&amp;alpha;-Ketoglutarate Application in Hemodialysis Patients Improves Amino Acid Metabolism

Riedel, E; Nündel, M.; Hampl, H.

doi:10.1159/000189319

Cited by 39 publications

(23 citation statements)

References 8 publications

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“…We presumed that the chronic dialyzed patients receiving keto acids should have a protein intake of at least 0.8 g/kg/day. One possible reason for keeping stable nutritional status may be related to the keto acid supplementation, which provided the essential amino acids and their corresponding keto acids, and thus decreased the degradation of branched-chain amino acids while increasing the essential amino acids, which may lead to stimulation of protein synthesis and reduction in protein degradation [20]. Keto acids raise the cycling utilization of urea nitrogen in the body to synthesize essential amino acids, which corrects negative nitrogen balance and improves the protein nutrition status [28,29].…”

Section: Discussionmentioning

confidence: 99%

“…A highly significant correlation has been observed between protein and phosphate intake [19]. The serum phosphorus level can certainly be reduced by a low-protein diet (LPD), and if the diet is supplemented with keto acids, which is a potent phosphate binder, the serum phosphorus level can be further reduced [20]. As early as 1988, Schaefer et al [21] have demonstrated the beneficial effects of LPD and keto acid supplementation on serum phosphorus and parathyroid hormone levels in uremic patients.…”

Section: Introductionmentioning

confidence: 99%

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Effect of Short-Term Low-Protein Diet Supplemented with Keto Acids on Hyperphosphatemia in Maintenance Hemodialysis Patients

Long

Shao

et al. 2010

Blood Purif

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Aim: To evaluate the effects of short-term restriction of dietary protein intake (DPI) supplemented with keto acids on hyperphosphatemia in maintenance hemodialysis (MHD) patients. Methods: Forty MHD patients with uncontrolled hyperphosphatemia were randomized to either low DPI with keto acid-supplemented (sLP) or normal DPI (NP) group for 8 weeks. After 8 weeks, the sLP group was shifted to NP for another 8 weeks. Low-protein diet (LPD) was individualized with total caloric intake 30–35 kcal/kg/day, protein intake of 0.8 g/kg/day and phosphate intake of 500 mg/day. Keto acids were supplied in a dosage of 12 pills per day. Calcium phosphorous metabolism index and nutritional index (serum albumin, total protein, somatometric measurements, 3-day diaries and Mini-Nutritional Assessment score) were recorded. C-reactive protein, CO₂ combining power and Kt/V were measured to evaluate the inflammation, metabolic acidosis and dialysis adequacy, respectively. Results: Serum phosphorus level and calcium-phosphate product were significantly decreased at the end of the first 8 weeks in the sLP group compared to the basal value and the NP group (p < 0.001). No difference was observed in C-reactive protein, Kt/V and nutritional index, while CO₂ combining power was significantly higher at week 8 in the sLP group (p < 0.001). Conclusion: Short-term restriction of DPI supplemented with keto acids could decrease hyperphosphatemia and calcium-phosphate product, while keeping stable nutritional status among MHD patients.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effect of Short-Term Low-Protein Diet Supplemented with Keto Acids on Hyperphosphatemia in Maintenance Hemodialysis Patients

Long

Shao

et al. 2010

Blood Purif

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“…Of particular note is the extensive oxidation of α-KG by enterocytes that may suppress GLN catabolism and ammonia production by intestinal cells (Yao et al 2012). The adverse side effect of α-KG administration may be catabolism of BCAA as demonstrated by increased levels of branched-chain keto acids in hemodialysis patients (Riedel et al 1996). …”

Section: Therapeutic Perspectivesmentioning

confidence: 99%

Evidence of a vicious cycle in glutamine synthesis and breakdown in pathogenesis of hepatic encephalopathy–therapeutic perspectives

Holeček

2013

Metab Brain Dis

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There is substantial clinical and experimental evidence that ammonia is a major factor in the pathogenesis of hepatic encephalopathy. In the article is demonstrated that in hepatocellular dysfunction, ammonia detoxification to glutamine (GLN) in skeletal muscle, brain, and likely the lungs, is activated. In addition to ammonia detoxification, enhanced GLN production may exert beneficial effects on the immune system and gut barrier function. However, enhanced GLN synthesis may exert adverse effects in the brain (swelling of astrocytes or altered neurotransmission) and stimulate catabolism of branched-chain amino acids (BCAA; valine, leucine, and isoleucine) in skeletal muscle. Furthermore, the majority of GLN produced is released to the blood and catabolized in enterocytes and the kidneys to ammonia, which due to liver injury escapes detoxification to urea and appears in peripheral blood. As only one molecule of ammonia is detoxified in GLN synthesis whereas two molecules may appear in GLN breakdown, these events can be seen as a vicious cycle in which enhanced ammonia concentration activates synthesis of GLN leading to its subsequent catabolism and increase in ammonia levels in the blood. These alterations may explain why therapies targeted to intestinal bacteria have only a limited effect on ammonia levels in patients with liver failure and indicate the needs of new therapeutic strategies focused on GLN metabolism. It is demonstrated that each of the various treatment options targeting only one the of the ammonia-lowering mechanisms that affect GLN metabolism, such as enhancing GLN synthesis (BCAA), suppressing ammonia production from GLN breakdown (glutaminase inhibitors and alpha-ketoglutarate), and promoting GLN elimination (phenylbutyrate) exerts substantial adverse effects that can be avoided if their combination is tailored to the specific needs of each patient.

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“…Unlike free Gln, AKG has a good water solubility, is non-toxic and relatively stable in water solutions, and thus represents an effective alternative Gln source for the composition of parenteral solutions (Filip and Pierzynowski, 2007). In addition, AKG can prevent uncontrolled nitrogen (N) loss from muscle protein in human patients suffering from post-surgical trauma, burns or chronic malnutrition, controlling the amino acid (AA) blood profile and reducing the blood urea in patients undergoing hemodialysis (Blomqvist et al, 1995;Riedel et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Anticatabolic activity of alpha-ketoglutaric acid in growing rats

Prandini

Morlacchini²,

Sigolo

et al. 2012

Italian Journal of Animal Science

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This study evaluated the anti-catabolic effect of a-ketoglutaric acid (AKG) in rats. Thirty Sprague Dowley male rats were divided into 3 groups of 10 animals each and fed ad libitum with protein-free diet (PFD) supplemented with 0, 3, and 6 g/kg feed of AKG for 14 consecutive days. The AKG administration had no effect on the growth performance of rats in the global trial period (0-14 d). After 7 d of excreta collection, the losses of endogenous nitrogen (N), both urinary and total, linearly reduced (P<0.05) following the administration of AKG, ranging from 35.00 mg/d to 28.00 mg/d, and from 45.28 mg/d to 36.36 mg/d, respectively. The villi and microvilli heights were lower when animals received 3 g/kg of AKG respecting to other tested AKG levels. Indeed, enterocytes length linearly increased (P<0.05) as the level of AKG increased in the diet by 25.0% (3 g/kg) and 49.0% (6 g/kg). The AKG levels quadratically influenced (P<0.05) the essential amino acids (EAA) concentrations in the blood, being EAA lower for animals treated with 6 g/kg of AKG (-21.6%) compared to the animals fed the control PFD and the PFD with 3 g/kg of AKG. In conclusion, AKG was effective in reducing catabolism and EAA depletion.

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α-Ketoglutarate Application in Hemodialysis Patients Improves Amino Acid Metabolism

Cited by 39 publications

References 8 publications

Effect of Short-Term Low-Protein Diet Supplemented with Keto Acids on Hyperphosphatemia in Maintenance Hemodialysis Patients

Effect of Short-Term Low-Protein Diet Supplemented with Keto Acids on Hyperphosphatemia in Maintenance Hemodialysis Patients

Evidence of a vicious cycle in glutamine synthesis and breakdown in pathogenesis of hepatic encephalopathy–therapeutic perspectives

Anticatabolic activity of alpha-ketoglutaric acid in growing rats

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