Urinary Excretion of Pyruvic Acid, Citric Acid and α-Ketogiutaric Acid after the Intravenous Injection of Pyruvate and Fructose in Diabetic Patients

Takanami, Akira; S, Ohya; Coto, Y.

doi:10.1620/tjem.72.163

Cited by 11 publications

(6 citation statements)

References 15 publications

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“…This finding is in agreement with previously reported work (Takanami et al, 1960;Anderson and Marks, 1962). After lactate ingestion the urinary pyruvate excretion was increased in the normal subjects and in all the diabetic groups.…”

Section: Discussionsupporting

confidence: 94%

See 1 more Smart Citation

Pyruvate and lactate excretion in diabetes mellitus after sodium lactate.

Anderson¹,

Thomas²,

Tomlinson³

1966

BMJ

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Section: Discussionsupporting

confidence: 94%

“…In diabetics, while the plasma concentration of pyruvate may be twice that of normal subjects, the urinary excretion of pyruvate is usually three or four times greater (Takanami et al, 1960 ;Anderson and Mazza, 1963 ;Anderson et al, 1964). Thus the reabsorptive capacity for pyruvate in the diabetic may be reaching a maximum.…”

mentioning

confidence: 99%

Pyruvate and lactate excretion in diabetes mellitus after sodium lactate.

Anderson¹,

Thomas²,

Tomlinson³

1966

BMJ

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“…In mild diabetes, and in well-balanced insulin-dependent diabetes, the fructose is mainly converted to pyruvate and Krebs cycle intermediates, as is shown by the increment in the serum levels of pyruvate, lactate, ac-ketoglutarate and citrate after fructose injection (Smith et al, 1953;Metz et al, 1967). Furthermore, pyruvate is effectively utilized by the peripheral tissues, and no more than a slight impairment in the assimilation of pyruvate is observable in diabetes (Takanami et al, 1960).…”

Section: Metabolism Of Fructose In Diabetes Mellitusmentioning

confidence: 99%

Fructose in medicine

Huttunen

1971

Postgraduate Medical Journal

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Summary A review is given of the metabolism of fructose in the mammalian organism, and its significance in medicine. Emphasis is laid upon the absorption and assimilation of fructose through pathways not identical with those of glucose. The metabolism of fructose is largely insulin-independent, although the ultimate fate of fructose carbons is determined by the presence or the absence of insulin. Clinical and experimental work has suggested that fructose may exert beneficial effects as a component of the diet for patients with mild and well-balanced diabetes. Fructose is absorbed slowly from the gut, and does not induce drastic changes in blood sugar levels. Secondly, fructose is metabolized by insulin-independent pathways in the liver, intestinal wall, kidney and adipose tissue. As a consequence of the rapid and efficient utilization of fructose, it has been used widely for intravenous feeding in medicine and surgery. However, it has been shown that the rapid infusion of large amounts of fruetose may cause accumulation of lactic acid in the extracellular fluid. The possibility of lactate acidosis, with concomitant impairment of the acid-base balance, already disturbed, constitutes a relative contraindication to the use of intravenous fructose in the treatment of diabetic ketoacidosis. Fructose is known to accelerate ethanol metabolism in the liver. No well-documented reports on the use of fructose in the treatment of ethanol intoxication have been published, although it has recently been suggested that fructose might be of value in the treatment of delirium tremens. Fructose may be less cariogenic than sucrose, at least in short-term experiments. Long-term trials are lacking, and thus the potential advantages of fructose in preventive odontology have not been determined. Fructose does not seem to have any side-effects when used in reasonable amounts. However, it has been reported that the administration of fructose in large amounts induces hyperlipidemia both in man and in experimental animals. Earlier suggestions concerned with the atherogenic properties of fructose have recently been challenged. The apparent increase in the incidence of coronary disease among sucrose users seems to be a statistical artefact, caused by the increased ingestion of coffee and soft drinks by cigarette smokers.

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“…The first intracoronary pyruvate infusion (totally 1.53 g and 3.05 g in 30 min, according to the calculation) was studied in eight patients with dilated cardiomyopathy in the Lancet in 1999; the hemodynamic measurements, including increases in the cardiac index and stroke volume and a decrease in pulmonary capillary wedge pressure, demonstrated the clinical cardio-protection due to pyruvate with a favorable inotropic effect (94). Additional reports on severe heart failure with intracoronary pyruvate of approximately 6.0 g in 30 min and others with cardioplegia on small doses of pyruvate and several IV loading tests of 10.0 g/4 min or 0.5 g/kg in 10 min all further demonstrated its clinical effectiveness and safety (39,91). The only report presents the case of a child with restrictive cardiomyopathy who received pyruvate infusion and died shortly after the pyruvate loading test (98); however, the causation between pyruvate and death was not confirmed (99).…”

Section: Safety and Feasibility Of Pyruvate Fluidsmentioning

confidence: 93%

“…One early study used IV 3.5 g% pyruvate at 10 mg/kg (20 ml/70 kg) for 1–1.5 min in 21 healthy subjects and 27 patients subjected to Vit B1 deficiency ( 89 ); another study used 18.8 g of 12% pyruvate in three non-psychotic and four schizophrenic patients ( 90 ). Then, 10 g of pyruvate (100 ml of 10% solution) was infused in 18 non-diabetic subjects and 19 diabetic patients to investigate the secretion of pyruvate in urine in 1960 ( 91 ). No unexpected effects were observed in all these subjects.…”

Section: Safety and Feasibility Of Pyruvate Fluidsmentioning

confidence: 99%

Pyruvate as a Potential Beneficial Anion in Resuscitation Fluids

Zhou

2022

Front. Med.

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There have been ongoing debates about resuscitation fluids because each of the current fluids has its own disadvantages. The debates essentially reflect an embarrassing clinical status quo that all fluids are not quite ideal in most clinical settings. Therefore, a novel fluid that overcomes the limitations of most fluids is necessary for most patients, particularly diabetic and older patients. Pyruvate is a natural potent antioxidant/nitrosative and anti-inflammatory agent. Exogenous pyruvate as an alkalizer can increase cellular hypoxia and anoxia tolerance with the preservation of classic glycolytic pathways and the reactivation of pyruvate dehydrogenase activity to promote oxidative metabolism and reverse the Warburg effect, robustly preventing and treating hypoxic lactic acidosis, which is one of the fatal complications in critically ill patients. In animal studies and clinical reports, pyruvate has been shown to play a protective role in multi-organ functions, especially the heart, brain, kidney, and intestine, demonstrating a great potential to improve patient survival. Pyruvate-enriched fluids including crystalloids and colloids and oral rehydration solution (ORS) may be ideal due to the unique beneficial properties of pyruvate relative to anions in contemporary existing fluids, such as acetate, bicarbonate, chloride, citrate, lactate, and even malate. Preclinical studies have demonstrated that pyruvate-enriched saline is superior to 0.9% sodium chloride. Moreover, pyruvate-enriched Ringer’s solution is advantageous over lactated Ringer’s solution. Furthermore, pyruvate as a carrier in colloids, such as hydroxyethyl starch 130/0.4, is more beneficial than its commercial counterparts. Similarly, pyruvate-enriched ORS is more favorable than WHO-ORS in organ protection and shock resuscitation. It is critical that attention first be paid to improving abnormal saline with pyruvate for ICU patients. Many clinical trials with a high dose of intravenous or oral pyruvate were conducted over the past half century, and results indicated its effectiveness and safety in humans. The long-term instability of pyruvate aqueous solutions and para-pyruvate cytotoxicity is not a barrier to the pharmaceutical manufacturing of pyruvate-enriched fluids for ICU patients. Clinical trials with sodium pyruvate-enriched solutions are urgently warranted.

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Urinary Excretion of Pyruvic Acid, Citric Acid and α-Ketogiutaric Acid after the Intravenous Injection of Pyruvate and Fructose in Diabetic Patients

Cited by 11 publications

References 15 publications

Pyruvate and lactate excretion in diabetes mellitus after sodium lactate.

Pyruvate and lactate excretion in diabetes mellitus after sodium lactate.

Fructose in medicine

Pyruvate as a Potential Beneficial Anion in Resuscitation Fluids

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