China
Africa
Explore chapters and articles related to this topic
Diabetic Ketoacidosis
Published in Stephen M. Cohn, Alan Lisbon, Stephen Heard, 50 Landmark Papers, 2021
Laboratory assessment of DKA includes testing for increased production of ketone bodies: ß-hydroxybutyric acid, acetoacetic acid, and acetone. The latter two are detectable in blood or urine by the semiquantitative nitroprusside test. This test fails to detect ß-hydroxybutyric acid, which is important because it is the predominant ketone in DKA, produced more than acetoacetic acid by a factor of 7–10. For this reason, the direct assay for ß-hydroxybutyric acid is preferred.
4-Hydroxybutyric aciduria
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
Other compounds found in the urine of patients include dicarboxylic acids, which might suggest a disorder of fatty acid oxidation [35]. 4-Hydroxybutyric acid is, after all, a short chain fatty acid. They could result from secondary inhibition of mitochondrial fatty acid oxidation. 4,5-dihydroxyhexanoic acid identified in the urine of these patients [35] has not been found in other metabolic diseases and so may be a specific marker for this disease. It could arise from the condensation of a 2-carbon moiety with succinic semialdehyde. The occurrence of 3-hydroxypropionic acid and glycine in the urine of some patients might suggest a diagnosis of a disorder of propionate metabolism. Identification of the key compound, 4-hydroxybutyric acid, should avoid any confusion. Glycine would be a product of glycolic acid, which can be formed from β-oxidation of 4-hydroxybutyric acid [36].
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.
The neurochemistry of hypnotic suggestion
Published in American Journal of Clinical Hypnosis, 2021
David J. Acunzo, David A. Oakley, Devin B. Terhune
Multiple reports imply that elevated GABA produces increased suggestibility. However, these data come from studies that lacked placebo-controlled trials and robust measures of suggestibility and thus should be considered preliminary. Early research suggested that amobarbital, a GABAA receptor agonist, increases suggestibility (Eysenck & Rees, 1945). Recent research has highlighted how the abuse of benzodiazepines, which include a large number of sedative GABAA agonists, produces automatism amnesia where individuals will perform seemingly automatic behaviors and display elevated suggestibility often followed by anterograde amnesia (Goullé & Anger, 2004; Marc et al., 2000). Benzodiazepines have also been cited as increasing suggestibility in the context of narcotherapy in functional neurological disorder (Rosebush & Mazurek, 2011). Gamma hydroxybutyric acid, a GABAB agonist used in the treatment of narcolepsy and as an anesthetic agent, has similarly been reported to increase suggestibility (e.g., Bismuth, Dally, & Borron, 1997). These encouraging, albeit preliminary, results point to a clear need to more rigorously assess the impact of GABA agonism on suggestibility, including an assessment of mediating factors to distinguish between competing interpretations of these results.
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].