein synthesis, or nutritional and endocrinal parameters.

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Section: Introductionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 99%

Does Increasing Blood pH Stimulate Protein Synthesis in Dialysis Patients?

et al. 2009

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“…The administration of long-chain fatty acids, unlike medium-chain triglycerides, also decreases leucine oxidation compared with controls (Keller et al 2002). In contrast, leucine oxidation is activated in healthy subjects by glucagon, (Pacy et al 1990) glucocorticosteroid therapy (Zimmerman et al 1989), and ammonium chloride-induced metabolic acidosis (Reaich et al 1992;Straumann et al 1992). Acute exercise induces activation of BCKD complex in human skeletal muscle, but after training the activity of this enzyme is reduced, along with an increase in BCKD kinase protein (Howarth et al 2007).…”

Section: Leucinementioning

confidence: 90%

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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“…Moreover, wasting of lean body mass is a common feature in patients with chronic uremic acidosis (13). The increase in whole body protein degradation reported in acute (14) and chronic (15) mineral acidosis in normal subjects might be an important pathogenic factor responsible for the loss of lean body mass in human uremia. In addition, the subjects with chronic mineral acidosis were also reported to exhibit a simultaneous increase in whole body protein synthesis and leucine oxidation in the post-absorptive state ( 15).…”

Section: Introductionmentioning

confidence: 99%

Chronic metabolic acidosis decreases albumin synthesis and induces negative nitrogen balance in humans.

Ballmer¹,

McNurlan²,

Hulter³

et al. 1995

J. Clin. Invest.

342

183

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Chronic metabolic acidosis has been previously shown to stimulate protein degradation. To evaluate the effects of chronic metabolic acidosis on nitrogen balance and protein synthesis we measured albumin synthesis rates and urinary nitrogen excretion in eight male subjects on a constant metabolic diet before and during two different degrees of chronic metabolic acidosis (NH4Cl 2.1 mmol/kg body weight, low dose group, and 4.2 mmol/kg body weight, high dose group, orally for 7 d). Albumin synthesis rates were measured by intravenous injection of [2H5ring]phenylalanine (43 mg/kg body weight, 7.5 atom percent and 15 atom percent, respectively) after an overnight fast. In the low dose group, fractional synthesis rates of albumin decreased from 9.9±1.0% per day in the control period to 8.4±0.7 (n.s.) in the acidosis period, and from 8.3±1.3% per day to 6.3±1.1 (P < 0.001) in the high dose group. Urinary nitrogen excretion increased significantly in the acidosis period (EA 634 mmol in the low dose group, 2,554 mmol in the high dose group). Plasma concentrations of insulin-like growth factor-I, free thyroxine and tri-iodothyronine were significantly lower during acidosis. In conclusion, chronic metabolic acidosis causes negative nitrogen balance and decreases albumin synthesis in humans. The effect on albumin synthesis may be mediated, at least in part, by a suppression of insulin-like growth factor-I, free thyroxine and tri-iodothyronine. (J. Clin. Invest. 1995. 95:39-45.) Key words: albumin * metabolic acidosis A protein synthesis * nitrogen balance * insulin-like growth factor-I

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Effect of acute acidosis and alkalosis on leucine kinetics in man

Cited by 27 publications

References 36 publications

Does Increasing Blood pH Stimulate Protein Synthesis in Dialysis Patients?

Does Increasing Blood pH Stimulate Protein Synthesis in Dialysis Patients?

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

Chronic metabolic acidosis decreases albumin synthesis and induces negative nitrogen balance in humans.

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