Basic Concepts of Acid–Base Physiology
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2020
The majority of the non-volatile or metabolic acids are derived from protein metabolism, primarily metabolism of exogenous protein in the form of methionine and phosphoproteins. Sulphuric acid is formed from sulphur-containing amino acids such as cysteine and methionine. Hydrochloric acid is formed from the degradation of lysine, arginine and histidine. Phosphoric acid is formed by the hydrolysis of phosphoproteins. A person consuming 100 g of protein a day produces about 1.1 mol of hydrogen ions during the conversion of protein nitrogen to urea. About 1500 mmol/day of lactic acid is produced by normal anaerobic metabolism of glucose and glycogen processes in the red blood cells, skin and skeletal muscle. The lactate is oxidized in the liver to regenerate bicarbonate. Excess lactic acid in the plasma indicates a diminished supply of oxygen to tissues. Acetoacetic acid and β-hydroxybutyric acid are produced by the metabolism of triglycerides during fasting. Acetoacetic acid and hydroxybutyric acids, in excess of normal amounts (e.g. in diabetic ketoacidosis), are excreted by the kidneys. Acetoacetic acid can be decarboxylated to acetone, which is excreted via the lungs and the kidneys. About 30 mmol of bicarbonate is lost in the faeces via the gastrointestinal tract, and this is equivalent to an acid load to the body.
Acid–base physiology
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2015
The majority of the non-volatile or metabolic acids are derived from protein metabolism, primarily metabolism of exogenous protein in the form of methionine and phosphoproteins. Sulphuric acid is formed from sulphur-containing amino acids such as cysteine and methionine. Hydrochloric acid is formed from the degradation of lysine, arginine and histidine. Phosphoric acid is formed by the hydrolysis of phosphoproteins. A person consuming 100 g of protein a day produces about 1.1 moles of hydrogen ions during the conversion of protein nitrogen to urea. About 1500 mmol/day of lactic acid is produced by normal anaerobic metabolism of glucose and glycogen processes in the red blood cell, skin and skeletal muscle. The lactate is oxidized in the liver to regenerate bicarbonate. Excess lactic acid in the plasma indicates a diminished supply of oxygen to tissues. Acetoacetic acid and β-hydroxybutyric acid are produced by the metabolism of triglycerides during fasting. Acetoacetic acid and hydroxybutyric acids, in excess of normal amounts (e.g., in diabetic ketoacidosis), are excreted by the kidneys. Acetoacetic acid can be decarboxylated to acetone, which is excreted via the lungs and the kidneys. About 30 mmol of bicarbonate is lost in the faeces via the gastrointestinal tract, and this is equivalent to an acid load to the body.
Botanicals and the Gut Microbiome
Namrita Lall in Medicinal Plants for Cosmetics, Health and Diseases, 2022
A decoction known as Yinchenhao, consisting mainly of Artemisia annua L., Gardenia jasminoides Ellis and Rheum palmatum L., is suggested to prevent liver injury, apoptosis of the liver cells, activation of hepatic stellate cells, synthesis of collagen and the promotion of bilirubin metabolism (Sakaida et al., 2003; Yamamoto et al., 2000, Yamamoto et al., 1996, Yamshiki et al., 2000, Huang et al., 2004; Lu et al., 2019). All of these mainly contribute to the Yinchenhao decoction in treating jaundice. Specifically, with regard to the gut microbiome, the study conducted by Liu et al. (2019) summarized that the protective effects seen in the liver injury was specifically related to the production of 3-hydroxybutyric acid through the changes in the availability of Clostridia and Clostridiales.
Serum metabolic alterations in peritoneal dialysis patients with excessive daytime sleepiness
Published in Renal Failure, 2023
Wei Chen, Ying Xu, Zheng-Hao Li, Ya-Chen Si, Hai-Yan Wang, Xiao-Lu Bian, Lu Li, Zhi-Yong Guo, Xue-Li Lai
For organic acid metabolism, we found that 3-hydroxybutyric acid levels were higher in EDS patients than in non-EDS patients. Interestingly, 3-hydroxybutyric acid is an inhibitor of histone deacetylases, resulting in the upregulation of genes involved in protection against oxidative stress and regulation of metabolism. It interacts with the inflammasome in immune cells to reduce the production of inflammatory cytokines and reduce inflammation [35]. Therefore, the change in 3-hydroxybutyric acid may be the compensatory mechanism by which oxidative stress and inflammation are inhibited. Previous studies have shown that sleep restriction increased 3-hydroxybutyric acid levels, which might be associated with increased hepatic fatty acid oxidation promoted by peroxisome proliferator-activated receptor α [36]. However, another trial demonstrated that plasma 3-hydroxybutyric acid levels were reduced in sleep restriction, which might be related to decreased nonesterified fatty acids [37]. In our study, EDS might promote fatty acid oxidation to produce energy, which is consistent with the low carnitine and high 3-hydroxybutyric acid levels. Ketogenic diet consumption and exogenous ketone supplementation have been attempted in a wide variety of neurological diseases, including epilepsy, neurotrauma, Alzheimer’s disease and Parkinson’s disease [38]. However, a ketogenic diet had no effect on subjective sleep quality in a sample of healthy individuals [39]. Thus, whether a ketogenic diet can improve EDS in PD patients needs further research.
Microbial polyhydroxyalkanoates as medical implant biomaterials
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2018
Guo-Qiang Chen, Junyu Zhang
The main component of PHBHHx is 3-hydroxybutyric acid (3HB), a ketone body that is also produced in vivo. Cheng et al. investigated the effects of 3HB treatment on murine fibroblast L929 cells, HUVECs and RACs. 0.005–0.10 g/L 3HB promoted cell proliferation for each cell line [134]. Cell cycle analysis indicated that 3HB had a stimulatory effect on DNA synthesis. In L929 cells, 0.02 g/L 3HB stimulated a rapid increase in the concentration of cytosolic calcium that was blocked by verapamil and diltiazem, inhibitors of L-type Ca2+ channels. Finally, verapamil inhibited 3HB-induced L929 cell proliferation. Collectively, these results indicated that 3HB had a stimulatory effect on cell cycle progression that is mediated by a signalling pathway dependent upon increases in intracellular Ca2+ concentration. 3HB also promoted proliferation of L929 cells in high-density cultures by preventing apoptotic and necrotic cell death [135]. These results indicated that PHBHHx degradation product 3HB was beneficial for L929 cell growth.
Impact of Acutely Increased Endogenous- and Exogenous Ketone Bodies on FGF21 Levels in Humans
Published in Endocrine Research, 2021
Esben Stistrup Lauritzen, Mads Vandsted Svart, Thomas Voss, Niels Møller, Mette Bjerre
In the ketone infusion study, we found no significant effects of OHB infusion (reaching 5.5 mmol/L) on FGF21 levels, but a trend to increased FGF21 levels was observed after 4 hours of OHB infusion compared with the control day. The OHB infusion was a racemic mixture of L and D-3 hydroxybutyric acid. The metabolic effects and metabolism of OHB are primarily investigated in the endogenous produced D enantiomer, whereas the metabolism and effects of the L enantiomer remain to be unraveled.33 Thus, we reached 2.75 mmol/L of D-hydroxybutyric acid. Comparisons between study 1/study 2 and study 3 are challenging since the endogenous production of ketone bodies include both OHB and acetoacetate. In study 3 we infused OHB, which previously has been shown to also increase acetoacetate levels,34 but the ratio between the two substances in plasma is probably determined by the mitochondrial redox state of the hepatocytes,1–2 which most likely was different between study1/study2 and study 3.
Related Knowledge Centers
- Chirality
- Enantiomer
- Fatty Acid Metabolism
- Liver
- Agonist
- Beta Hydroxy Acid
- Chemical Formula
- Conjugate
- G Protein-Coupled Receptor
- Butyric Acid