ライフサイエンスコーパス: ketone body

1 P) to generate beta-hydroxybutyrate (BHB), a ketone body.

2 le with diabetes to monitor both glucose and ketone bodies.

3 ty acids, glucose, lactate, amino acids, and ketone bodies.

4 of insulin on these and free fatty acids and ketone bodies.

5 demic, and have higher than normal levels of ketone bodies.

6 expression has been associated with elevated ketone bodies.

7 oxidized for ATP synthesis, or conversion to ketone bodies.

8 reased circulating concentrations of KIC and ketone bodies.

9 y metabolism toward increased utilization of ketone bodies.

10 rbs energy metabolism as indicated by higher ketone bodies.

11 ike effects and results in the production of ketone bodies.

12 acids, amino acids, glycolysis measures and ketone bodies.

13 o tumours while fuelling normal tissues with ketone bodies.

14 ed to lipids, lipoproteins, fatty acids, and ketone bodies.

15 ed in lipid catabolism and the production of ketone bodies.

16 hagic flux and the production of glucose and ketone bodies.

17 cluded amino acids, fatty acids, lipids, and ketone bodies.

18 amino acids, glycolysis related measures and ketone bodies.

19 c production and extrahepatic utilization of ketone bodies.

20 is closely correlated with the production of ketone bodies.

21 oketogenesis facilitated the labeling of the ketone bodies [1-(13)C]acetoacetate and [1-(13)C]beta-hy

22 no acid, 2 glycolysis-related metabolites, 2 ketone bodies, 2 triglyceride, and 6 lipoprotein subclas

23 requires consideration of effects on ISR by ketone bodies; 2) ISR responses to FFA/beta-OHB were def

24 r by supplementing either vitamin B12 or the ketone bodies 3-hydroxybutyrate (3HB) and acetoacetate (

25 etabolic substrate utilization, favoring the ketone body 3-hydroxybutyrate as energy source.

26 Acute increases in circulating levels of ketone body 3-hydroxybutyrate have beneficial acute hemo

27 Conversely, the ketone body 3-hydroxybutyrate, branched chain amino acid

28 ylcarnitines, together with increases in the ketone body 3-hydroxybutyrate.

29 Ketone bodies, 3-hydroxybutyrate, and acetoacetate, were

30 igh fat-fed livers contained, in addition to ketone bodies, a new metabolite, identified as AMP, whic

31 ncreased autophagic flux, mild elevations in ketone bodies, a reduction in oxidative stress, and the

32 ncreased autophagic flux, mild elevations in ketone bodies, a reduction in oxidative stress, and the

33 udy demonstrates that elevated levels of the ketone body AA can increase lipid peroxidation and lower

34 Second, ketone body AA treatment increases TNF-alpha secretion,

35 fasting (12-36 h) were protected from blood ketone-body accumulation, unlike control and Ppp1r3b(Del

36 frequently encounter elevated levels of the ketone bodies acetoacetate (AA), beta-hydroxybutyrate (B

37 Conversion of the ketone body acetoacetate (AcAc) to beta-hydroxybutyrate

38 -CoA lyase and promotes the formation of the ketone body acetoacetate, which subsequently enhances BR

39 U937 cells were cultured with ketone bodies (acetoacetate [AA] and beta-hydroxybutyrat

40 lly attributed to the 'acidic' nature of the ketone bodies (acetoacetate, 3-hydroxybutyrate, and acet

41 tabolism in AD is of particular interest, as ketone bodies (acetone, acetoacetate (AcAc), and beta-hy

42 A third ketone body, acetone, was significantly lower in the 30

43 oxylate fuels such as lactate, pyruvate, and ketone bodies across brain endothelial cells is mediated

44 Extrahepatic tissues which oxidise ketone bodies also have the capacity to accumulate them

45 id measures, glycolysis-related metabolites, ketone bodies, amino acids, and acute-phase reaction mar

46 y metabolites such as lactate, pyruvate, and ketone bodies and are expressed in most tissues.

47 ty for fatty acid oxidation and increases in ketone bodies and branched chain amino acids.

48 by nuclear Oxct1) cannot terminally oxidize ketone bodies and develop lethal hyperketonemic hypoglyc

49 en storage without increased serum levels of ketone bodies and free fatty acid suggesting that they a

50 t, it markedly reduced levels of both plasma ketone bodies and hepatic expression of the rate-limitin

51 -TGH KO mice presented with increased plasma ketone bodies and hepatic fatty acid oxidation.

52 Data regarding ketone bodies and incident type 2 diabetes are scarce.

53 ated a potential association between fasting ketone bodies and incident type 2 diabetes in the genera

54 and mitochondrial pathways such as glycogen, ketone bodies and nucleosides.

55 Mass isotopomer analysis of C(4) and C(5) ketone bodies and of related acyl-CoA esters reveal that

56 l metabolism toward increased utilization of ketone bodies and that increasing cardiac ketone deliver

57 I activity and carbon flux from palmitate to ketone bodies and to CO2 in the absence and presence of

58 As glucose output increased, ketone body and acetate release increased while CO(2) re

59 Beta-hydroxybutyrate (BHB) is a ketone body and has recently been reported to exert anti

60 ultured rat hepatocytes were used to explore ketone body and insulin regulation of CYP2E1 expression.

61 excess acetyl groups as acetylcarnitine and ketone bodies, and (iii) the channeling of mitochondrial

62 rsistent AF, unraveling a potential role for ketone bodies, and demonstrated that discordant metaboli

63 amino acids, gluconeogenesis intermediates, ketone bodies, and fatty acid composition and saturation

64 ncreases in plasma glycerol, fatty acids and ketone bodies, and hepatic triglycerides.

65 ed 1) circulating levels of free fatty acid, ketone bodies, and long-chain acylcarnitines and 2) card

66 oncentrations of 5'-GMP, ribose-5-phosphate, ketone bodies, and purines.

67 nsated by elevated plasma levels of FFAs and ketone bodies; and 3) approximately two times more insul

68 Ketone bodies are a critical cardiac fuel and have diver

69 Ketone bodies are alternative fuels produced when glucos

70 Ketone bodies are comprised of three compounds (beta-hyd

71 C enrichment of glutamate when (13)C-labeled ketone bodies are delivered in vivo or ex vivo, indicati

72 Ketone bodies are energy-rich metabolites and signaling

73 n-specific and cell-type-specific effects of ketone bodies are important to consider as prospective t

74 Ketone bodies are readily oxidized by cardiomyocytes and

75 Ketone bodies are the most energy-efficient fuel and yie

76 ophied and failing heart shifts to oxidizing ketone bodies as a fuel source in the context of reduced

77 he hypertrophied and failing heart shifts to ketone bodies as a significant fuel source for oxidative

78 ucose loss include reduced fat mass and more ketone bodies as additional fuel.

79 betes mellitus, and they support the role of ketone bodies as an alternative fuel and myocardial keto

80 Certain types of cancer use ketone bodies as an energy source(9,10) that may rely on

81 mmatory cytokine production, a shift towards ketone bodies as the metabolic substrate for the heart a

82 ioxide production ( VCO2 ) and production of ketone bodies (B-hydroxybutyrate).

83 The ketone bodies beta-hydroxybutyrate (BHB) and acetoacetat

84 The ketone bodies beta-hydroxybutyrate and acetoacetate are

85 A, a receptor for the vitamin niacin and the ketone body beta-hydroxybutyrate (beta-HB).

86 The ketone body beta-hydroxybutyrate (BHB) is synthesized in

87 d the effects of glucose deprivation and the ketone body beta-hydroxybutyrate (BHB) on inflammatory g

88 ar Cell, Tang et al.(1) demonstrate that the ketone body beta-hydroxybutyrate (BHB) promotes the biog

89 KD (CKD), or dietary supplementation of the ketone body beta-hydroxybutyrate (BHB), which is an endo

90 of ketogenic diets are recapitulated by the ketone body beta-hydroxybutyrate (BHB), which reduces th

91 We found that a diet enriched with the ketone body beta-hydroxybutyrate during early developmen

92 Further, the ketone body beta-hydroxybutyrate, another metabolite tha

93 t we show encodes a transporter of the major ketone body beta-hydroxybutyrate.

94 nduced high-amplitude daily rhythms in blood ketone bodies (beta-hydroxybutyrate [betaOHB]) that corr

95 Physiological concentrations of ketone bodies (beta-hydroxybutyrate or acetoacetate) red

96 ioxide production ( VCO2 ) and production of ketone bodies (beta-hydroxybutyrate).

97 e, we discovered that the major component of ketone body, beta-hydroxybutyrate (BHB), improved mitoch

98 Moreover, the most abundant ketone body, beta-hydroxybutyrate, inhibits the NLRP3 in

99 f hepatic beta-hydroxybutyrate and repressed ketone body biosynthesis gene expression.

100 d group received intravenous infusion of the ketone body BOHB (beta-hydroxybutyrate) during the MI in

101 lic acid (TCA) cycle and is also involved in ketone-body breakdown in animals.

102 body was sufficient to potently lower plasma ketone bodies but failed to normalize elevated levels of

103 SCD1-/- mice have increased levels of plasma ketone bodies but reduced levels of plasma insulin and l

104 LDL cholesterol, free fatty acids, and total ketone bodies by 25, 49, and 116%, respectively.

105 yrate, consistent with earlier findings that ketone bodies can affect K(ATP) activity.

106 actic acidosis and ketoacidosis, lactate and ketone bodies can be converted back to bicarbonate if th

107 porting the view that fatty acids as well as ketone bodies can be metabolized by the brain.

108 The demonstration that ketone bodies can distinguish between normal and respira

109 alance between production and removal of the ketone bodies cannot be excluded.

110 This occurs both because ketone body carbon is metabolized to glutamine and becau

111 We also present evidence that treatment with ketone bodies caused "heteroplasmic shifting" not only a

112 Baseline fasting ketone body concentrations were measured by nuclear magn

113 age-related metabolic shift toward enhanced ketone body consumption as an alternative source of ener

114 tended to restore cardiac metabolism through ketone bodies could both refuel and 'repair' the failing

115 esenting a molecular mechanism through which ketone bodies could influence systemic physiology and ch

116 Ketone bodies could serve as a potential biomarker for c

117 it might also catalyze the oxidation of the ketone body d-3-hydroxybutyrate.

118 We report that the ketone body d-beta-hydroxybutyrate (betaOHB) is an endog

119 Here we show that the infusion of the ketone body d-beta-hydroxybutyrate (DbetaHB) in mice con

120 Ketone bodies (d-beta-hydroxybutyrate, acetoacetate) are

121 Here we show that the fatty acid-derived ketone body (D)-beta-hydroxybutyrate ((D)-beta-OHB) spec

122 Supplementation of cellular energy with a ketone body, D-beta-hydroxybutyrate, decreased rotenone

123 Fasting for 20 h caused a 9-fold increase in ketone body delivery to the brain but had no effect on a

124 dioprotective potential of empagliflozin and ketone bodies during acute myocardial infarction (MI).

125 The salutary effects of ketone bodies during HF may also include extra-cardiac r

126 ions of anticatabolic effects of protein and ketone bodies during inflammation, and using a novel mod

127 Consistent with an anticonvulsant role, the ketone body effect is larger for cells that fire more ra

128 This study shows that ketone bodies, either combined or as individual subspeci

129 d replication regression analyses, including ketone bodies, fatty acids, glycolysis-related molecules

130 al morphology, number, and respiration, plus ketone body, fatty acid, and glucose oxidation in isolat

131 upport a model in which C. elegans relies on ketone bodies for energy when vitamin B12 levels are low

132 ctive dependence of the brain on glucose and ketone bodies for energy, and on amino acids for neurotr

133 ody homeostasis, including the production of ketone bodies for peripheral tissues to use as energy so

134 ficiency results in an inherited disorder of ketone body formation.

135 zing various nutrients as carbon sources for ketone body formation.

136 thesis and an upregulation of an alternative ketone-body formation pathway.

137 When glucose levels are limited, ketone bodies generated in the liver and lactate derived

138 G-CoA) lyase catalyzes the terminal steps in ketone body generation and leucine degradation.

139 nsor toward minimally invasive monitoring of ketone bodies has been demonstrated in a phantom gel ski

140 Indeed, ketone bodies have been shown to influence a variety of

141 c fuel utilization that elevates circulating ketone bodies; however, the consequences of these compou

142 C infusion for 8 hrs substantially increased ketone bodies in blood and liver, in comparison with the

143 ice exhibited significantly higher levels of ketone bodies in both blood and urine compared to fastin

144 iprocal effects on metabolism of glucose and ketone bodies in brain cells.

145 e recently shown the potential importance of ketone bodies in cardio-metabolic health.

146 Exposure to ketone bodies in early development can reduce neurologic

147 research demonstrates beneficial effects of ketone bodies in heart failure.

148 anisms involved in the beneficial effects of ketone bodies in HF have yet to be defined and represent

149 tic capacity, controlling the utilization of ketone bodies in ketotic states.

150 rection for modulating circulating levels of ketone bodies in metabolic diseases.

151 lts indicate the critical metabolic roles of ketone bodies in neonatal metabolism and suggest that di

152 hondrial enzyme involved in the breakdown of ketone bodies in the extrahepatic tissues, was identifie

153 Because of the safety record of ketone bodies in the treatment of epilepsy and their abi

154 To examine the effects of ketone bodies in vivo, studies were performed that showe

155 ficant increase in blood and urine levels of ketone bodies in wild-type (WT) mice.

156 hydroxybutyrate, the predominant circulating ketone body in mammals.

157 he rate-limiting enzyme in the production of ketone bodies, including beta-hydroxybutyrate (betaOHB),

158 ere we have investigated the hypothesis that ketone bodies induce CMA.

159 Sustained modulation of circulating ketone bodies is a potential treatment principle in pati

160 al fluid (ISF), the continuous monitoring of ketone bodies is yet to be addressed.

161 Ketone bodies (KB) are an important alternative metaboli

162 Ketone bodies (KB) are products of fatty acid oxidation

163 ial fuel metabolism away from glucose toward ketone bodies (KB), which improves myocardial energy pro

164 ad a significant increase in fatty acids and ketone body (KB) content compared with baseline.

165 her beta-hydroxybutyrate (betaOHB), the main ketone body (KB) produced in ketogenic diet (KD), is neu

166 Circulating ketone bodies (KBs) are increased in patients with heart

167 Since ketone bodies (KBs) can trigger repair mechanisms in res

168 The interest in ketone bodies (KBs) has intensified recently as they pla

169 nvestigated the association of the levels of ketone bodies (KBs) with hyperglycemia and with 62 genet

170 Here, we identified ketone bodies (KBs)-including beta-hydroxybutyrate (beta

171 Despite higher catecholamine and ketone body levels and muscle insulin resistance, KO mic

172 In conclusion, fasting plasma ketone body levels are strongly positively associated wi

173 In Kaplan-Meier analysis, sex-stratified ketone body levels strongly positively associated with i

174 ificant changes in blood glucose and fasting ketone body levels.

175 ficult to identify, therefore, the amount of ketone bodies (mainly beta-hydroxybutyric acid, BHB) is

176 Ketone bodies may be recycled into anabolic substrates,

177 Ketone bodies may form an alternative substrate source,

178 Ketone bodies may have anabolic effects in skeletal musc

179 In addition, ketone bodies may help to restore cardiac function by mi

180 The induction of CMA by ketone bodies may provide an important physiological mec

181 s a seizure gate in the hippocampus and that ketone-body-mediated augmentation of the activity-depend

182 y of organ failure was related to increasing ketone body metabolism (3 Hydroxybutyric Acid-1 and - 3;

183 acids (Glutamine - 0.682; Alanine - 0.594), ketone body metabolism (Acetone - 0.64; 3-Hydroxybutyric

184 ion, suggesting a potential coupling between ketone body metabolism and cardiac function.

185 , boosting energy efficiency through altered ketone body metabolism and mitigating inflammation and o

186 Here, we show that PDA cells can activate ketone body metabolism and that beta-hydroxybutyrate (be

187 ochondrial defects, and the up-regulation of ketone body metabolism genes.

188 on of amino acid catabolism, glycolysis, and ketone body metabolism in a subset of UK Biobank.

189 ole of the NLRP3 inflammasome and microglial ketone body metabolism in AD pathogenesis.

190 d investigated the alterations in myocardial ketone body metabolism in diabetic rats.

191 Unlike the acute effects of ketone body metabolism in the perfused working heart, th

192 we found that BDH2 deficiency did not alter ketone body metabolism in vivo.

193 the ways in which changes in fatty acid and ketone body metabolism modulate insulin secretion by the

194 beta-hydroxybutyrate, the major substrate in ketone body metabolism, along with an increase in ketoge

195 y regulatory roles in hepatic amino acid and ketone body metabolism, as well as mitochondrial turnove

196 ntions have markedly intensified interest in ketone body metabolism.

197 that reduce glucose utilization and promote ketone body metabolism.

198 that during aging, liver-derived circulating ketone bodies might be more important for deactivating t

199 bstrate for cardiac mitochondrial oxidation, ketone bodies modulate myocardial utilization of glucose

200 sent the first use of a real-time continuous ketone bodies monitoring (CKM) microneedle platform.

201 he ketone ester diet had elevated mean blood ketone bodies of 3.5 mm and lowered plasma glucose, insu

202 However, the role of SGLT2i or ketone bodies on myocardial ischemia reperfusion injury

203 tested for an acute effect of physiological ketone bodies on neuronal firing rates and excitability,

204 We propose that ketone bodies or glycolytic restriction treat epilepsy b

205 e brain's fuel source from glucose to either ketone bodies or lactate, i.e. a cerebral substrate swit

206 aging in dissociated VMH neurons showed that ketone bodies overrode normal FA sensing, primarily by e

207 Furthermore, reduced ketone body oxidation correlates with failure of ketone

208 The increased ketone body oxidation in the diabetic hearts correlated

209 asive and real time monitoring of myocardial ketone body oxidation in vivo, which offers a powerful t

210 CoA-transferase (SCOT), to demonstrate that ketone body oxidation is required for postnatal survival

211 ther, these results indicate that peripheral ketone body oxidation prevents hypoglycemia and supports

212 e use this model to demonstrate that loss of ketone body oxidation, an exclusively extrahepatic proce

213 early-adult metabolic shift, favoring lipid/ketone body oxidation, triggers inflammatory degradation

214 ibit specific metabolic responses to loss of ketone body oxidation.

215 tty acids (SCFAs), substrates in the colonic ketone body pathway, are increased in stool, which corre

216 These observations show that ketone bodies play an important role in the regulation o

217 Ketone bodies play significant roles in organismal energ

218 mation may explain the altered metabolism of ketone bodies present in these disorders.

219 w-molecular-weight metabolites (amino acids, ketone bodies), processed using (1)H nuclear magnetic re

220 beta-hydroxybutyrate (BHB), one of the main ketone bodies produced, can have an anti-inflammatory an

221 Beta-hydroxybutyrate (betaHB), a ketone body produced during fasting or adherence to a ke

222 gression, with only one-3-hydroxybutyrate, a ketone body produced during fasting-showing significant

223 icated downshifting of fatty acid oxidation, ketone body production and breakdown, and the tricarboxy

224 in liver size, and to a pronounced defect in ketone body production and ketogenic gene expression on

225 ic intake as a consequence of FA-induced VMH ketone body production by astrocytes.

226 late protein-sparing phase of fasting, when ketone body production by the liver supplies compensator

227 2 (Clk2) suppresses fatty acid oxidation and ketone body production during diet-induced obesity.

228 Elevated ketone body production in NKT cell-deficient mice result

229 atus during low-flow ischaemia would support ketone body production in the heart.

230 t the following biochemical transformations: ketone body production, glucose synthesis and transamina

231 le, sparing fatty acids for triglyceride and ketone body production.

232 loss of dhgd-1 causes lethality by limiting ketone body production.

233 sion of the rate-limiting enzyme involved in ketone body production.

234 th severer ketonemia, acetoacetate and total ketone-body production and oxidation rates were higher b

235 Rates of plasma acetoacetate and total ketone-body production and oxidation to CO2 were determi

236 The maximum rates of total ketone-body production and oxidation were about 150 g/24

237 l ketonuria, rates of acetoacetate and total ketone-body production and oxidation were directly relat

238 Although an increased ketone-body production was the primary factor responsibl

239 reakdown are altered, potentially leading to ketone-body production.

240 Ketone bodies provide fuel particularly to brain, heart,

241 channels were higher in the presence of the ketone body R-beta-hydroxybutyrate, consistent with earl

242 The arterial ketone body ratio was profoundly compromised by chronic

243 acid and indocyanine green uptake, arterial ketone body ratio, orthotopic liver transplantation) exp

244 Although ketone bodies recently received a renewed interest as po

245 The two ketone body redox partners, acetoacetate and D-B-hydroxy

246 et exhibit increased fasting levels of blood ketone bodies, reduced respiratory exchange ratio, and i

247 the free-fed state, impairs triglyceride and ketone body release from the liver during prolonged fast

248 nneling, the labeling of acetylcarnitine and ketone bodies released by the heart are not proxies of t

249 es of urea, ammonium, urate, creatinine, and ketone bodies remained unchanged.

250 in which we grow cells in medium containing ketone bodies, replacing glucose as the carbon source.

251 an produce the life-sustaining quantities of ketone bodies required for survival during fasting or ke

252 Provision of ketone bodies restored energy status, calcium homeostasi

253 of this muscle diversion, serum-free FA and ketone bodies rose much less after fasting in SJL/J mice

254 In vitro and in vivo experiments showed that ketone bodies selectively inhibited bifidobacterial grow

255 Ketone bodies serve as an energy source, especially in t

256 fected, causing an increase in production of ketone bodies, suggesting lipids were used as an alterna

257 To determine whether ketone bodies sustain neuronal function as energy substr

258 have decreased CO2 production but increased ketone body synthesis, suggesting that altered redox sta

259 the bioenergetic and pleiotropic effects of ketone bodies that could potentially contribute to its c

260 ne sampling to investigate urea, creatinine, ketone bodies, the thyroid hormone triiodothyronine (T3)

261 d P < 0.05), as synthesis and degradation of ketone bodies; the alanine, aspartate and glutamate meta

262 ght NLRP3 inflammasome inhibition by several ketone body therapies as a promising new treatment strat

263 fat and low carbohydrate diet that produces ketone bodies through imitation of starvation.

264 ce of skeletal muscle and heart from fat and ketone bodies to glucose.

265 ate intake, mammals convert energy stored in ketone bodies to high energy phosphates.

266 ne body oxidation correlates with failure of ketone bodies to inhibit fatty acid oxidation.

267 In some physiological states, cells rely on ketone bodies to satisfy their metabolic needs, especial

268 liver where they are metabolized to generate ketone bodies to serve as fuels for other tissues.

269 mouse liver and primary hepatocytes consumed ketone bodies to support fatty acid biosynthesis via bot

270 s in enabling adequate supply of glucose and ketone bodies to the circulation.

271 ation to acetoacetate but no contribution of ketone bodies to the tricarboxylic acid cycle.

272 AMP and ketone bodies together can therefore inhibit lipogenesis

273 l step in fasting energy metabolism: hepatic ketone body transport.

274 the present work suggests that MCT1-mediated ketone-body transport is needed to maintain acid-base ba

275 incorporation of 13C-labeled acetyl-CoA into ketone bodies, tricarboxylic acid cycle intermediates, a

276 ther normalized glucose uptake nor decreased ketone body uptake have a positive effect on the mitocho

277 IN1), lipid droplet formation (BTN1A1, XDH), ketone body utilization (BDH1), and transcription regula

278 ogrammed the expression of genes involved in ketone body utilization and normalized myocardial ATP pr

279 This suggests an increase in ketone body utilization in the diabetic heart, with the

280 However, techniques to determine myocardial ketone body utilization in vivo are lacking.

281 eveloped a novel method to assess myocardial ketone body utilization in vivo using hyperpolarized [3-

282 ately reprograms multiple metabolic pathways-ketone body utilization, glycolysis, pentose phosphate s

283 (SCOT) activity, the rate-limiting enzyme of ketone body utilization, in the diabetic heart.

284 cle engages a metabolic response that limits ketone body utilization.

285 rs, and myocardial metabolism is directed to ketone body utilization.

286 SCOT is a key enzyme for ketone body utilization.

287 The effect of ketone bodies was abolished by eliminating the metabolic

288 etabolite pools, including acylcarnitine and ketone bodies, was similar amongst the groups, suggestin

289 Although BDH2 has been proposed to oxidize ketone bodies, we found that BDH2 deficiency did not alt

290 Glucose, lactate, glutamine, glutamate and ketone bodies were also found to be important external m

291 Elevated levels of ketone bodies were confirmed in the blood following KD.

292 serum metabolomics or levels of circulating ketone bodies were observed.

293 zation, as well as muscle acylcarnitines and ketone bodies, were remarkably similar between groups.

294 SGLT2i increases circulating levels of ketone bodies, which has been demonstrated to enhance my

295 etabolic acidosis due to the accumulation of ketone bodies, which requires people with diabetes to mo

296 n endotoxemia, probably by its conversion to ketone bodies, which serve as an alternative energy subs

297 -deficient mice induced a higher increase of ketone bodies, which up-regulate CYP2E1 through protein

298 c metabolites, such as lactate, pyruvate, or ketone bodies, which will enable the correlation of panc

299 ferritin, beta-hydroxybutyrate, acetone, and ketone bodies, with an increase in apolipoprotein A-1, w

300 iabetic model, there is an overproduction of ketone-bodies within the vessels using an alternative tr