Response of hepatic amino acid consumption to chronic metabolic acidosis

Boon, Louis; Blommaart, P. J. E.; Meijer, Alfred J.; Lamers, Wouter H.; Schoolwerth, Anton C.

doi:10.1152/ajprenal.1996.271.1.f198

Cited by 13 publications

(11 citation statements)

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“…While the directional differences observed in the ureagenic response to CMA in the humans of the present study and those reported previously in rats (6,19,23,27) remain unresolved, the degree of acidosis reported in the rat studies was modest and of lesser magnitude than that in the human data. Future studies exploring CMA in multiple species and over a range of magnitudes will be of great interest.…”

contrasting

confidence: 70%

“…In acute metabolic acidosis in rats induced by HCl administration, results have been modestly supportive of the hepatic regulator theory, as both decreases (3,5) and no change (8,13) in ureagenesis were reported. In chronic metabolic acidosis (CMA) in rats, however, the results have been reasonably uniform in support of the hepatic acid-base control theory inasmuch as significant reductions in urea production have been observed consistently (6,19,23,27), although one of the reports found only a transient reduction (19). Hepatic control of acid-base homeostasis may also operate in chronic metabolic alkalosis, as chronic alkali exposure in the walking catfish has been recently reported to greatly increase ureagenesis (25).…”

mentioning

confidence: 84%

“…The findings of both increased flux in the glutamine synthetase pathway and decreased flux in the glutaminase pathway in perfused liver have been confirmed with detailed in vitro flux measurements in incubated liver cells from rats with CMA (22). In vivo data in rats with either acute metabolic acidosis or CMA, however, have not confirmed acidosisinduced increases in hepatic glutamine release (5,6).…”

mentioning

confidence: 94%

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Ureagenesis: evidence for a lack of hepatic regulation of acid-base equilibrium in humans

Hosch¹,

Muser²,

Hulter³

et al. 2004

American Journal of Physiology-Renal Physiology

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Ureagenesis in the liver consumes up to 1,000 mmol of HCO3-/day in humans as a result of 2NH4+ + 2HCO3- --> urea + CO2 + 3H2O. Whether the liver contributes to the regulation of acid-base equilibrium by controlling the rate of ureagenesis and, therefore, HCO3- consumption in response to changes in plasma acidity has not been adequately evaluated in humans. Rates of ureagenesis were measured in eight healthy volunteers during control, chronic metabolic acidosis (induced by oral administration of CaCl2 3.2 mmol.kg body wt-1.day-1 for 11 days), and recovery as well as during bicarbonate infusion (200 mmol over 240 min; acute metabolic alkalosis). Rates of ureagenesis were correlated negatively with plasma HCO3- concentration both during adaption to metabolic acidosis and during the chronic, steady-state phase. Thus ureagenesis, an acidifying process, increased rather than decreased in metabolic acidosis. During bicarbonate infusion, rates of ureagenesis decreased significantly. Thus ureagenesis did not appear to be involved in the regulated elimination of excess HCO3-. The finding of a negative correlation between ureagenesis and plasma HCO3- concentration over a wide range of HCO3- concentrations, altered both chronically and acutely, suggests that the ureagenic process per se is maladaptive for acid-base regulation and that ureagenesis has no discernible homeostatic effect on acid-base equilibrium.

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contrasting

confidence: 70%

mentioning

confidence: 84%

mentioning

confidence: 94%

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Ureagenesis: evidence for a lack of hepatic regulation of acid-base equilibrium in humans

Hosch¹,

Muser²,

Hulter³

et al. 2004

American Journal of Physiology-Renal Physiology

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“…As Mn# + can allosterically activate hepatic arginase in a pHsensitive fashion, it has been suggested that pH-dependent regulation of arginase activity may contribute to the pHdependence of hepatic urea production [211]. However, changes in hepatic amino acid transport [212,213] and possibly also in activities of key enzymes involved in amino acid catabolism, rather than changes in activities of the urea-cycle enzymes per se, are probably much more important in regulating pH-dependent alterations in hepatic urea synthesis.…”

Section: Arginase and Ureagenesismentioning

confidence: 99%

Arginine metabolism: nitric oxide and beyond

Morris

1998

Biochemical Journal

2,450

2,036

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Arginine is one of the most versatile amino acids in animal cells, serving as a precursor for the synthesis not only of proteins but also of nitric oxide, urea, polyamines, proline, glutamate, creatine and agmatine. Of the enzymes that catalyse rate-controlling steps in arginine synthesis and catabolism, argininosuccinate synthase, the two arginase isoenzymes, the three nitric oxide synthase isoenzymes and arginine decarboxylase have been recognized in recent years as key factors in regulating newly identified aspects of arginine metabolism. In particular, changes in the activities of argininosuccinate synthase, the arginases, the inducible isoenzyme of nitric oxide synthase and also cationic amino acid transporters play major roles in determining the metabolic fates of arginine in health and disease, and recent studies have identified

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“…Furthermore, an oxidation of labeled leucine was found to correlate inversely with lipid oxidation in obese women [59]. Second, the metabolic acidosis, existing in these subjects at the fast state [23], may result in a decrease in urea synthesis due to an inhibition of amino acids transport across the liver plasma membranes as it has been shown in rats with acute HCl-induced metabolic acidosis [60].…”

Section: Discussionmentioning

confidence: 99%

Anthropometric correlates of morning plasma cortisol level and hormonal and biochemical response to fasting in obese premenopausal women

Melnikov¹,

Kim²

2017

Integr Obesity Diabetes

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Numerous studies have established associations between hormonal parameters and body shape but they focused on the patterns of body fat distribution and, mainly, abdominal fat deposition. Based on the anthropometric features of patients with Cushing's syndrome, we hypothesized that there are somatometric predictors, other than waist-to-hip ratio, of increased cortisol production. To test this hypothesis and to identify the indicators of endocrine and metabolic responsiveness to shortterm fasting, we searched associations among 37 anthropometric traits and metabolic and hormonal parameters. An observational repeated measures study was performed on 64 moderately obese women using the partial correlation analysis. Blood glucose, serum lipids and urea concentrations, morning plasma cortisol, serum triiodthyronine (T3), thyroxin levels, and insulin activity (IRI) were examined before and after 4-and 7-day total fasting. The morning plasma cortisol level (RIA) showed the strongest correlation, independent of total fatness, with chest-hip circumference ratio (CHR) (r=0.48, p<0.005), whereas no significant association could be found with waist-hip ratio (WHR). IRI level correlated directly with WHR (r=0.47, p<0.001). The 4-day fasting significantly raised cortisol levels (+23%), free fatty acids (FFAs) (+79%), and triglyceride (TGs) (+34%) concentrations, and lowered IRI (-43%), T3 (-33%) and glucose (-27%) levels. The cortisol response to 4-day fasting tended to relate with age (r=0.25) and age-independently correlated with body height (r=-0.30) and WHR (r=-0.27). Both basal levels and fast changes in glucose and TGs concentrations correlated with age (glucose, r=0.38; TGs, r=0.24; d-glucose, r=-0.32; d-TG, r=-0.24). The relative weight loss after the 27-day weight-loss program increased with increasing basal FFAs and thyroxin levels. In conclusion, CHR was found to be a powerful predictor for morning plasma cortisol level. The relation established seems to reflect the differential sensitivity of the upper and lower body subcutaneous adipocytes to the metabolic stimuli of the hormone and/or other factors associated with glucocorticoids.level. In addition to this primary objective, there were two aims: (1) to describe anthropometric correlates for the response of endocrine variables and the patterns of protein, glucose, and lipid metabolism to short-term fasting, and (2) to verify hormonal, metabolic and somatometric predictors for the weight reduction during weight-loss program (WLP). Taking into account the sex-dependence of cortisol metabolism in obesity [18] we performed this research on obese women who were usually being investigated from the standpoint under study. Subjects and methods SubjectsThe study was undertaken on 64 Russian fertile women living in Novosibirsk city and referred to the endocrine division of the academic clinic for treatment of obesity by a WLP. The patients' free and informed consent to participate in the study was obtained. No women had signs of hirsutism, other endocrine disorders, ...

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Response of hepatic amino acid consumption to chronic metabolic acidosis

Cited by 13 publications

References 0 publications

Ureagenesis: evidence for a lack of hepatic regulation of acid-base equilibrium in humans

Ureagenesis: evidence for a lack of hepatic regulation of acid-base equilibrium in humans

Arginine metabolism: nitric oxide and beyond

Anthropometric correlates of morning plasma cortisol level and hormonal and biochemical response to fasting in obese premenopausal women

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