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1 lipogenesis is energy wasteful and precludes ketogenesis.
2 rhagic shock has any salutary effects on gut ketogenesis.
3 iagenesis, ureagenesis, gluconeogenesis, and ketogenesis.
4 ycemia causes the increases in lipolysis and ketogenesis.
5 y augment S100A9 for preventing unrestrained ketogenesis.
6  the stimulation of fatty acid oxidation and ketogenesis.
7 dependent pathway able to normalize diabetic ketogenesis.
8  fasting on hepatic fatty acid oxidation and ketogenesis.
9  therapeutic target for restraining diabetic ketogenesis.
10 europathology caused by insufficient hepatic ketogenesis.
11  factor 21 (FGF21) are primary regulators of ketogenesis.
12 nitive decline caused by compromised hepatic ketogenesis.
13 rcadian clock is a regulator of diet-induced ketogenesis.
14 ne contacts in hepatic lipid utilization and ketogenesis.
15 colysis and AMPK-deficient cell resorting to ketogenesis.
16 ficient to repress PPARa-responsive genes or ketogenesis.
17 d metabolism, pentose phosphate pathway, and ketogenesis.
18 s of hepatic glucose production, and hepatic ketogenesis.
19 amined whether OS phagocytosis was linked to ketogenesis.
20  glucose concentrations and rates of HGP and ketogenesis.
21 nzymes required for fatty acid oxidation and ketogenesis.
22 ered TGD, and stimulated lipolysis, LOx, and ketogenesis.
23 stress hormones that stimulate lipolysis and ketogenesis.
24 blast growth factor 21 expression and intact ketogenesis.
25 with consequent diversion of acetyl-CoA into ketogenesis.
26 a-hydroxybutyryate, without evidence of true ketogenesis.
27 o-glucagon ratio) favors glucose release and ketogenesis.
28 ng liver and kidney, which was essential for ketogenesis.
29 pha target genes in fatty acid oxidation and ketogenesis.
30 ive hepatic fatty acid oxidation and fasting ketogenesis.
31 c fatty acid oxidation, gluconeogenesis, and ketogenesis.
32 ient to prevent the ageing-induced defect in ketogenesis.
33 c gluconeogenesis, fatty acid oxidation, and ketogenesis.
34 d fast and have impaired gluconeogenesis and ketogenesis.
35 lglycerol synthesis and toward oxidation and ketogenesis.
36 riptional programmes of lipid metabolism and ketogenesis.
37 on of mitochondrial fatty acid oxidation and ketogenesis.
38 itioning of the resulting fatty acids toward ketogenesis (+232%) due to reductions in serum insulin c
39 pression of the terminal enzyme required for ketogenesis, 3-Hydroxy-3-Methylglutaryl-CoA Lyase (HMGCL
40 e liver that catalyses the first reaction in ketogenesis: 3-hydroxymethylglutaryl-CoA synthase 2 (HMG
41 hepatic G0S2 knockdown also showed increased ketogenesis, accelerated gluconeogenesis, and decelerate
42  suppress a PPARa transcriptional program or ketogenesis after fasting.
43 sis, which was sufficient to prevent rise in ketogenesis, also prevented a fall in leptin.
44 lic pathways including fatty acid oxidation, ketogenesis, amino acid catabolism, and the urea and tri
45 atic beta-oxidation, dramatically increasing ketogenesis and decreasing reliance on the TCA cycle.
46 ndomized trials and the close association of ketogenesis and erythrocytosis with the cardioprotective
47 s is distinguished by 2 intriguing features: ketogenesis and erythrocytosis.
48 er and skeletal muscle, resulting in hepatic ketogenesis and glucocorticoid-driven muscle catabolism,
49 es encoding enzymes of fatty acid oxidation, ketogenesis and glycolysis.
50  HMGCS2-deficient mice which lack endogenous ketogenesis and have poor outcomes after MI.
51 ipid droplet numbers in vitro, and decreased ketogenesis and hepatic mitochondrial activity in vivo F
52 ha agonist induced hepatic fat oxidation via ketogenesis and hepatic TCA cycle activity but failed to
53                    Here, we analyze steps in ketogenesis and identify four potential sources: adipocy
54  in the periphery including the induction of ketogenesis and immunoregulation.
55  recombinant S100A9 administration restrains ketogenesis and improves hyperglycemia without causing h
56 pidomics to establish a link between hepatic ketogenesis and lipid anabolism.
57 y correlated with hepatic beta-oxidation and ketogenesis and positively correlated with citrate synth
58 vates selective translation, which underlies ketogenesis and provides a tailored diet intervention th
59  regulator of PPARalpha function and hepatic ketogenesis and suggest a role for mTORC1 activity in pr
60 more acetyl-CoA away from lipogenesis toward ketogenesis and TCA cycle, a milieu which can hasten oxi
61 rn promotes hepatic fatty acid oxidation and ketogenesis and ultimately leads to increased energy exp
62 duced lipid droplet formation and subsequent ketogenesis and, ultimately, for maintaining systemic en
63 at SGLT2 inhibitors promote gluconeogenesis, ketogenesis, and erythrocytosis and reduce uricemia, the
64 f genes involved in fatty acid oxidation and ketogenesis, and increased expression of genes that cont
65 etabolic alterations related to lipogenesis, ketogenesis, and inflammation in db/db mice.
66          HMG-CoA lyase (HMGCL) is crucial to ketogenesis, and inherited human mutations are potential
67 nic diet induced hepatic lipid oxidation and ketogenesis, and produced multifaceted changes in flux t
68 oneogenesis and fatty acid oxidation) drives ketogenesis, and working in concert with AMPK, it can di
69           These studies suggest that FAO and ketogenesis are key to supporting the metabolism of the
70 demonstrate the importance of HMGCS2-induced ketogenesis as a means to regulate metabolic response to
71 icit in hepatic gluconeogenesis and enhanced ketogenesis as expected but were able to maintain system
72 es PDA aggressiveness and identify HMGCL and ketogenesis as metabolic targets for limiting PDA progre
73 wed fasting hepatic steatosis and diminished ketogenesis associated with decreased expression of gene
74 ne palmitoyltransferase (CPT I) over hepatic ketogenesis because its role in controlling this pathway
75 es are depleted, hepatic gluconeogenesis and ketogenesis become major energy sources.
76 tivated receptor alpha (PPARa) signaling and ketogenesis, but the molecular determinants of this regu
77  was impaired twofold secondary to decreased ketogenesis, but tricarboxylic acid (TCA) cycle activity
78 epatic glucose production (HGP), and hepatic ketogenesis by 50% within 6 hours and were independent o
79 BP contributes to hepatic LCFA oxidation and ketogenesis by a nontranscriptional mechanism, whereas L
80 st this hypothesis, we conditionally ablated ketogenesis by disrupting expression of the terminal enz
81                                              Ketogenesis can dispose of much of the fat that enters t
82 t these genes were significantly involved in ketogenesis, cardiovascular disease, apoptosis and other
83 ual flux control coefficients for CPT I over ketogenesis, CO2 production and total carbon flux (0.51
84         Increased rates of fat oxidation and ketogenesis combined with lower rates of DNL are suggest
85               Maintaining beta-oxidation and ketogenesis could prevent liver injury, and targeting Sh
86            Patients with CFRD rarely develop ketogenesis, despite insulin deficiency.
87    The induction of fatty acid oxidation and ketogenesis during fasting is mainly driven by interrela
88  proteomic profiling revealed that HDACi and ketogenesis enhanced ICB efficacy through both cancer ce
89 urinary metabolome from sugar degradation to ketogenesis-evidence of negative energy balance.
90                  Pentoxifylline promotes gut ketogenesis following trauma-hemorrhage and resuscitatio
91 e by the liver are similar, the rate of C(5) ketogenesis from heptanoate is much lower than the rate
92 ptanoate is much lower than the rate of C(4) ketogenesis from octanoate.
93                                         C(5) ketogenesis from propionate is virtually nil because ace
94 xidation (LOx; by indirect calorimetry), and ketogenesis (from circulating beta-hydroxybutyrate conce
95 n the expression of fatty acid oxidation and ketogenesis genes in the liver.
96 ent deprivation sensor that does not promote ketogenesis) has not been shown to reduce heart failure
97 to potential mediators, such as induction of ketogenesis, immunomodulating effects, and/or reduction
98 d virus-driven HMGCS2 overexpression induced ketogenesis in adult CMs and recapitulated CM dedifferen
99                                Activation of ketogenesis in aged mice expands tissue protective yd T
100 1), a co-repressor of PPARalpha, reactivates ketogenesis in cells and livers with hyperactive mTORC1
101 tin-induced decreases in lipolysis, HGP, and ketogenesis in DKA were also nullified by relatively sma
102 CPT I exerts significantly less control over ketogenesis in hepatocytes isolated from suckling rats t
103 alpha can induce genes of beta-oxidation and ketogenesis in hepatocytes, but these effects do not req
104 ous FGF21 does not drive starvation-mediated ketogenesis in humans.
105 e body is unclear even though AMPK regulates ketogenesis in liver.
106 le, induction of lipolysis, acetogenesis and ketogenesis in livers exposed to 12 h-NMP.
107            Here we show that mTORC1 controls ketogenesis in mice in response to fasting.
108 epatic overexpression of CLSTN3beta promotes ketogenesis in mice.
109 lysed starvation-induced gluconeogenesis and ketogenesis in mouse strains lacking autophagy in liver,
110 A synthase (HMGCS2) to determine the role of ketogenesis in preventing diet-induced steatohepatitis.
111                   Inhibiting P-eIF4E impairs ketogenesis in response to fasting and a ketogenic diet.
112 nt to suppress PPARa signaling and therefore ketogenesis in the fasted state.
113  impairment of fatty acid beta-oxidation and ketogenesis in the liver under chronic fasting or ketoge
114  other specialized tissue functions, such as ketogenesis in the liver.
115 downregulation of hepatic beta-oxidation and ketogenesis in the neonatal chicken.
116 d the connection between OS phagocytosis and ketogenesis in wild-type mice and mice with defects in p
117 hydroxy-3-methylglutarate-CoA synthase 2 (in ketogenesis) in wild-type (Pxr(+/+)) mice only.
118 F21 induces hepatic fatty acid oxidation and ketogenesis, increases insulin sensitivity, blocks somat
119 -specific loss of CLSTN3beta in mice impairs ketogenesis independent of changes in PPARalpha activati
120          These findings suggest that hepatic ketogenesis influences PUFA metabolism, representing a m
121 ediates and gluconeogenesis in the livers of ketogenesis-insufficient animals.
122       Together, these findings indicate that ketogenesis is a critical regulator of hepatic acyl-CoA
123                                              Ketogenesis is a dynamic metabolic conduit supporting he
124 al molecular stimulus to gluconeogenesis and ketogenesis is activation of SIRT1 (sirtuin-1) and its d
125 e are the first data to propose that hepatic ketogenesis is required to maintain cognition and mitoch
126 s the first set of data that suggest hepatic ketogenesis is required to maintain cognition, synaptic
127 oreover, any effect of glucagon to stimulate ketogenesis is severely limited by its insulinotropic ac
128 ittle or no glycolytic reserve; (iii) marked ketogenesis; (iv) depletion of intracellular NTPs; (v) a
129                                 Unrestrained ketogenesis leads to life-threatening ketoacidosis whose
130 ion in the absorptive state and suggest that ketogenesis may modulate fatty liver disease.
131 nt, Ppar alpha-regulated increase in hepatic ketogenesis occurs, and myocardial metabolism is directe
132                     In addition, CR reversed ketogenesis pathway enzymes and the enhanced autophagy,
133                                      Hepatic ketogenesis plays an important role in catabolism of fat
134 investigated the interrelations between C(4) ketogenesis (production of beta-hydroxybutyrate + acetoa
135 f beta-hydroxybutyrate + acetoacetate), C(5) ketogenesis (production of beta-hydroxypentanoate + beta
136 BAT in response to the cold, suggesting that ketogenesis provides an alternative fuel source to compe
137 ochondrial fluxes and redox state to promote ketogenesis rather than synthesis of IHTG.
138 al effects have been attributed to increased ketogenesis, reduced cardiac fatty acid oxidation, and d
139 expression of lipogenic genes, and increased ketogenesis relative to controls.
140 al and extramitochondrial LCFA oxidation and ketogenesis remained at wild-type levels.
141                                              Ketogenesis requires fatty acid flux from intracellular
142 c (endogenous glucose production, lipolysis, ketogenesis) responses to exercise; 2) antecedent hypogl
143 h-fat diet feeding of mice with insufficient ketogenesis resulted in extensive hepatocyte injury and
144             The AMPK-MNK-eIF4E axis controls ketogenesis, revealing a new lipid-mediated kinase signa
145 ed acyl-CoA esters reveal that C(4) and C(5) ketogenesis share the same pool of acetyl-CoA.
146 the flux control coefficients for CPT I over ketogenesis specifically and over total carbon flux (< 0
147 c TLR4 in non-parenchymal cells mediates the ketogenesis-suppressing action of S100A9.
148 bited decreased rates of lipolysis, HGP, and ketogenesis; these effects were reversed by corticostero
149                While insulin therapy reduces ketogenesis this approach is sub-optimal.
150 stimulating mitochondrial beta-oxidation and ketogenesis through the XBP1s-PPARalpha axis.
151 ediated kinase signalling pathway that links ketogenesis to translation control.
152 , we find HMG-CoA lyase (HMGCL), involved in ketogenesis, to be among the most deregulated metabolic
153      PDA cells activate enzymes required for ketogenesis, utilizing various nutrients as carbon sourc
154 array analysis revealed that upregulation of ketogenesis was central to this process.
155                    However, the capacity for ketogenesis was not reduced: BHB plasma levels were rest
156                               No increase in ketogenesis was observed following ingestion of oxidized
157 e production (EGP), lipolytic responses, and ketogenesis were also significantly attenuated (P<0.01)
158 a3-adrenergic agonist, in vivo lipolysis and ketogenesis were decreased in G0S2 transgenic mice when
159 es participating in fatty acid oxidation and ketogenesis were induced more slowly (24 h), following a
160 le genes responsible for lipid oxidation and ketogenesis were up-regulated in HRFI group.
161 echanisms range broadly and include enhanced ketogenesis, where the mild ketosis associated with SGLT
162 promote lipolysis, fatty acid oxidation, and ketogenesis, whereas refeeding suppresses its expression
163 ing mimicry are enhanced gluconeogenesis and ketogenesis, which are not seen with other antihyperglyc
164 ORC1, livers from aged mice have a defect in ketogenesis, which correlates with an increase in mTORC1
165                 We hypothesized that chronic ketogenesis will worsen metabolic dysfunction and oxidat

 
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