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1 yrate, the central metabolite of therapeutic ketosis.
2 eline, week 9 in ketosis, and week 13 out of ketosis.
3 modulates the appetite suppressant effect of ketosis.
4 ketone oxidation after sustained nutritional ketosis.
5 tory genes that affect clinical/ subclinical ketosis.
6 of ChREBP to the cytoplasm during periods of ketosis.
7     Higher HbA1c levels were correlated with ketosis.
8 and specificity of HbA1c as an indicator for ketosis.
9 s inhibiting fat synthesis during periods of ketosis.
10  diabetic ketoacidosis or hyperglycemia with ketosis.
11 lism by increasing gluconeogenesis (GNG) and ketosis.
12 ges associated with starvation, which create ketosis.
13 uction in beta-cell mass with progression to ketosis.
14 lasticity factor, Bdnf, in the brain without ketosis.
15 fasting durations are associated with higher ketosis.
16 group and 2 in the BGM group), hyperglycemia/ketosis (1 participant with an event in CGM group and 4
17 ly in its study and development, therapeutic ketosis across the spectrum of HF holds significant prom
18                                              Ketosis also led to significantly reduced aortic CCR2 co
19 act of WL-induced changes in appetite and if ketosis alters these responses.
20 ed by increased availability due to systemic ketosis and a cardiac autonomous upregulation of ketolyt
21  less restrictive, therapy that also creates ketosis and can lower the number of seizures.
22 usly to be associated with susceptibility to ketosis and clinical mastitis in Jersey and Holstein dai
23 tment and retention rates and achievement of ketosis and glucose control.
24 Rats receiving KD and EKB reached a state of ketosis and had significant reduction in AAA expansion a
25          Ketogenic diets promote nutritional ketosis and have shown benefits on glycaemic control, in
26 act on serum lipids without the accompanying ketosis and have the potential to provide a nutritionall
27 ing of 10% kcal protein also caused moderate ketosis and hepatic fat accumulation, which were again a
28 hur Mirsky, and George Cahill) had described ketosis and ketoacidosis induced by administration of th
29 ions remain regarding the use of therapeutic ketosis and mechanism of action in HF, current evidence
30 elation (r = 0.36, P < 0.05; n = 34) between ketosis and oxidative stress as well as between oxidativ
31 served a strong inverse relationship between ketosis and patterns of MGU.
32 ly, our data suggest that fasting-associated ketosis and the ketogenic effects of SGLT2 inhibitors oc
33 line restricted (~300 mg/kg) provokes robust ketosis and weight loss in mice, but through unknown mec
34       These diets induce a moderate level of ketosis and, in some studies, have been shown to improve
35 ic program, including glycolysis, lipolysis, ketosis, and nucleotide breakdown.
36 ppetite were measured at baseline, week 9 in ketosis, and week 13 out of ketosis.
37                                              Ketosis appears to have a greater beneficial impact on G
38  an emphasis on the therapeutic potential of ketosis as a treatment for heart failure (HF).
39 include enhanced ketogenesis, where the mild ketosis associated with SGLT2i use is presumed to be ben
40 th HF, and (4) the potential significance of ketosis associated with sodium-glucose cotransporter 2 i
41 ve study consisted of 253 T2DM patients with ketosis at Shanghai 10th People's Hospital during a peri
42                                     However, ketosis (beta-hydroxybutyrate levels >500 mumol/L) was a
43  with uDM, hyperglucagonemia is required for ketosis but not for increased HGP or hyperglycemia.
44                                        Under ketosis, C75 was also less efficient at stimulating mTOR
45                        In extreme conditions ketosis can progress to ketoacidosis, a dangerous and po
46  AAA expansion, and that its modulation with ketosis can reduce AAA pathology.
47 glucose production (HGP), hyperglycemia, and ketosis characteristic of uncontrolled insulin-deficient
48 ant renal epithelial cell death, (6) induces ketosis characterized by an increase in serum level of b
49         Three weeks of sustained nutritional ketosis, compared with the HCLF diet, had no effect on s
50                                              Ketosis (defined as 3-hydroxybutyrate >500 muM) was achi
51 ketosis) versus ketone ester ([KE] exogenous ketosis) drink.
52  participants were in a state of nutritional ketosis during post-KD assessments (baseline: 0.2 +/- 0.
53 ike transcriptional paradigm, with increased ketosis, erythropoietin, and autophagic flux in addition
54 t mice has hyperlipidemia, hypoglycemia, and ketosis exacerbated by fasting.
55 l body weight for height and maximal urinary ketosis for seizure control.
56 butyrate-based novel approach of therapeutic ketosis for treating DKD.
57 high: all 17 patients maintained nutritional ketosis (&gt;= 0.3 mM/dL) > 50% of study days.
58 y suggest that 3 wk of sustained nutritional ketosis had no effect on cognitive performance, mood, or
59  overnight fastings of 11 +/- 1 h and during ketosis-hyperglycemia events for the minors.
60 l process of defective energy production and ketosis in A(-)beta(+) KPD.
61 asible, safe, well tolerated and resulted in ketosis in all patients in the intervention group, with
62 he failing heart, (3) effects of therapeutic ketosis in animals and humans with HF, and (4) the poten
63  BHB) is used as an indicator of subclinical ketosis in cows.
64                                              Ketosis in dairy cattle has been shown to cause a high m
65 oncentrations have a strong correlation with ketosis in dairy cattle.
66 d pathways potentially affecting subclinical ketosis in North American Holstein dairy cattle.
67      HbA1c is a potential screening tool for ketosis in patients with T2DM.
68                                              Ketosis in patients with type 2 diabetes mellitus (T2DM)
69 moglobin A1c (HbA1c) as a screening tool for ketosis in T2DM patients.
70 lism, glucagon has been described to promote ketosis in the fasted state.
71  inflammation, we evaluated whether systemic ketosis in vivo could reduce CCR2 and AAA progression.
72 BHB concentrations (indicator of subclinical ketosis) in the first lactation (SCK1) and second and la
73            Burgeoning evidence suggests that ketosis, in particular B-hydroxybutyrate, exerts a benef
74      This study examined the hypothesis that ketosis increases the TNF-alpha secretion, both in a cel
75      We conclude that both hyperglycemia and ketosis independently cause reductions in cerebral high-
76  most abundant BHB-amino acid, BHB-Phe, is a ketosis-inducible congener of Lac-Phe that activates hyp
77 iver triglyceride accumulation in vivo via a ketosis induction protocol in multiparous dairy cows per
78       This raises the question of why severe ketosis is accompanied by acidosis.
79 ing that neither fasting- nor SGLT2i-induced ketosis is altered by interruption of glucagon signaling
80 r the benefit and feasibility of therapeutic ketosis is examined in preclinical and clinical studies.
81                                              Ketosis is much more likely with HbA1c values at >/=10.1
82                                              Ketosis is one of the most important health problems in
83 B-HB in adults, including animals in dietary ketosis, is unaffected.
84 tress induced by 2-DG can, in the absence of ketosis, lead to the transcription of genes involved in
85 y was undertaken to test the hypothesis that ketosis might increase lipid peroxidation and lower glut
86 ms, hepatocellular injury, hyperglycemia and ketosis, neurologic illnesses, ocular symptoms, and derm
87 of severe hypoglycemia or hyperglycemia with ketosis occurred.
88  adipogenesis, beta-oxidation of lipids, and ketosis of carbohydrates, lipids, and proteins.
89 the independent effects of hyperglycemia and ketosis on cerebral metabolism, blood flow, and water di
90 cal studies that will evaluate the impact of ketosis on human AAA disease.
91 ere are few data on carbohydrate content and ketosis on motivation to eat and ad libitum intake.
92 highest proportion of retinopathy (20%); and ketosis-prone (6%) with the highest proportion of kidney
93                                              Ketosis-prone atypical diabetes is mostly recorded in pe
94 f an adult patient with an unusual course of ketosis-prone diabetes (KPD) and lacking islet autoantib
95                                              Ketosis-prone diabetes (KPD) is a rare form of type 2 di
96                                  A(-)beta(+) ketosis-prone diabetes (KPD) is an emerging syndrome of
97 and near-normoglycemic, patients with "A-B+" ketosis-prone diabetes (KPD) manifest accelerated leucin
98                                              Ketosis-prone diabetes mellitus (KPD) is a subtype of ty
99 ying mechanisms for beta-cell dysfunction in ketosis-prone type 2 diabetes are not known; however, pr
100 group consisted of 221 T2DM patients without ketosis randomly selected from inpatients during the sam
101 athways and a lack of metabolic switching to ketosis resulting in a deficit in GABAergic signaling an
102 a key biomarker for diagnosis of subclinical ketosis (SCK), and provides information on the health st
103 ified in previous studies as associated with ketosis susceptibility and immune response, and also fou
104                                              Ketosis symptoms, however, are difficult to identify, th
105 ketones make it possible to reach a state of ketosis that may improve metabolic control in humans.
106 f adult mice led to lethal hyperglycemia and ketosis that were attributed to loss of beta cell functi
107 n is metabolized to glutamine and because in ketosis there is increased consumption of acetate, which
108 , noninferiority trial of the KD (endogenous ketosis) versus ketone ester ([KE] exogenous ketosis) dr
109 abilized by ketones, irrespective of whether ketosis was achieved with a ketogenic diet or exogenous
110 he response of the minors to the presence of ketosis was consistent but unique for each individual.
111          Body weight was measured daily, and ketosis was monitored by analysis of plasma and urine sa
112  As 2-OPP formation appears to increase upon ketosis, we emphasize the importance of avoiding catabol
113 ately 10 days their severe hyperglycemia and ketosis were corrected.
114                   Only physiologic levels of ketosis were observed.
115                          The LC diet induced ketosis with mean 3-hydroxybutyrate concentrations of 1.
116 ed serious adverse events (hyperglycaemia or ketosis without acidosis) resulting in hospital admissio

 
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