Journal articles: 'Plasma ketone'

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Bentourkia, M'hamed, Sébastien Tremblay, Fabien Pifferi, Jacques Rousseau, Roger Lecomte, and Stephen Cunnane. "PET study of 11C-acetoacetate kinetics in rat brain during dietary treatments affecting ketosis." American Journal of Physiology-Endocrinology and Metabolism 296, no. 4 (April 2009): E796—E801. http://dx.doi.org/10.1152/ajpendo.90644.2008.

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Normally, the brain's fuel is glucose, but during fasting it increasingly relies on ketones (β-hydroxybutyrate, acetoacetate, and acetone) produced in liver mitochondria from fatty acid β-oxidation. Although moderately raised blood ketones produced on a very high fat ketogenic diet have important clinical effects on the brain, including reducing seizures, ketone metabolism by the brain is still poorly understood. The aim of the present work was to assess brain uptake of carbon-11-labeled acetoacetate (11C-acetoacetate) by positron emission tomography (PET) imaging in the intact, living rat. To vary plasma ketones, we used three dietary conditions: high carbohydrate control diet (low plasma ketones), fat-rich ketogenic diet (raised plasma ketones), and 48-h fasting (raised plasma ketones). 11C-acetoacetate metabolism was measured in the brain, heart, and tissue in the mouth area. Using 11C-acetoacetate and small animal PET imaging, we have noninvasively quantified an approximately seven- to eightfold enhanced brain uptake of ketones on a ketogenic diet or during fasting. This opens up an opportunity to study brain ketone metabolism in humans.

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O’Malley, Trevor, Etienne Myette-Cote, Cody Durrer, and Jonathan P. Little. "Nutritional ketone salts increase fat oxidation but impair high-intensity exercise performance in healthy adult males." Applied Physiology, Nutrition, and Metabolism 42, no. 10 (October 2017): 1031–35. http://dx.doi.org/10.1139/apnm-2016-0641.

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This study investigated the impact of raising plasma beta-hydroxybutyrate (β-OHB) through ingestion of ketone salts on substrate oxidation and performance during cycling exercise. Ten healthy adult males (age, 23 ± 3 years; body mass index, 25 ± 3 kg/m2, peak oxygen uptake, 45 ± 10 mL/(kg·min)−1) were recruited to complete 2 experimental trials. Before enrollment in the experimental conditions, baseline anthropometrics and cardiorespiratory fitness (peak oxygen uptake) were assessed and familiarization to the study protocol was provided. On experimental days, participants reported to the laboratory in the fasted state and consumed either 0.3 g/kg β-OHB ketone salts or a flavour-matched placebo at 30 min prior to engaging in cycling exercise. Subjects completed steady-state exercise at 30%, 60%, and 90% ventilatory threshold (VT) followed by a 150-kJ cycling time-trial. Respiratory exchange ratio (RER) and total substrate oxidation were derived from indirect calorimetry. Plasma glucose, lactate, and ketones were measured at baseline, 30 min post-supplement, post–steady-state exercise, and immediately following the time-trial. Plasma β-OHB was elevated from baseline and throughout the entire protocol in the ketone condition (p < 0.05). RER was lower at 30% and 60% VT in the ketone compared with control condition. Total fat oxidation was greater in the ketone versus control (p = 0.05). Average time-trial power output was ∼7% lower (–16 W, p = 0.029) in the ketone condition. Ingestion of ketone salts prior to exercise increases fat oxidation during steady-state exercise but impairs high-intensity exercise performance.

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Nestler, James R. "Metabolic substrate change during daily torpor in deer mice." Canadian Journal of Zoology 69, no. 2 (February 1, 1991): 322–27. http://dx.doi.org/10.1139/z91-052.

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Various metabolic substrates were measured in plasma (glucose, free fatty acids (FFA), ketones, lactate), heart, liver, and skeletal muscle (glycogen, ketones, lactate) of deer mice (Peromyscus maniculatus) in association with their daily torpor cycle. Immediately after feeding, substrate levels were similar to those observed in other mammals. However, within 8–10 h carbohydrate indices (glucose, glycogen) decreased significantly in plasma, liver, and skeletal muscle, with prominent increases in FAA and ketones. Thus the metabolic condition of normothermic deer mice (body temperature 35–38 °C) resembled that seen during acute starvation. Conditions during the actual torpor bout (body temperature 19–24 °C) were similar to those immediately prior to torpor entrance. Glycogen levels in heart were actually highest during daily torpor, possibly as an 'anticipatory' response prior to arousal. Following arousal no repletion of glucose or glycogen was noted, while ketone levels exceeded 5 mM (plasma) and 5 μmol/g (tissues). Adjustments in FFA and ketone utilization may be important in sparing carbohydrate and protein during daily torpor, enabling foraging activity necessary for restoration of endogenous fuel following arousal.

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Avogaro, A., P. E. Cryer, and D. M. Bier. "Epinephrine's ketogenic effect in humans is mediated principally by lipolysis." American Journal of Physiology-Endocrinology and Metabolism 263, no. 2 (August 1, 1992): E250—E260. http://dx.doi.org/10.1152/ajpendo.1992.263.2.e250.

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To quantify epinephrine's effects on acetoacetate and beta-hydroxybutyrate kinetics, we infused subjects with 0.3 and 2.5 micrograms/min epinephrine, either alone or with a concomitant somatostatin infusion with insulin, glucagon, and growth hormone replaced at postabsorptive levels (islet clamp). Additional subjects received no epinephrine but sequential infusions of heparin plus 10% Intralipid at rates of 0.5 and 3.0 ml/min. Both epinephrine and Intralipid increased ketone body appearance (unaffected by islet clamp), augmented the interconversion rates between ketone bodies and, during the 2.5 micrograms/min infusion, caused a marked increase in beta-hydroxybutyrate appearance. The fraction of plasma free fatty acid (FFA) flux appearing as plasma ketones increased from 6 to 7% in the basal state to 11% at the high-epinephrine infusion. This fraction was also unaffected by the islet clamp and was not different from values obtained at similar Intralipid plus heparin-induced elevations in plasma FFA levels. We conclude that epinephrine's ketogenic effect in humans is primarily the result of its lipolytic effect, is accompanied by a significantly increased rate of ketone body interconversion, is manifest largely as an increase in plasma beta-hydroxybutyrate appearance at high plasma epinephrine values, and is not limited by portal insulin at post-absorptive levels.

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Leshem, M., F. W. Flynn, and A. N. Epstein. "Brain glucoprivation and ketoprivation do not promote ingestion in the suckling rat pup." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 258, no. 2 (February 1, 1990): R365—R375. http://dx.doi.org/10.1152/ajpregu.1990.258.2.r365.

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We examined the possibility that brain glucose or ketone availability may control suckling or precocious feeding in the preweanling rat. Brain glucoprivation induced by 5-thio-D-glucose injection into the 4th ventricle did not increase feeding on orally infused milk until 30 days of age, although hyperglycemia was evoked as early as 9 days by the same treatment. Plasma ketone levels varied with suckling status, but pharmacological blockade of hepatic free fatty acid oxidation, which restricts ketone availability (ketoprivation), failed to increase suckling. Because the suckling rat can switch energy substrates under nutritional duress, we combined glucoprivation and ketoprivation. Feeding was suppressed, and suckling was not affected. Finally, we injected ketones into the 3rd brain ventricle and found that they increased feeding. Thus, in contrast to the adult rat, reduced glucose or ketone utilization by the brain does not increase food intake in the preweanling, but increased circulating and brain ketone concentrations may arouse feeding.

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Valenzuela, Pedro L., Javier S. Morales, Adrián Castillo-García, and Alejandro Lucia. "Acute Ketone Supplementation and Exercise Performance: A Systematic Review and Meta-Analysis of Randomized Controlled Trials." International Journal of Sports Physiology and Performance 15, no. 3 (March 1, 2020): 298–308. http://dx.doi.org/10.1123/ijspp.2019-0918.

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Purpose: To determine the acute effects of ketone supplementation on exercise performance (primary outcome) and physiological and perceptual responses to exercise (secondary outcomes). Methods: A systematic search was conducted in PubMed, Web of Science, and SPORTDiscus (since inception to July 21, 2019) to find randomized controlled trials assessing the effects of acute ketone supplementation compared with a drink containing no ketones (ie, control intervention). The standardized mean difference (Hedges g) between interventions and 95% confidence interval (CI) were computed using a random-effects model. Results: Thirteen studies met all inclusion criteria. No significant differences were observed between interventions for overall exercise performance (Hedges g = −0.05; 95% CI, −0.30 to 0.20; P = .68). Subanalyses revealed no differences between interventions when analyzing endurance time-trial performance (g = −0.04; 95% CI, −0.35 to 0.28; P = .82) or when assessing the separate effects of supplements containing ketone esters (g = −0.07; 95% CI, −0.38 to 0.24; P = .66) or salts (g = −0.02; 95% CI, −0.45 to 0.41; P = .93). All studies reported increases in plasma ketone concentration after acute ketone supplementation, but no consistent effects were reported on the metabolic (plasma lactate and glucose levels), respiratory (respiratory exchange ratio, oxygen uptake, and ventilatory rate), cardiovascular (heart rate), or perceptual responses to exercise (rating of perceived exertion). Conclusions: The present findings suggest that ketone supplementation exerts no clear influence on exercise performance (from sprints to events lasting up to ∼50 min) or metabolic, respiratory, cardiovascular, or perceptual responses to exercise. More research is needed to elucidate if this strategy could provide ergogenic effects on other exercise types (eg, ultraendurance exercise).

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Ferrier, B., M. Martin, B. Janbon, and G. Baverel. "Transport of beta-hydroxybutyrate and acetoacetate along rat nephrons: a micropuncture study." American Journal of Physiology-Renal Physiology 262, no. 5 (May 1, 1992): F762—F769. http://dx.doi.org/10.1152/ajprenal.1992.262.5.f762.

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The transport of ketone bodies across the luminal membrane of the nephron was studied by means of micropuncture techniques in rats in normal acid-base state. The concentration of beta-hydroxybutyrate (beta-HB) and acetoacetate (AcAc) in plasma, tubular fluid and urine was measured by an ultramicromethod using enzymatic cycling. At endogenous plasma ketone body concentration, approximately 80% of the filtered load of beta-HB and AcAc was reabsorbed in the proximal convoluted tubule, the remaining fraction being almost completely reabsorbed between the late proximal convoluted and the distal tubule; under these conditions, the urinary excretion of ketone bodies was less than 1% of the filtered load. A progressive elevation to steady-state levels of plasma beta-HB resulted in a progressive reduction of the fractional reabsorption of beta-HB and AcAc in the proximal convoluted tubule, which means that reabsorption of ketone bodies in this nephron segment is saturable. No net secretion of ketone bodies could be demonstrated along the nephron even at the highest plasma ketone body concentrations reached. In clearance experiments, the capacity of the rat kidney for reabsorbing both beta-HB and AcAc was found to be limited by a maximal tubular capacity (Tm). The data suggest that, in the young Wistar rat nephron, most of the reabsorption of ketone bodies is carrier mediated.

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Rittig, Nikolaj, Mads Svart, Henrik Holm Thomsen, Esben Thyssen Vestergaard, Jens Frederik Rehfeld, Bolette Hartmann, Jens Juul Holst, Mogens Johannsen, Niels Møller, and Niels Jessen. "Oral D/L-3-Hydroxybutyrate Stimulates Cholecystokinin and Insulin Secretion and Slows Gastric Emptying in Healthy Males." Journal of Clinical Endocrinology & Metabolism 105, no. 10 (July 27, 2020): e3597-e3605. http://dx.doi.org/10.1210/clinem/dgaa483.

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Abstract Background D-3-hydroxybutyrate (D-3-OHB) is a ketone body that serves as an alternative nutritional fuel but also as an important signaling metabolite. Oral ketone supplements containing D/L-3-OHB are becoming a popular approach to achieve ketosis. Aim To explore the gut-derived effects of ketone supplements. Methods Eight healthy lean male volunteers were investigated on 2 separate occasions: An acetaminophen test was performed to evaluate gastric emptying and blood samples were obtained consecutively throughout the study period. Results We show that oral consumption of D/L-3-OHB stimulates cholecystokinin release (P = 0.02), elevates insulin (P = 0.03) and C-peptide (P < 0.001) concentrations, and slows gastric emptying (P = 0.01) compared with matched intravenous D/L-3-OHB administration. Measures of appetite and plasma concentrations of glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) were unaffected by interventions. Conclusion Our findings show that D/L-3-OHB exert incretin effects and indicate luminal sensing in the gut endothelium. This adds to our understanding of ketones as signaling metabolites and displays the important difference between physiological ketosis and oral ketone supplements.

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Kanikarla-Marie, Preeti, and Sushil K. Jain. "Role of Hyperketonemia in Inducing Oxidative Stress and Cellular Damage in Cultured Hepatocytes and Type 1 Diabetic Rat Liver." Cellular Physiology and Biochemistry 37, no. 6 (2015): 2160–70. http://dx.doi.org/10.1159/000438573.

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Background/Aims: Type 1 diabetic (T1D) patients have a higher incidence of liver disease. T1D patients frequently experience elevated plasma ketone levels along with hyperglycemia. However, no study has examined whether hyperketonemia per se has any role in excess liver damage in T1D. This study investigates the hypothesis that hyperketonemia can induce oxidative stress and cellular dysfunction. Methods: STZ treated diabetic rats, FL83B hepatocytes, and GCLC knocked down (GSH deficient) hepatocytes were used. Results: The blood levels of ALT and AST, biomarkers of liver damage, and ketones were elevated in T1D rats. An increase in NOX4 and ROS along with a reduction in GSH and GCLC levels was observed in T1D rat livers in comparison to those seen in non-diabetic control or type 2 diabetic rats. MCP-1 and ICAM-1 were also elevated in T1D rat livers and ketone treated hepatocytes. Macrophage markers CCR2 and CD11A that interact with MCP-1, and ICAM-1 respectively, were also elevated in the T1D liver, indicating macrophage infiltration. Additionally, activated macrophages increased hepatocyte damage with ketone treatment, which was similar to that seen in GCLC knockdown hepatocytes without ketones. Conclusion: Hyperketonemia per se can induce macrophage mediated damage to hepatocytes and the liver, caused by GSH depletion and oxidative stress up regulation in T1D.

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Mey, Jacob T., Adithya Hari, Christopher L. Axelrod, Ciarán E. Fealy, Melissa L. Erickson, John P. Kirwan, Raed A. Dweik, and Gustavo A. Heresi. "Lipids and ketones dominate metabolism at the expense of glucose control in pulmonary arterial hypertension: a hyperglycaemic clamp and metabolomics study." European Respiratory Journal 55, no. 4 (February 27, 2020): 1901700. http://dx.doi.org/10.1183/13993003.01700-2019.

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Individuals with idiopathic pulmonary arterial hypertension (PAH) display reduced oral glucose tolerance. This may involve defects in pancreatic function or insulin sensitivity but this hypothesis has not been tested; moreover, fasting nutrient metabolism remains poorly described in PAH. Thus, we aimed to characterise fasting nutrient metabolism and investigated the metabolic response to hyperglycaemia in PAH.12 participants (six PAH, six controls) were administered a hyperglycaemic clamp, while 52 (21 PAH, 31 controls) underwent plasma metabolomic analysis. Glucose, insulin, C-peptide, free fatty acids and acylcarnitines were assessed from the clamp. Plasma metabolomics was conducted on fasting plasma samples.The clamp verified a reduced insulin response to hyperglycaemia in PAH (−53% versus control), but with similar pancreatic insulin secretion. Skeletal muscle insulin sensitivity was unexpectedly greater in PAH. Hepatic insulin extraction was elevated in PAH (+11% versus control). Plasma metabolomics identified 862 metabolites: 213 elevated, 145 reduced in PAH (p<0.05). In both clamp and metabolomic cohorts, lipid oxidation and ketones were elevated in PAH. Insulin sensitivity, fatty acids, acylcarnitines and ketones correlated with PAH severity, while hepatic extraction and fatty acid:ketone ratio correlated with longer six-min walk distance.Poor glucose control in PAH could not be explained by pancreatic β-cell function or skeletal muscle insulin sensitivity. Instead, elevated hepatic insulin extraction emerged as an underlying factor. In agreement, nutrient metabolism in PAH favours lipid and ketone metabolism at the expense of glucose control. Future research should investigate the therapeutic potential of reinforcing lipid and ketone metabolism on clinical outcomes in PAH.

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El Midaoui, Adil, Jean Louis Chiasson, Gilles Tancrède, and André Nadeau. "Physical training reverses the increased activity of the hepatic ketone body synthesis pathway in chronically diabetic rats." American Journal of Physiology-Endocrinology and Metabolism 290, no. 2 (February 2006): E207—E212. http://dx.doi.org/10.1152/ajpendo.00608.2004.

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This study was designed to examine whether the training-induced improvement in the plasma concentration of ketone bodies in experimental diabetes mellitus could be explained by changes in the activity of the hepatic ketone body synthesis pathway and/or the plasma free fatty acid levels. Diabetes mellitus was induced by an intravenous injection of streptozotocin (50 mg/kg), and training was carried out on a treadmill. The plasma concentration of β-hydroxybutyric acid was increased ( P < 0.001) in sedentary diabetic rats, and this was partly reversed by training ( P < 0.001). The plasma concentration of free fatty acids was increased ( P < 0.001) in sedentary diabetic rats, and this was reversed to normal by training ( P < 0.001). Diabetes was also associated with an increased activity of the hepatic ketone body synthesis pathway. When the data are expressed as per total liver, physical training decreased the activity of the hepatic ketone body synthesis pathway by 18% in nondiabetic rats ( P < 0.05) and by 22% in diabetic rats ( P < 0.01), the activity present in trained diabetic rats being not statistically different from that of sedentary control rats. These data suggest that the beneficial effects of physical training on the plasma β-hydroxybutyric acid levels in the diabetic state are probably explained in part by a decrease in the activity of the hepatic ketone body synthesis pathway and in part by a decrease in plasma free fatty acid levels.

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Keller, U., P. P. Gerber, and W. Stauffacher. "Fatty acid-independent inhibition of hepatic ketone body production by insulin in humans." American Journal of Physiology-Endocrinology and Metabolism 254, no. 6 (June 1, 1988): E694—E699. http://dx.doi.org/10.1152/ajpendo.1988.254.6.e694.

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To investigate whether elevated plasma insulin or glucagon concentrations are capable of modifying hepatic ketogenesis independently of plasma free fatty acid (FFA) concentrations, ketone body production was determined by [3–14C]acetoacetate infusions in overnight-fasted normal subjects during exogenous supply of FFA (Intralipid and heparin infusion). When plasma FFA concentrations were elevated from 0.73 +/- 0.07 to 1.53 +/- 0.16 mmol/l during low insulin concentrations (approximately equal to 13 microU/ml) in group A (n = 7), total ketone body production increased from 3.6 +/- 0.6 to 8.2 +/- 1.0 mumol.kg-1.min-1 (P less than 0.001). When plasma FFA were similarly elevated during raised plasma insulin concentrations (approximately equal to 110 microU/ml) in group B (n = 5), total ketone body production was only 3.8 +/- 0.8 mumol.kg-1.min-1 (P less than 0.01 vs. group A). Low plasma FFA and low insulin concentrations resulted in total ketone body production of 0.70 +/- 0.18 mumol.kg-1.min-1 in group C (n = 7; P less than 0.01 vs. groups A and B). Elevation of plasma glucagon during Intralipid infusion in group D (n = 7) failed to affect ketogenesis, but the beta-hydroxybutyrate-to-acetoacetate concentration ratio decreased significantly (P less than 0.01). The data indicate that elevation of plasma insulin to high physiological concentrations restrains FFA-induced ketogenesis.

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Vandenberghe, Camille, Christian-Alexandre Castellano, Mathieu Maltais, Mélanie Fortier, Valérie St-Pierre, Isabelle J. Dionne, and Stephen C. Cunnane. "A short-term intervention combining aerobic exercise with medium-chain triglycerides (MCT) is more ketogenic than either MCT or aerobic exercise alone: a comparison of normoglycemic and prediabetic older women." Applied Physiology, Nutrition, and Metabolism 44, no. 1 (January 2019): 66–73. http://dx.doi.org/10.1139/apnm-2018-0367.

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The objectives of this study were to determine (i) whether a 5-day aerobic exercise (AE) program combined with a medium-chain triglyceride (MCT) supplement would increase the plasma ketone response in older women more than either intervention alone and (ii) whether ketonemia after these combined or separate treatments was alike in normoglycemic (NG) and prediabetic (PD) women. Older women (NG, n = 10; PD, n = 9) underwent a 4-h metabolic study after each of 4 different treatments: (i) no treatment (control), (ii) 5 days of MCT alone (30 g·day−1), (iii) 1 session of 30 min of AE alone, and (iv) 5 days of MCT and AE combined (MCT+AE). Blood was sampled every 30 min over 4 h for analysis. In NG, MCT+AE induced the highest area under the curve (AUC) for plasma ketones (835 ± 341 μmol·h·L−1); this value was 69% higher than that observed with MCT alone (P < 0.05). AUCs were not different between MCT alone and MCT+AE in PD, but both treatments induced a significantly higher AUC than the control or AE alone (P < 0.05). Although there was a trend towards a higher ketone AUC in NG versus PD with AE alone (P = 0.091), there was no significant difference between the ketone AUCs in PD and NG. In conclusion, MCT+AE was more ketogenic in older women than MCT or AE alone. MCT+AE had a synergistic effect on ketonemia in NG but not in PD. Whether improving insulin sensitivity with a longer term AE intervention can improve the ketogenic effect of MCT in PD and thereby increase brain ketone uptake in older people merits further investigation.

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Neudorf, Helena, Étienne Myette-Côté, and Jonathan P. Little. "The Impact of Acute Ingestion of a Ketone Monoester Drink on LPS-Stimulated NLRP3 Activation in Humans with Obesity." Nutrients 12, no. 3 (March 23, 2020): 854. http://dx.doi.org/10.3390/nu12030854.

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Activation of the NOD-like receptor pyrin-domain containing 3 (NLRP3) inflammasome is associated with chronic low-grade inflammation in metabolic diseases such as obesity. Mechanistic studies have shown that β-hydroxybutyrate (OHB) attenuates activation of NLRP3, but human data are limited. In a randomized, double-blind, placebo-controlled crossover trial (n = 11) we tested the hypothesis that acutely raising β-OHB by ingestion of exogenous ketones would attenuate NLRP3 activation in humans with obesity. Blood was sampled before and 30 min post-ingestion of a ketone monoester drink ((R)-3-hydroxybutyl (R)-3-hydroxybutyrate, 482 mg/kg body mass) or placebo. A 75 g oral glucose load was then ingested, and a third blood sample was obtained 60 min following glucose ingestion. NLRP3 activation was quantified by assessing monocyte caspase-1 activation and interleukin (IL)-1β secretion in ex vivo lipopolysaccharide (LPS)-stimulated whole-blood cultures. LPS-stimulated caspase-1 activation increased following glucose ingestion (main effect of time; p = 0.032), with no differences between conditions. IL-1β secretion did not differ between conditions but was lower 60 min post-glucose ingestion compared to the fasting baseline (main effect of time, p = 0.014). Plasma IL-1β was detectable in ~80% of samples and showed a decrease from fasting baseline to 60 min in the ketone condition only (condition × time interaction, p = 0.01). In individuals with obesity, an excursion into hyperglycemia following ingestion of a glucose load augments LPS-induced activation of caspase-1 in monocytes with no apparent impact of raising circulating β-OHB concentration via ingestion of exogenous ketones. Exogenous ketone supplementation may impact plasma IL-1β, but these findings require confirmation in studies with larger sample sizes.

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Prins, Philip J., Andrew P. Koutnik, Dominic P. D’Agostino, Christopher Q. Rogers, Jacob F. Seibert, Jillian A. Breckenridge, Daniel S. Jackson, Edward J. Ryan, Jeffrey D. Buxton, and Dana L. Ault. "Effects of an Exogenous Ketone Supplement on Five‐Kilometer Running Performance." Journal of Human Kinetics 72, no. 1 (March 31, 2020): 115–27. http://dx.doi.org/10.2478/hukin-2019-0114.

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AbstractNumerous oral ketone supplements are marketed with the claim that they will rapidly induce ketosis and improve exercise performance. The purpose of this study was to assess exercise performance time and related physiological, metabolic and perceptual responses of recreational endurance runners after ingestion of a commercially available oral ketone supplement. Recreational endurance runners (n = 10; age: 20.8 ± 1.0 years; body mass: 68.9 ± 5.6 kg; height: 175.6 ± 4.9 cm) participated in a double-blind, crossover, repeated-measures study where they were randomized to 300 mg.kg-1 body weight of an oral β-hydroxybutyrate-salt + Medium Chain Triglyceride (βHB-salt+MCT) ketone supplement or a flavor matched placebo (PLA) 60 min prior to performing a 5-km running time trial (5KTT) on a treadmill. Time, HR, RPE, affect, RER, VO2, VCO2, and VE were measured during the 5-km run. The Session RPE and affect (Feeling Scale) were obtained post-5KTT. Plasma glucose, lactate and ketones were measured at baseline, 60-min post-supplement, and immediately post-5KTT. Plasma R-βHB (endogenous isomer) was elevated from baseline and throughout the entire protocol under the βHB-salt+MCT condition (p < 0.05). No significant difference (58.3 ± 100.40 s; 95% CI: -130.12 – 13.52; p = 0.100) was observed between the βHB-salt+MCT supplement (1430.0 ± 187.7 s) and the PLA (1488.3 ± 243.8 s) in time to complete the 5KTT. No other differences (p > 0.05) were noted in any of the other physiological, metabolic or perceptual measures.

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Vandenberghe, Camille, Valérie St-Pierre, Alexandre Courchesne-Loyer, Marie Hennebelle, Christian-Alexandre Castellano, and Stephen C. Cunnane. "Caffeine intake increases plasma ketones: an acute metabolic study in humans." Canadian Journal of Physiology and Pharmacology 95, no. 4 (April 2017): 455–58. http://dx.doi.org/10.1139/cjpp-2016-0338.

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Brain glucose uptake declines during aging and is significantly impaired in Alzheimer’s disease. Ketones are the main alternative brain fuel to glucose so they represent a potential approach to compensate for the brain glucose reduction. Caffeine is of interest as a potential ketogenic agent owing to its actions on lipolysis and lipid oxidation but whether it is ketogenic in humans is unknown. This study aimed to evaluate the acute ketogenic effect of 2 doses of caffeine (2.5; 5.0 mg/kg) in 10 healthy adults. Caffeine given at breakfast significantly stimulated ketone production in a dose-dependent manner (+88%; +116%) and also raised plasma free fatty acids. Whether caffeine has long-term ketogenic effects or could enhance the ketogenic effect of medium chain triglycerides remains to be determined.

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Hawkins, R. A., A. M. Mans, and D. W. Davis. "Regional ketone body utilization by rat brain in starvation and diabetes." American Journal of Physiology-Endocrinology and Metabolism 250, no. 2 (February 1, 1986): E169—E178. http://dx.doi.org/10.1152/ajpendo.1986.250.2.e169.

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The rate of ketone body (beta-hydroxybutyrate and acetoacetate) metabolism was measured in individual cerebral structures of fed, starved, and diabetic rats. This was done by infusing beta-[3-14C]hydroxybutyrate intravenously and measuring the incorporation of 14C into brain by quantitative autoradiography. The capacity of the brain to use ketone bodies, expressed as plasma clearance, increased in starvation and diabetes by approximately 50-60%. Plasma clearance was near maximal after 2 days starvation and was not significantly increased after 4 days starvation, 6 days of diabetes or 28 days of diabetes. In all situations the ketone bodies provided only a modest amount of fuel for brain energy metabolism; 3.2% after 2 days starvation and 6.5 and 9.9% after 6 and 28 days of diabetes. The fraction of their energy requirement which the various structures could derive from the ketone bodies differed widely. In general the telencephalon made greatest use of ketone bodies, whereas the hindbrain used least. There was no correlation between the energy requirement of structures (estimated from glucose use in fed rats) and the fraction of energy they could derive from ketone bodies.

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McCarthy, Devin G., William Bostad, Fiona J. Powley, Jonathan P. Little, Douglas L. Richards, and Martin J. Gibala. "Increased cardiorespiratory stress during submaximal cycling after ketone monoester ingestion in endurance-trained adults." Applied Physiology, Nutrition, and Metabolism 46, no. 8 (August 2021): 986–93. http://dx.doi.org/10.1139/apnm-2020-0999.

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There is growing interest in the effect of exogenous ketone body supplementation on exercise responses and performance. The limited studies to date have yielded equivocal data, likely due in part to differences in dosing strategy, increase in blood ketones, and participant training status. Using a randomized, double-blind, counterbalanced design, we examined the effect of ingesting a ketone monoester (KE) supplement (600 mg/kg body mass) or flavour-matched placebo in endurance-trained adults (n = 10 males, n = 9 females; V̇O2peak = 57 ± 8 mL/kg/min). Participants performed a 30-min cycling bout at ventilatory threshold intensity (71 ± 3% V̇O2peak), followed 15 min later by a 3 kJ/kg body mass time-trial. KE versus placebo ingestion increased plasma β-hydroxybutyrate concentration before exercise (3.9 ± 1.0 vs 0.2 ± 0.3 mM, p < 0.0001, dz = 3.4), ventilation (77 ± 17 vs 71 ± 15 L/min, p < 0.0001, dz = 1.3) and heart rate (155 ± 11 vs 150 ± 11 beats/min, p < 0.001, dz = 1.2) during exercise, and rating of perceived exertion at the end of exercise (15.4 ± 1.6 vs 14.5 ± 1.2, p < 0.01, dz = 0.85). Plasma β-hydroxybutyrate concentration remained higher after KE vs placebo ingestion before the time-trial (3.5 ± 1.0 vs 0.3 ± 0.2 mM, p < 0.0001, dz = 3.1), but performance was not different (KE: 16:25 ± 2:50 vs placebo: 16:06 ± 2:40 min:s, p = 0.20; dz = 0.31). We conclude that acute ingestion of a relatively large KE bolus dose increased markers of cardiorespiratory stress during submaximal exercise in endurance-trained participants. Novelty: Limited studies have yielded equivocal data regarding exercise responses after acute ketone body supplementation. Using a randomized, double-blind, placebo-controlled, counterbalanced design, we found that ingestion of a large bolus dose of a commercial ketone monoester supplement increased markers of cardiorespiratory stress during cycling at ventilatory threshold intensity in endurance-trained adults.

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El Midaoui, Adil, Jean Louis Chiasson, Gilles Tancrède, and André Nadeau. "Physical training reverses defect in 3-ketoacid CoA-transferase activity in skeletal muscle of diabetic rats." American Journal of Physiology-Endocrinology and Metabolism 288, no. 4 (April 2005): E748—E752. http://dx.doi.org/10.1152/ajpendo.00515.2004.

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To investigate one potential mechanism whereby physical training improves the plasma concentration of ketone bodies in experimental diabetes mellitus, we measured the activity of 3-ketoacid CoA-transferase, the key enzyme in the peripheral utilization of ketone bodies. Diabetes was induced with streptozotocin (50 mg/kg) and training carried out on a treadmill with a progressive 10-wk program. Diabetes resulted in an increase ( P < 0.001) in plasma concentration of β-hydroxybutyric acid in sedentary rats, which was partly reversed by training ( P < 0.001). Diabetes was also associated with a decreased activity of 3-ketoacid CoA-transferase in gastrocnemius muscle. When expressed per total gastrocnemius, training increased the activity of 3-ketoacid CoA-transferase by 66% in nondiabetic rats ( P < 0.001) and by 150% in diabetic rats ( P < 0.001), the decrease present in diabetic rats being fully reversed by training. Simple linear regression between the log of 3-ketoacid CoA-transferase activity and the log of plasma β-hydroxybutyric acid levels showed a statistically significant ( r = 0.563, P < 0.001) negative correlation. The beneficial effects of training on plasma ketone bodies in diabetic rats are probably explained, at least in part, by an increase in ketone body utilization, mediated by an increase in skeletal muscle 3-ketoacid CoA-transferase activity.

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Mey, Jacob T., Melissa L. Erickson, Christopher L. Axelrod, William T. King, Chris A. Flask, Arthur J. McCullough, and John P. Kirwan. "β-Hydroxybutyrate is reduced in humans with obesity-related NAFLD and displays a dose-dependent effect on skeletal muscle mitochondrial respiration in vitro." American Journal of Physiology-Endocrinology and Metabolism 319, no. 1 (July 1, 2020): E187—E195. http://dx.doi.org/10.1152/ajpendo.00058.2020.

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Nonalcoholic fatty liver disease (NAFLD) is characterized by hepatic fat accumulation and impaired insulin sensitivity. Reduced hepatic ketogenesis may promote these pathologies, but data are inconclusive in humans and the link between NAFLD and reduced insulin sensitivity remains obscure. We investigated individuals with obesity-related NAFLD and hypothesized that β-hydroxybutyrate (βOHB; the predominant ketone species) would be reduced and related to hepatic fat accumulation and insulin sensitivity. Furthermore, we hypothesized that ketones would impact skeletal muscle mitochondrial respiration in vitro. Hepatic fat was assessed by 1H-MRS in 22 participants in a parallel design, case control study [Control: n = 7, age 50 ± 6 yr, body mass index (BMI) 30 ± 1 kg/m2; NAFLD: n = 15, age 57 ± 3 yr, BMI 35 ± 1 kg/m2]. Plasma assessments were conducted in the fasted state. Whole body insulin sensitivity was determined by the gold-standard hyperinsulinemic-euglycemic clamp. The effect of ketone dose (0.5–5.0 mM) on mitochondrial respiration was conducted in human skeletal muscle cell culture. Fasting βOHB, a surrogate measure of hepatic ketogenesis, was reduced in NAFLD (−15.6%, P < 0.01) and correlated negatively with liver fat ( r2 = 0.21, P = 0.03) and positively with insulin sensitivity ( r2 = 0.30, P = 0.01). Skeletal muscle mitochondrial oxygen consumption increased with low-dose ketones, attributable to increases in basal respiration (135%, P < 0.05) and ATP-linked oxygen consumption (136%, P < 0.05). NAFLD pathophysiology includes impaired hepatic ketogenesis, which is associated with hepatic fat accumulation and impaired insulin sensitivity. This reduced capacity to produce ketones may be a potential link between NAFLD and NAFLD-associated reductions in whole body insulin sensitivity, whereby ketone concentrations impact skeletal muscle mitochondrial respiration.

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21

Metcalfe, H. K., J. P. Monson, S. G. Welch, and R. D. Cohen. "Carrier-mediated efflux of ketone bodies in isolated rat hepatocytes." Clinical Science 71, no. 6 (December 1, 1986): 755–61. http://dx.doi.org/10.1042/cs0710755.

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1. The rate of efflux of ketone bodies has been studied in isolated hepatocytes prepared from starved rats and preloaded with d-3-[14C]hydroxybutyrate. 2. Efflux of ketone bodies was temperature-dependent, saturable and inhibited by α-cyano-3-hydroxycinnamate and phloretin. The rate of efflux was also reduced by 6 mmol/l lactate and pyruvate added to the external medium. 3. Under conditions of simulated metabolic acidosis in the hepatocyte suspension medium, ketone body efflux rate was reduced. 4. The experimental data suggest that hepatic plasma membrane ketone body transit is carrier-mediated.

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22

Courchesne-Loyer, Alexandre, Etienne Croteau, Christian-Alexandre Castellano, Valérie St-Pierre, Marie Hennebelle, and Stephen C. Cunnane. "Inverse relationship between brain glucose and ketone metabolism in adults during short-term moderate dietary ketosis: A dual tracer quantitative positron emission tomography study." Journal of Cerebral Blood Flow & Metabolism 37, no. 7 (October 1, 2016): 2485–93. http://dx.doi.org/10.1177/0271678x16669366.

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Ketones (principally β-hydroxybutyrate and acetoacetate (AcAc)) are an important alternative fuel to glucose for the human brain, but their utilisation by the brain remains poorly understood. Our objective was to use positron emission tomography (PET) to assess the impact of diet-induced moderate ketosis on cerebral metabolic rate of acetoacetate (CMRa) and glucose (CMRglc) in healthy adults. Ten participants (35 ± 15 y) received a very high fat ketogenic diet (KD) (4.5:1; lipid:protein plus carbohydrates) for four days. CMRa and CMRglc were quantified by PET before and after the KD with the tracers, 11C-AcAc and 18F-fluorodeoxyglucose (18F-FDG), respectively. During the KD, plasma ketones increased 8-fold ( p = 0.005) while plasma glucose decreased by 24% ( p = 0.005). CMRa increased 6-fold ( p = 0.005), whereas CMRglc decreased by 20% ( p = 0.014) on the KD. Plasma ketones were positively correlated with CMRa (r = 0.93; p < 0.0001). After four days on the KD, CMRa represented 17% of whole brain energy requirements in healthy adults with a 2-fold difference across brain regions (12–24%). The CMR of ketones (AcAc and β-hydroxybutyrate combined) while on the KD was estimated to represent about 33% of brain energy requirements or approximately double the CMRa. Whether increased ketone availability raises CMR of ketones to the same extent in older people as observed here or in conditions in which chronic brain glucose hypometabolism is present remains to be determined.

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Uno, S., O. Takehiro, R. Tabata, and K. Ozawa. "Enzymatic method for determining ketone body ratio in arterial blood." Clinical Chemistry 41, no. 12 (December 1, 1995): 1745–50. http://dx.doi.org/10.1093/clinchem/41.12.1745.

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Abstract We have developed a new, sensitive, and rapid method for measuring the ketone body concentration in arterial blood and determining the arterial blood ketone body ratio. The procedure involves the sequential use of the enzymes 3-hydroxybutyrate dehydrogenase (3-HBDH; EC 1.1.1.30) and NADH oxidase, followed by a color-generating reaction with the hydrogen peroxide produced by the oxidase reaction. The amount of oxidized chromogen produced is proportional to the 3-hydroxybutyrate (3-HBA) concentration. The acetoacetate (AcAc) concentration is obtained after complete conversion of the AcAc to 3-HBA, in the presence of 3-HBDH. The total 3-HBA concentration is measured and then subtracted from the total ketone body concentration to give the AcAc concentration. This procedure may be applied to plasma samples and the absorbance change measured with an automated chemistry analyzer. Ketone body concentration may be determined over the range 0 to 400 mumol/L. The analysis takes approximately 12 min and requires only 30 microL of plasma.

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24

Zhang, Yifan, Youzhi Kuang, Kui Xu, Donald Harris, Zhenghong Lee, Joseph LaManna, and Michelle A. Puchowicz. "Ketosis Proportionately Spares Glucose Utilization in Brain." Journal of Cerebral Blood Flow & Metabolism 33, no. 8 (June 5, 2013): 1307–11. http://dx.doi.org/10.1038/jcbfm.2013.87.

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The brain is dependent on glucose as a primary energy substrate, but is capable of utilizing ketones such as β-hydroxybutyrate and acetoacetate, as occurs with fasting, starvation, or chronic feeding of a ketogenic diet. The relationship between changes in cerebral metabolic rates of glucose (CMRglc) and degree or duration of ketosis remains uncertain. To investigate if CMRglc decreases with chronic ketosis, 2-[18F]fluoro-2-deoxy-D-glucose in combination with positron emission tomography, was applied in anesthetized young adult rats fed 3 weeks of either standard or ketogenic diets. Cerebral metabolic rates of glucose (μmol/min per 100 g) was determined in the cerebral cortex and cerebellum using Gjedde-Patlak analysis. The average CMRglc significantly decreased in the cerebral cortex (23.0 ±4.9 versus 32.9 ±4.7) and cerebellum (29.3 ± 8.6 versus 41.2 ±6.4) with increased plasma ketone bodies in the ketotic rats compared with standard diet group. The reduction of CMRg|c in both brain regions correlates linearly by ∼9% for each 1 mmol/L increase of total plasma ketone bodies (0.3 to 6.3 mmol/L). Together with our meta-analysis, these data revealed that the degree and duration of ketosis has a major role in determining the corresponding change in CMRglc with ketosis.

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25

Song, Jiang-Ping, Liang Chen, Xiao Chen, Jie Ren, Ning-Ning Zhang, Tiara Tirasawasdichai, Zhen-Liang Hu, et al. "Elevated plasma β-hydroxybutyrate predicts adverse outcomes and disease progression in patients with arrhythmogenic cardiomyopathy." Science Translational Medicine 12, no. 530 (February 12, 2020): eaay8329. http://dx.doi.org/10.1126/scitranslmed.aay8329.

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Sudden death could be the first symptom of patients with arrhythmogenic cardiomyopathy (AC), a disease for which clinical indicators predicting adverse progression remain lacking. Recent findings suggest that metabolic dysregulation is present in AC. We performed this study to identify metabolic indicators that predicted major adverse cardiac events (MACEs) in patients with AC and their relatives. Comparing explanted hearts from patients with AC and healthy donors, we identified deregulated metabolic pathways using quantitative proteomics. Right ventricles (RVs) from patients with AC displayed elevated ketone metabolic enzymes, OXCT1 and HMGCS2, suggesting higher ketone metabolism in AC RVs. Analysis of matched coronary artery and sinus plasma suggested potential ketone body synthesis at early-stage AC, which was validated using patient-derived induced pluripotent stem cell–derived cardiomyocytes (iPSC-CMs) in vitro. Targeted metabolomics analysis in RVs from end-stage AC revealed a “burned-out” state, with predominant medium-chain fatty acid rather than ketone body utilization. In an independent validation cohort, 65 probands with mostly non–heart failure manifestations of AC had higher plasma β-hydroxybutyrate (β-OHB) than 62 healthy volunteers (P < 0.001). Probands with AC with MACE had higher β-OHB than those without MACE (P < 0.001). Among 94 relatives of probands, higher plasma β-OHB distinguished 25 relatives having suspected AC from nonaffected relatives. This study demonstrates that elevated plasma β-OHB predicts MACE in probands and disease progression in patients with AC and their clinically asymptomatic relatives.

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26

Inaba, T., W. Kalow, T. Someya, S. Takahashi, S. W. Cheung, and S. W. Tang. "Haloperidol reduction can be assayed in human red blood cells." Canadian Journal of Physiology and Pharmacology 67, no. 11 (November 1, 1989): 1468–69. http://dx.doi.org/10.1139/y89-237.

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One metabolite of haloperidol present in plasma is "reduced haloperidol." This study demonstrates that human red blood cells are capable of converting haloperidol to reduced haloperidol in vitro. The reductase involved requires NADPH, as does haloperidol (ketone) reductase in human liver cytosol.Key words: haloperidol reductase, human red blood cells, ketone reductase.

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27

Kumar, Dileep, Muhammad Zubair Nasim, Bilal Ahmad Shoukat, and Syed Shabahat Ali Shah. "Presentation of mixed diabetic ketoacidosis and metabolic acidosis due to ileal neobladder reconstruction." BMJ Case Reports 14, no. 2 (February 2021): e223668. http://dx.doi.org/10.1136/bcr-2017-223668.

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Diabetic ketoacidosis (DKA) is one of the most serious acute metabolic complications of diabetes mellitus. It is characterised by the biochemical triad of hyperglycaemia, ketonemia/ketonuria, and an increased anion gap metabolic acidosis. In this case, a 40-year-old male patient presented to the emergency department, with vomiting, nausea, polydipsia, polyuria and weight loss. He was found to have an elevated plasma glucose, despite having no known history of diabetes mellitus. His medical history was significant for spina bifida and ileal neobladder reconstruction. The plasma glucose level was 38 mmol/L. Blood gas analysis showed normal anion gap metabolic acidosis with high chloride and low bicarbonate. His plasma ketone level was 4.5 mmol/L. No significant reason for hyperchloraemia was identified. On initiation of DKA regimen, his condition improved and serum ketones normalised. Due to persistent hyperchloraemic metabolic acidosis, bicarbonate infusion was administered and his metabolic acidosis resolved.

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Zeugswetter, Florian, Stephanie Handl, Christine Iben, and Ilse Schwendenwein. "Efficacy of plasma ß-hydroxybutyrate concentration as a marker for diabetes mellitus in acutely sick cats." Journal of Feline Medicine and Surgery 12, no. 4 (April 2010): 300–305. http://dx.doi.org/10.1016/j.jfms.2009.10.002.

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Urine ketone measurement is routinely performed in cats with diabetes mellitus to identify impending or established ketoacidosis. Studies using the urinary ketone dipstick test have shown that ketonuria is common in cats with newly diagnosed untreated diabetes mellitus. This test has a low sensitivity as it quantifies the less abundant ketone acetoacetate. The objective of the present study was to determine if ketonaemia is an inherent biochemical finding in untreated feline diabetes mellitus by measuring plasma ß-hydroxybutyrate (ß-OHB) in acutely sick cats. In 122 sick cats (37 diabetic and 85 non-diabetic cats) plasma ß-OHB, glucose, fructosamine, total protein and thyroxine were measured as part of the routine work up. Diabetic cats had significantly elevated ß-OHB values and ß-OHB measurement was a sensitive and specific test to identify diabetes mellitus. The area under the receiver operating characteristic (ROC) curve was 0.93. The cut off value with the highest positive likelihood ratio was 0.58 mmol/l. These results suggest that determination of plasma ß-OHB concentration is a useful method to distinguish between diabetic and non-diabetic sick cats.

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Hasselbalch, S. G., G. M. Knudsen, J. Jakobsen, L. P. Hageman, S. Holm, and O. B. Paulson. "Blood-brain barrier permeability of glucose and ketone bodies during short-term starvation in humans." American Journal of Physiology-Endocrinology and Metabolism 268, no. 6 (June 1, 1995): E1161—E1166. http://dx.doi.org/10.1152/ajpendo.1995.268.6.e1161.

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The blood-brain barrier (BBB) permeability for glucose and beta-hydroxybutyrate (beta-OHB) was studied by the intravenous double-indicator method in nine healthy subjects before and after 3.5 days of starvation. In fasting, mean arterial plasma glucose decreased and arterial concentration of beta-OHB increased, whereas cerebral blood flow remained unchanged. The permeability-surface area product for BBB glucose transport from blood to brain (PS1) increased by 55 +/- 31%, whereas no significant change in the permeability from brain back to blood (PS2) was found. PS1 for beta-OHB remained constant during starvation. The expected increase in PS1 due to the lower plasma glucose concentration was calculated to be 22% using previous estimates of maximal transport velocity and Michaelis-Menten affinity constant for glucose transport. The determined increase was thus 33% higher than the expected increase and can only be partially explained by the decrease in plasma glucose. It is concluded that a modest upregulation of glucose transport across the BBB takes place after starvation. Brain transport of beta-OHB did not decrease as expected from the largely increased beta-OHB arterial level. This might be interpreted as an increase in brain transport of beta-OHB, which could be caused by induction mechanisms, but the large nonsaturable component of beta-OHB transport makes such a conclusion difficult. However, beta-OHB blood concentration and beta-OHB influx into the brain increased by > 10 times. This implies that the influx of ketone bodies into the brain is largely determined by the amount of ketones present in the blood, and any condition in which ketonemia occurs will lead to an increased ketone influx.

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30

Castellini, M. A., and D. P. Costa. "Relationships between plasma ketones and fasting duration in neonatal elephant seals." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 259, no. 5 (November 1, 1990): R1086—R1089. http://dx.doi.org/10.1152/ajpregu.1990.259.5.r1086.

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Long-duration fasting in mammals can ultimately lead to stage three terminal starvation, which is characterized by depleted fat stores, a metabolic shift away from fat metabolism toward lean tissue catabolism, and a sharp decline in circulating levels of plasma fatty acids and ketone bodies. However, this biochemical shift has never been observed outside of the laboratory in a naturally fasting, nonhibernating mammal. In the current study, plasma levels of the ketone body D-beta-hydroxybutyrate (beta-HBA) were assayed in 10 Northern elephant seal pups during suckling and the postweaning fast and in 12 fasting adult seals. Plasma beta-HBA concentration in the pups was minimal during suckling (0.09 +/- 0.06 mM; n = 10) and began to increase immediately after weaning. The concentration rose until about 55 days into the fast (1.34 +/- 0.36 mM; n = 10) and then declined sharply. Within 10 days of this deflection point, the seal pups left for sea. By contrast, adult elephant seals showed consistently low levels of beta-HBA after several months of fasting (0.06 +/- 0.07 mM; n = 12). The data suggest that the duration of fasting in elephant seal pups may be determined, in part, by biochemical shifts that occur near the end of the fast and that the regulation of ketone concentration is different in fasting neonatal and adult elephant seals.

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Note, Reine, Caroline Maisonneuve, Philippe Lettéron, Gilles Peytavin, Fatima Djouadi, Anissa Igoudjil, Marie-Christine Guimont, Michel Biour, Dominique Pessayre, and Bernard Fromenty. "Mitochondrial and Metabolic Effects of Nucleoside Reverse Transcriptase Inhibitors (NRTIs) in Mice Receiving One of Five Single- and Three Dual-NRTI Treatments." Antimicrobial Agents and Chemotherapy 47, no. 11 (November 2003): 3384–92. http://dx.doi.org/10.1128/aac.47.11.3384-3392.2003.

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ABSTRACT Although treatments with nucleoside reverse transcriptase inhibitors (NRTIs) can modify fat metabolism and fat distribution in humans, the mechanisms of these modifications and the roles of diverse NRTIs are unknown. We studied the mitochondrial and metabolic effects of stavudine (d4T), zidovudine (AZT), didanosine (ddI), lamivudine (3TC), zalcitabine (ddC), and three combinations (AZT-3TC, d4T-3TC, and d4T-ddI) in mice treated for 2 weeks with daily doses equivalent to the human dose per body area. Concentrations of AZT and d4T in plasma were lower when these drugs were administered with 3TC or ddI. Whatever the treatment, mitochondrial DNA was not significantly decreased in muscle, heart, brain, or white adipose tissue but was moderately decreased in liver tissue after the administration of AZT, 3TC, or d4T alone. Blood lactate was unchanged, even when NRTIs were administered at supratherapeutic doses. In contrast, the level of plasma ketone bodies increased with the administration of AZT or high doses of d4T but not with ddC, 3TC, or ddI, suggesting that the thymine moiety could be involved. Indeed, the levels of plasma ketone bodies increased in mice treated with β-aminoisobutyric acid, a thymine catabolite. Treatment with AZT, d4T, or β-aminoisobutyric acid increased hepatic carnitine palmitoyltransferase I (CPT-I) mRNA expression and the mitochondrial generation of ketone bodies from palmitate. In conclusion, therapeutic doses of NRTIs have no or moderate effects on mitochondrial DNA and no effects on plasma lactate in mice. However, AZT and high doses of d4T increase the levels of hepatic CPT-I, mitochondrial fatty acid β-oxidation, and ketone bodies, and these catabolic effects are reproduced by β-aminoisobutyric acid, a thymine metabolite.

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Amiel, Stephanie A., Helen R. Archibald, Gary Chusney, Alistair J. K. Williams, and Edwin A. M. Gale. "Ketone infusion lowers hormonal responses to hypoglycaemia: Evidence for acute cerebral utilization of a non-glucose fuel." Clinical Science 81, no. 2 (August 1, 1991): 189–94. http://dx.doi.org/10.1042/cs0810189.

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1. The effect of hyperketonaemia on counter-regulatory hormone responses to hypoglycaemia has been examined in six healthy subjects. 2. A controlled, step-wise reduction in blood glucose concentration was achieved by adjusting the rate of glucose infusion during a primed-continuous infusion of soluble insulin (1.5 m-units min−1 kg−1 body weight, plasma insulin concentration approximately 90 m-units/l). Simultaneous infusion of either saline or β-hydroxybutyrate (3 mg min−1 kg−1 body weight) was administered in a single-blind fashion, in random order. Despite a need for 40% more glucose during the ketone infusion, an identical fall in blood glucose concentration was achieved in each study. 3. The glycaemic threshold for stimulating an adrenaline response of 0.41 nmol/l was reduced from 3.1 to 2.8 mmol/l (P < 0.05) during ketone infusion, and that for stimulating a response of more than 50% of basal from 3.6 to 3.1 mmol/l (P < 0.001). The peak adrenaline response fell from 7.97 to 2.6 nmol/l (P < 0.04). Peak noradrenaline, cortisol and growth hormone responses were also significantly lower during ketone infusion (P = 0.04, 0.001 and 0.006, respectively). Glucagon responses alone were unaffected by hyperketonaemia. 4. The provision of an alternate metabolic fuel thus produced immediate changes in the neurohumoral responses to hypoglycaemia. This is consistent with the hypothesis that human nervous tissue can metabolize ketones acutely.

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Tordoff, M. G., and M. I. Friedman. "Hepatic control of feeding: effect of glucose, fructose, and mannitol infusion." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 254, no. 6 (June 1, 1988): R969—R976. http://dx.doi.org/10.1152/ajpregu.1988.254.6.r969.

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Plasma fuels, pancreatic hormones, liver glycogen, and food and water intake were measured immediately before or during the nocturnal feeding period of rats given hepatic portal or jugular infusions of glucose, fructose, and mannitol (0.3 M x 10 ml/2 h). Compared with mock and saline control infusions, hepatic portal glucose, fructose, and mannitol reliably and equally decreased food intake. Jugular fructose and mannitol also decreased food intake when infused before rats ate but not while they ate. Jugular glucose infusion did not affect food intake. Hepatic portal glucose did not reliably elevate systemic plasma glucose or insulin but increased hepatic glycogen content, indicating that most infused glucose was taken up by the liver. In contrast, jugular glucose increased systemic plasma glucose and insulin but did not affect hepatic glycogen. Hepatic portal fructose decreased plasma ketones and increased triglycerides and liver glycogen. Jugular fructose also decreased ketone levels and tended to increase liver glycogen. Mannitol by either route decreased plasma glucose and increased plasma free fatty acids. These results indicate that hepatic portal infusions that produce changes in plasma fuel concentrations within the physiological range decrease food intake. They strongly suggest this is accomplished by a direct action of the infusates on the metabolism of the liver.

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Blomqvist, G., M. Alvarsson, V. Grill, G. Von Heijne, M. Ingvar, J. O. Thorell, S. Stone-Elander, L. Widén, and K. Ekberg. "Effect of acute hyperketonemia on the cerebral uptake of ketone bodies in nondiabetic subjects and IDDM patients." American Journal of Physiology-Endocrinology and Metabolism 283, no. 1 (July 1, 2002): E20—E28. http://dx.doi.org/10.1152/ajpendo.00294.2001.

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Using R-β-[1-11C]hydroxybutyrate and positron emission tomography, we studied the effect of acute hyperketonemia (range 0.7–1.7 μmol/ml) on cerebral ketone body utilization in six nondiabetic subjects and six insulin-dependent diabetes mellitus (IDDM) patients with average metabolic control (HbA1c = 8.1 ± 1.7%). An infusion of unlabeled R-β-hydroxybutyrate was started 1 h before the bolus injection of R-β-[1-11C]hydroxybutyrate. The time course of the radioactivity in the brain was measured during 10 min. For both groups, the utilization rate of ketone bodies was found to increase nearly proportionally with the plasma concentration of ketone bodies (1.0 ± 0.3 μmol/ml for nondiabetic subjects and 1.3 ± 0.3 μmol/ml for IDDM patients). No transport of ketone bodies from the brain could be detected. This result, together with a recent study of the tissue concentration of R-β-hydroxybutyrate in the brain by magnetic resonance spectroscopy, indicate that, also at acute hyperketonemia, the rate-limiting step for ketone body utilization is the transport into the brain. No significant difference in transport and utilization of ketone bodies could be detected between the nondiabetic subjects and the IDDM patients.

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Miyamoto, Junki, Ryuji Ohue-Kitano, Hiromi Mukouyama, Akari Nishida, Keita Watanabe, Miki Igarashi, Junichiro Irie, et al. "Ketone body receptor GPR43 regulates lipid metabolism under ketogenic conditions." Proceedings of the National Academy of Sciences 116, no. 47 (November 4, 2019): 23813–21. http://dx.doi.org/10.1073/pnas.1912573116.

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Ketone bodies, including β-hydroxybutyrate and acetoacetate, are important alternative energy sources during energy shortage. β-Hydroxybutyrate also acts as a signaling molecule via specific G protein-coupled receptors (GPCRs); however, the specific associated GPCRs and physiological functions of acetoacetate remain unknown. Here we identified acetoacetate as an endogenous agonist for short-chain fatty acid (SCFA) receptor GPR43 by ligand screening in a heterologous expression system. Under ketogenic conditions, such as starvation and low-carbohydrate diets, plasma acetoacetate levels increased markedly, whereas plasma and cecal SCFA levels decreased dramatically, along with an altered gut microbiota composition. In addition, Gpr43-deficient mice showed reduced weight loss and suppressed plasma lipoprotein lipase activity during fasting and eucaloric ketogenic diet feeding. Moreover, Gpr43-deficient mice exhibited minimal weight decrease after intermittent fasting. These observations provide insight into the role of ketone bodies in energy metabolism under shifts in nutrition and may contribute to the development of preventive medicine via diet and foods.

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Evans, Rhys D., Vera Ilic, and Dermot H. Williamson. "Acute administration of tumour necrosis factor-α or interleukin-1-α does not mimic the hypoketonaemia associated with sepsis and inflammatory stress in the rat." Clinical Science 82, no. 2 (February 1, 1992): 205–9. http://dx.doi.org/10.1042/cs0820205.

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1. Administration of tumour necrosis factor (cachectin) and of interleukin-1-α increased the plasma level of non-esterified fatty acids in fed rats, and in the case of interleukin-1-α the blood glycerol level was also increased, suggesting stimulation of adipose tissue lipolysis. There were parallel increases in the plasma level of triacylglycerols. Neither cytokine had significant effects on blood or liver total ketone body (acetoacetate plus 3-hydroxybutyrate) concentrations. 2. In starved rats, the higher plasma non-esterified fatty acid concentration was not increased further by the cytokines. The plasma triacylglycerol level was increased, although the absolute change was less than in fed rats. The ketonaemia associated with starvation tended to be increased by the cytokines, but this was only significant in the case of interleukin-1-α. Parallel changes occurred in hepatic ketone bodies. 3. It is concluded that tumour necrosis factor-α and interleukin-1-α are not responsible for the hypoketonaemia associated with sepsis or other inflammatory states.

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Feingold, Kenneth R., Carl Grunfeld, Josef G. Heuer, Akanksha Gupta, Martin Cramer, Tonghai Zhang, Judy K. Shigenaga, et al. "FGF21 Is Increased by Inflammatory Stimuli and Protects Leptin-Deficient ob/ob Mice from the Toxicity of Sepsis." Endocrinology 153, no. 6 (April 2, 2012): 2689–700. http://dx.doi.org/10.1210/en.2011-1496.

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The acute phase response (APR) produces marked alterations in lipid and carbohydrate metabolism including decreasing plasma ketone levels. Fibroblast growth factor 21 (FGF21) is a recently discovered hormone that regulates lipid and glucose metabolism and stimulates ketogenesis. Here we demonstrate that lipopolysaccharide (LPS), zymosan, and turpentine, which induce the APR, increase serum FGF21 levels 2-fold. Although LPS, zymosan, and turpentine decrease the hepatic expression of FGF21, they increase FGF21 expression in adipose tissue and muscle, suggesting that extrahepatic tissues account for the increase in serum FGF21. After LPS administration, the characteristic decrease in plasma ketone levels is accentuated in FGF21−/− mice, but this is not due to differences in expression of carnitine palmitoyltransferase 1α or hydroxymethyglutaryl-CoA synthase 2 in liver, because LPS induces similar decreases in the expression of these genes in FGF21−/− and control mice. However, in FGF21−/− mice, the ability of LPS to increase plasma free fatty acid levels is blunted. This failure to increase plasma free fatty acid could contribute to the accentuated decrease in plasma ketone levels because the transport of fatty acids from adipose tissue to liver provides the substrate for ketogenesis. Treatment with exogenous FGF21 reduced the number of animals that die and the rapidity of death after LPS administration in leptin-deficient ob/ob mice and to a lesser extent in control mice. FGF21 also protected from the toxic effects of cecal ligation and puncture-induced sepsis. Thus, FGF21 is a positive APR protein that protects animals from the toxic effects of LPS and sepsis.

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Blomqvist, G., J. O. Thorell, M. Ingvar, V. Grill, L. Widen, and S. Stone-Elander. "Use of R-beta-[1-11C]hydroxybutyrate in PET studies of regional cerebral uptake of ketone bodies in humans." American Journal of Physiology-Endocrinology and Metabolism 269, no. 5 (November 1, 1995): E948—E959. http://dx.doi.org/10.1152/ajpendo.1995.269.5.e948.

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A method for determining regional cerebral utilization of ketone bodies in humans is described. After a bolus injection of R-beta-[1-11C]hydroxybutyrate, the time course of the tracer in the brain was measured with positron emission tomography in five healthy volunteers. The regional cerebral blood flow was measured separately. The tracer uptake in the brain could be well described by a single rate constant, indicating that the concentration of unmetabolized ketone bodies in the brain is very low and that transport across the blood-brain barrier is the rate-limiting step. At an average plasma concentration of beta-hydroxybutyrate of 0.043 mumol/ml, the utilization rate was estimated to be 0.48 nmol.ml-1.min-1. In accordance with previous animal studies, the utilization rate was found to increase almost linearly with increasing plasma concentration of beta-hydroxybutyrate. Furthermore, the utilization was higher in gray than in white matter. Finally, the ratio between the utilization in the basal ganglia and the brain as a whole was lower for ketone bodies than for glucose.

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Tardif, Annie, Nathalie Julien, Amélie Pelletier, Gaétan Thibault, Ashok K. Srivastava, Jean-Louis Chiasson, and Lise Coderre. "Chronic exposure to β-hydroxybutyrate impairs insulin action in primary cultures of adult cardiomyocytes." American Journal of Physiology-Endocrinology and Metabolism 281, no. 6 (December 1, 2001): E1205—E1212. http://dx.doi.org/10.1152/ajpendo.2001.281.6.e1205.

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Type 1 and type 2 diabetic patients often show elevated plasma ketone body concentrations. Because ketone bodies compete with other energetic substrates and reduce their utilization, they could participate in the development of insulin resistance in the heart. We have examined the effect of elevated levels of ketone bodies on insulin action in primary cultures of adult cardiomyocytes. Cardiomyocytes were cultured with the ketone body β-hydroxybutyrate (β-OHB) for 4 or 16 h, and insulin-stimulated glucose uptake was evaluated. Although short-term exposure to ketone bodies was not associated with any change in insulin action, our data demonstrated that preincubation with β-OHB for 16 h markedly reduced insulin-stimulated glucose uptake in cardiomyocytes. This effect is concentration dependent and persists for at least 6 h after the removal of β-OHB from the media. Ketone bodies also decreased the stimulatory effect of phorbol 12-myristate 13-acetate and pervanadate on glucose uptake. This diminution could not be explained by a change in either GLUT-1 or GLUT-4 protein content in cardiomyocytes. Chronic exposure to β-OHB was associated with impaired protein kinase B activation in response to insulin and pervanadate. These results indicate that prolonged exposure to ketone bodies altered insulin action in cardiomyocytes and suggest that this substrate could play a role in the development of insulin resistance in the heart.

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Lundgren, J., A. Mans, and B. K. Siesjo. "Ischemia in normoglycemic and hyperglycemic rats: plasma energy substrates and hormones." American Journal of Physiology-Endocrinology and Metabolism 258, no. 5 (May 1, 1990): E767—E774. http://dx.doi.org/10.1152/ajpendo.1990.258.5.e767.

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Seizures are a documented complication to cerebral ischemia. After 10 min of forebrain ischemia in rats, preischemic hyperglycemia invariably leads to severe, most often fatal epileptic attacks. This outcome is related to the exaggerated lactic acidosis, which has been suggested as a possible contributor to severe membrane changes and widespread edema. To find out if circulating hormones or plasma energy substrates modulate this additive damage caused by the hyperglycemia, plasma concentrations of of corticosterone, epinephrine, norepinephrine, dopamine, glucagon, insulin, glucose, free fatty acids (FFA), 3-hydroxybutyrate, and acetoacetate were measured before and in the early recirculation period after 15 min of forebrain ischemia in the rat. Plasma corticosterone levels did not differ between the normo- and hyperglycemic groups. Although not significantly different from control, the catecholamine levels showed a tendency to be higher in the hyperglycemic groups. Therefore, because catecholamines have been reported to have a protective effect during ischemia the present result cannot explain why hyperglycemia aggravates the ischemic damage. Insulin levels seemed to increase during ischemia but not significantly. Levels quickly returned to normal after 30 min of recirculation. FFA concentrations were reduced after the induction of ischemia and appeared lower in all hyperglycemic groups. The level of one of the ketone bodies, 3-hydroxybutyrate, showed a significant decrease in hyperglycemic ischemia in all groups compared with normoglycemic ischemia. The same tendency was seen for acetoacetate. Results are compatible with a protective role of ketone bodies in ischemia. It is concluded that among the hormones and substrates studied only the ketone body concentrations qualify as a modulator of the exaggerated brain damage after ischemia in hyperglycemic subjects.

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Pan, Jullie W., Douglas L. Rothman, Kevin L. Behar, Daniel T. Stein, and Hoby P. Hetherington. "Human Brain β-Hydroxybutyrate and Lactate Increase in Fasting-Induced Ketosis." Journal of Cerebral Blood Flow & Metabolism 20, no. 10 (October 2000): 1502–7. http://dx.doi.org/10.1097/00004647-200010000-00012.

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Ketones are known to constitute an important fraction of fuel for consumption by the brain, with brain ketone content generally thought to be low. However, the recent observation of 1-mmol/L levels of brain β-hydroxybutyrate (BHB) in children on the ketogenic diet suggests otherwise. The authors report the measurement of brain BHB and lactate in the occipital lobe of healthy adults using high field (4-T) magnetic resonance spectroscopy, measured in the nonfasted state and after 2-and 3-day fasting-induced ketosis. A 9-mL voxel located in the calcarine fissure was studied, detecting the BHB and lactate upfield resonances using a 1H homonuclear editing sequence. Plasma BHB levels also were measured. The mean brain BHB concentration increased from a nonfasted level of 0.05 ± 0.05 to 0.60 ± 0.26 mmol/L (after second day of fasting), increasing further to 0.98 ± 0.16 mmol/L (after the third day of fasting). The mean nonfasted brain lactate was 0.69 ± 0.17 mmol/L, increasing to 1.47 ± 0.22 mmol/L after the third day. The plasma and brain BHB levels correlated well ( r = 0.86) with a brain–plasma slope of 0.26. These data show that brain BHB rises significantly with 2-and 3-day fasting-induced ketosis. The lactate increase likely results from ketones displacing lactate oxidation without altering glucose phosphorylation and glycolysis.

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Kimura, M., K. Kobayashi, A. Matsuoka, K. Hayashi, and Y. Kimura. "Head-space gas-chromatographic determination of 3-hydroxybutyrate in plasma after enzymic reactions, and the relationship among the three ketone bodies." Clinical Chemistry 31, no. 4 (April 1, 1985): 596–98. http://dx.doi.org/10.1093/clinchem/31.4.596.

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Abstract In this sensitive, reproducible method for determination of D-3-hydroxybutyrate (3-OHB) in plasma, it is converted to acetone by use of 3-hydroxybutyrate dehydrogenase (EC 1.1.1.30)/lactate dehydrogenase (EC 1.1.1.27) coupled with acetoacetate decarboxylase (EC 4.1.1.4). The resulting acetone is detected by head-space gas chromatography. The lowest concentration of 3-OHB detectable in plasma was 2 mumol/L. The calibration curve showed a linear relationship for 3-OHB concentration from 0 to 5 mmol/L (r = 0.999). Analytical recovery of 3-OHB (50 mumol/L) was 97.9 (SD 3.8)%. The method was developed for determination of the three ketone bodies in plasma. The ratio of acetone to acetoacetate was not significantly different (p greater than 0.2) between normals (n = 31) and diabetics (n = 86). In normal subjects, the ratio of 3-OHB to acetoacetate was 1.20 (SD 0.44). In diabetic patients, the ratio correlated with the logarithm of the total ketone body concentration (r = 0.828).

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Chowdhury, Golam MI, Lihong Jiang, Douglas L. Rothman, and Kevin L. Behar. "The Contribution of Ketone Bodies to Basal and Activity-Dependent Neuronal Oxidation in Vivo." Journal of Cerebral Blood Flow & Metabolism 34, no. 7 (April 30, 2014): 1233–42. http://dx.doi.org/10.1038/jcbfm.2014.77.

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The capacity of ketone bodies to replace glucose in support of neuronal function is unresolved. Here, we determined the contributions of glucose and ketone bodies to neocortical oxidative metabolism over a large range of brain activity in rats fasted 36 hours and infused intravenously with [2,4- 13 C2]-D-β-hydroxybutyrate (BHB). Three animal groups and conditions were studied: awake ex vivo, pentobarbital-induced isoelectricity ex vivo, and halothane-anesthetized in vivo, the latter data reanalyzed from a recent study. Rates of neuronal acetyl-CoA oxidation from ketone bodies ( VaccoA-kbN) and pyruvate ( VpdhN), and the glutamate-glutamine cycle ( Vcyc) were determined by metabolic modeling of 13C label trapped in major brain amino acid pools. VacCoA-kbN increased gradually with increasing activity, as compared with the steeper change in tricarboxylic acid (TCA) cycle rate ( VtcaN), supporting a decreasing percentage of neuronal ketone oxidation: ˜100% (isoelectricity), 56% (halothane anesthesia), 36% (awake) with the BHB plasma levels achieved in our experiments (6 to 13 mM). In awake animals ketone oxidation reached saturation for blood levels > 17 mM, accounting for 62% of neuronal substrate oxidation, the remainder (38%) provided by glucose. We conclude that ketone bodies present at sufficient concentration to saturate metabolism provides full support of basal (housekeeping) energy needs and up to approximately half of the activity-dependent oxidative needs of neurons.

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Guo, J., R. R. Peters, and R. A. Kohn. "Modeling Nutrient Fluxes and Plasma Ketone Bodies in Periparturient Cows." Journal of Dairy Science 91, no. 11 (November 2008): 4282–92. http://dx.doi.org/10.3168/jds.2007-0960.

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Fishel, Derry L., and Jerry E. Hunt. "Californium-252 plasma desorption mass spectrometry of ketone trimethylhydrazinium derivatives." Organic Mass Spectrometry 22, no. 12 (December 1987): 799–801. http://dx.doi.org/10.1002/oms.1210221208.

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Cherel, Yves, Jean-Patrice Robin, Astrid Nehlig, Henri Girard, Agnès Lacombe, Michel Frain, and Yvon Le Maho. "Ambient temperature and ketone body plasma concentration in fasting geese." Pflügers Archiv 407, no. 1 (July 1986): 119–21. http://dx.doi.org/10.1007/bf00580732.

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Bougneres, P. F., L. Castano, F. Rocchiccioli, H. P. Gia, B. Leluyer, and P. Ferre. "Medium-chain fatty acids increase glucose production in normal and low birth weight newborns." American Journal of Physiology-Endocrinology and Metabolism 256, no. 5 (May 1, 1989): E692—E697. http://dx.doi.org/10.1152/ajpendo.1989.256.5.e692.

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To study the pathogenesis of hypoglycemia in low birth weight infants, glucose production was measured in five hypotrophic and four premature newborns with glycemia of 45 +/- 6 and 59 +/- 10 mg/dl, respectively. Hepatic glucose output averaged 5.7 +/- 0.4 and 5.3 +/- 0.5 mg.kg-1.min-1 in these neonates vs. 8.2 +/- 0.5 mg.kg-1.min-1 in five normal at term newborns and was correlated with glycemia (P less than 0.02). Despite normal plasma free fatty acids, the low birth weight infants had low ketone levels of 163 +/- 72 and 126 +/- 65 vs. 263 +/- 60 microM in normals. Oral administration of medium-chain triglycerides to the neonates increased their circulating ketones by two- to threefold and restored near-normal glycemia (51 +/- 9 and 76 +/- 8 mg/dl) and production of glucose (6.7 +/- 0.7 and 6.6 +/- 0.8 mg.kg-1.min-1) in the hypotrophic and premature vs. normals (8.7 +/- 0.7 mg.kg-1.min-1). Individual rates of glucose production correlated with ketone concentrations (P less than 0.02). We conclude that the hypoglycemia characterizing low birth weight neonates is primarily due to impaired glucose production. That exogenous lipids were able to increase glucose production indicates that fatty acid oxidation plays an important glucoregulatory role in the human newborn.

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Garcia, Erwin, Irina Shalaurova, Steven P. Matyus, David N. Oskardmay, James D. Otvos, Robin P. F. Dullaart, and Margery A. Connelly. "Ketone Bodies Are Mildly Elevated in Subjects with Type 2 Diabetes Mellitus and Are Inversely Associated with Insulin Resistance as Measured by the Lipoprotein Insulin Resistance Index." Journal of Clinical Medicine 9, no. 2 (January 23, 2020): 321. http://dx.doi.org/10.3390/jcm9020321.

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Background: Quantifying mildly elevated ketone bodies is clinically and pathophysiologically relevant, especially in the context of disease states as well as for monitoring of various diets and exercise regimens. As an alternative assay for measuring ketone bodies in the clinical laboratory, a nuclear magnetic resonance (NMR) spectroscopy-based test was developed for quantification of β-hydroxybutyrate (β-HB), acetoacetate (AcAc) and acetone. Methods: The ketone body assay was evaluated for precision, linearity and stability and method comparisons were performed. In addition, plasma ketone bodies were measured in the Insulin Resistance Atherosclerosis Study (IRAS, n = 1198; 373 type 2 diabetes mellitus (T2DM) subjects). Results: β-HB and AcAc quantified using NMR and mass spectrometry and acetone quantified using NMR and gas chromatography/mass spectrometry were highly correlated (R2 = 0.996, 0.994, and 0.994 for β-HB, AcAc, acetone, respectively). Coefficients of variation (%CVs) for intra- and inter-assay precision ranged from 1.3% to 9.3%, 3.1% to 7.7%, and 3.8% to 9.1%, for β-HB, AcAc and acetone, respectively. In the IRAS, ketone bodies were elevated in subjects with T2DM versus non-diabetic individuals (p = 0.011 to ≤0.001). Age- and sex-adjusted multivariable linear regression analysis revealed that total ketone bodies and β-HB were associated directly with free fatty acids (FFAs) and T2DM and inversely with triglycerides and insulin resistance as measured by the Lipoprotein Insulin Resistance Index. Conclusions: Concentrations of the three main ketone bodies can be determined by NMR with good clinical performance, are elevated in T2DM and are inversely associated with triglycerides and insulin resistance.

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Lee, Hae-In, Chan Seo, Man-Jeong Paik, and Mi-Kyung Lee. "Monitoring of Energy Metabolism by Organic Acid Profiling Analysis in Plasma of Type 2 Diabetic Mice." Current Metabolomics and Systems Biology 7, no. 1 (September 6, 2020): 42–50. http://dx.doi.org/10.2174/2666338407666190828155646.

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Objective:: This study was conducted to investigate energy metabolism based on changes in organic acids in diabetes and to establish a correlation between metabolites or bone microarchitecture and the glucose index in type 2 diabetic mice. Method:: Seven-week-old male C57BL/6 mice were randomly divided into a non-diabetic group and a diabetic group. The diabetic group was fed a high-fat diet (HFD) that induced insulin resistance for 5 weeks. Afterwards, diabetes was induced by a single streptozotocin injection. Both the groups were fed a normal diet and HFD diet for 9 weeks. Results:: The fasting blood glucose level glycosylated hemoglobin (HbA1c) significantly increased in diabetic mice. Bone-alkaline phosphatase activity decreased in the diabetic group. Diabetes increased the levels of ketone bodies, including 3-hydroxybutyric, acetoacetic and butyric acid, whereas it decreased Krebs cycle components, including succinic acid and malic acid, as well as levels of glycolytic products, including lactic acid. Diabetes also induced a shortage of trabecular bone mineral density (BMD) by the regulation of trabecular morphometric parameters in the femur and tibia. Correlation analysis indicated that BMD, Krebs cycle components and lactic acid levels were negatively correlated with HbA1c, whereas ketone bodies were positively correlated with HbA1c. Conclusion: : This research suggested that uncontrolled HbA1c can affect bone loss, production of ketone bodies and utilization of glucose metabolites for energy production in type 2 diabetes.

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Rofe, A. M., R. Bais, and R. A. Conyers. "Ketone-body metabolism in tumour-bearing rats." Biochemical Journal 233, no. 2 (January 15, 1986): 485–91. http://dx.doi.org/10.1042/bj2330485.

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During starvation for 72 h, tumour-bearing rats showed accelerated ketonaemia and marked ketonuria. Total blood [ketone bodies] were 8.53 mM and 3.34 mM in tumour-bearing and control (non-tumour-bearing) rats respectively (P less than 0.001). The [3-hydroxybutyrate]/[acetoacetate] ratio was 1.3 in the tumour-bearing rats, compared with 3.2 in the controls at 72 h (P less than 0.001). Blood [glucose] and hepatic [glycogen] were lower at the start of starvation in tumour-bearing rats, whereas plasma [non-esterified fatty acids] were not increased above those in the control rats during starvation. After functional hepatectomy, blood [acetoacetate], but not [3-hydroxybutyrate], decreased rapidly in tumour-bearing rats, whereas both ketone bodies decreased, and at a slower rate, in the control rats. Blood [glucose] decreased more rapidly in the hepatectomized control rats. Hepatocytes prepared from 72 h-starved tumour-bearing and control rats showed similar rates of ketogenesis from palmitate, and the distribution of [1-14C] palmitate between oxidation (ketone bodies and CO2) and esterification was also unaffected by tumour-bearing, as was the rate of gluconeogenesis from lactate. The carcinoma itself showed rapid rates of glycolysis and a poor ability to metabolize ketone bodies in vitro. The results are consistent with the peripheral, normal, tissues in tumour-bearing rats having increased ketone-body and decreased glucose metabolic turnover rates.

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Journal articles on the topic 'Plasma ketone'

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