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Botanicals and the Gut Microbiome
Published in Namrita Lall, 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.
Improvement of Cognitive Function in Patients with Alzheimer’s Disease using Ketogenic Diets
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Diet-induced ketosis was reported to upregulate GLUT1 as well as monocarboxylate transporters in rat brains, which may increase the utilization of not only ketone bodies but also glucose in the brain (Puchowicz et al. 2007). In-vitro studies demonstrated that β-hydroxybutyric acid protected hippocampal cells from β-amyloid-induced toxicity. β-Amyloid activates mitochondrial protein kinases, which inactivate the pyruvate dehydrogenase complex by phosphorylation. It is possible that β-hydroxybutyric acid bypasses a block at mitochondrial pyruvate dehydrogenase and supplies substrates for the TCA cycle, which helps maintain mitochondrial function (Kashiwaya et al. 2000). β-Hydroxybutyric acid has been demonstrated to act as an agonist to G-protein coupling receptor (GPR)-109A, which is expressed on glial cells and suppresses inflammation (Fu et al. 2015). These biological functions of ketone bodies beyond energy source may be involved in the improvement in cognitive function of patients with AD via ketogenic diets. A better understanding of these mechanisms would contribute to the development of more efficient management and therapies for AD.
Basic Concepts of Acid–Base Physiology
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
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.
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.
Ipragliflozin and sodium glucose transporter 2 inhibitors to reduce liver fat: will the prize we sought be won?
Published in Expert Opinion on Pharmacotherapy, 2018
Kalliopi Pafili, Efstratios Maltezos, Nikolaos Papanas
More recently, Ohta et al. [17] have investigated the effect of 24-week therapy with this agent (50 mg per day) in 20 T2DM Japanese patients (with mean body mass index: 29.7 ± 3.2kg/m2, body weight: 82.2 ± 11.3 kg, HbA1c: 8.2 ± 1.3%, VFV: 6303.9 ± 1907.3 cm3, SFV 7904.2 ± 2097 cm3). Primary outcome measures included change in VFV, abdominal SFV (assessed by whole abdominal computed tomography scanning), and IHLC (measured by proton magnetic resonance spectroscopy) after 12 and 24 weeks of treatment. Secondary end points included change of body fat and lean mass (assessed by dual X-ray absorptiometry) [17]. The authors reported that 12-week ipragliflozin administration resulted in reduction of body weight, body mass index, HbA1c, aminotransferases, fasting plasma glucose (FPG), and homeostasis model assessment of insulin resistance (HOMA-IR). However, only the first four aforementioned parameters decreased further at 24 weeks of therapy, whilst at that time point, a marginal increase of 3-hydroxybutyric acid was observed [17]. Further reductions were reported for fat mass, limbs lean mass, SFV, VFV, and IHLC at 12 and 24 weeks (p < 0.05 for all parameters at weeks 12 and 24 in comparison with baseline), but only VFV was further significantly reduced at week 24 as compared with reduction described at week 12 [17].
Microbial polyhydroxyalkanoates as medical implant biomaterials
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2018
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.