ライフサイエンスコーパス: ketone body

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

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

3 expression has been associated with elevated ketone bodies.

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

5 reased circulating concentrations of KIC and ketone bodies.

6 amino acids, glycolysis related measures and ketone bodies.

7 c production and extrahepatic utilization of ketone bodies.

8 is closely correlated with the production of ketone bodies.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

94 that reduce glucose utilization and promote ketone body metabolism.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 2 (Clk2) suppresses fatty acid oxidation and ketone body production during diet-induced obesity.

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

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

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

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

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

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

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

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

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

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

123 Ketone bodies provide fuel particularly to brain, heart,

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

125 The arterial ketone body ratio was profoundly compromised by chronic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 AMP and ketone bodies together can therefore inhibit lipogenesis

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

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

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

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

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

146 SCOT is a key enzyme for ketone body utilization.

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

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

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

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

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

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

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

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