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1 r (PTG(OE)), which results in an increase in liver glycogen.
2 f glucose and normal postprandial amounts of liver glycogen.
3 d after fasting for 16 h and 48 h to deplete liver glycogen.
4 e used during exercise comes from muscle and liver glycogen.
5 a related isoform essential for synthesizing liver glycogen.
6                               In conclusion, liver glycogen accumulation caused a reduced food intake
7                                              Liver glycogen accumulation during period 2 was 21 +/- 1
8  were able to cause significant increases in liver glycogen accumulation in dose-dependent fashion.
9 ements of postprandial changes in muscle and liver glycogen and lipid content, and assessment of DNL
10 e derived from ingested carbohydrate, stored liver glycogen and newly synthesized glucose (gluconeoge
11 t in db/db mice, in association with reduced liver glycogen and reduced liver enzyme activity in seru
12                Feeding rats glucose elevated liver glycogen and significantly reduced hepatocellular
13 treated with AdCMV-GKL had 5.4 times as much liver glycogen as AdCMV-betaGAL-treated controls; no sig
14       In addition, we measured how enhancing liver glycogen by feeding glucose to the rat donors affe
15 od to improve the donor liver, but elevating liver glycogen by glucose supplementation is possible an
16 rved and characterized by depleted levels of liver glycogen, choline, taurine, trimethylamine N-oxide
17 photoperiod exhibiting 13.8 times more total liver glycogen compared to treefrogs in the early-season
18                 After the liquid mixed meal, liver glycogen concentration rose from 207 +/- 22 to 316
19 d reduced birthweight (>=30 mg/kg), depleted liver glycogen concentrations (all doses), hypoglycemia
20 ((13)C MRS) was applied to assess muscle and liver glycogen concentrations before and immediately aft
21                                              Liver glycogen concentrations increased from 110 +/- 44
22 ence of carbohydrate intake (CON) muscle and liver glycogen concentrations remained unchanged during
23 ose ingestion (1.2 g/kg BM/h) fully restored liver glycogen concentrations well within 6 h of post-ex
24                                   Muscle and liver glycogen concentrations were again assessed at 6 a
25                                              Liver glycogen concentrations were significantly higher
26 enables in vivo assessments of muscle and/or liver glycogen concentrations.
27                                The amount of liver glycogen consumed during exercise was similar for
28  liver to generate Akita mice with increased liver glycogen content (Akita-PTG(OE)).
29 sly demonstrated that strategies to increase liver glycogen content in a high-fat-diet mouse model of
30 109 +/- 28 mg/dl 6 days after injection) and liver glycogen content in STZ-injected rats.
31 ults demonstrate that strategies to increase liver glycogen content lead to the long-term reduction o
32                                              Liver glycogen content was elevated, but the nitric oxid
33   In rats subjected to compound A treatment, liver glycogen content was increased.
34 ernight fast, PTG(OE) animals presented high liver glycogen content, lower liver triacylglycerol cont
35 counterregulatory axis that is responsive to liver glycogen content.
36 atory responses that resulted from increased liver glycogen content.
37  deficiency, and have a 95% reduction in fed liver glycogen content.
38 s indicated from serum metabolite levels and liver glycogen content.
39  non-invasive measurement of both muscle and liver glycogen contents before and after exercise, and a
40 arge amounts of carbohydrate both muscle and liver glycogen contents increase rapidly, with liver gly
41 ise recovery, the time required to replenish liver glycogen contents is less evident.
42  compared to the control, whereas soleus and liver glycogen contents were less (P < 0.01 and P < 0.01
43 ob mice pretreated with 14C-glucose to label liver glycogen, CP-91149 administration reduced 14C-glyc
44  become markedly hypoglycemic as a result of liver glycogen depletion.
45 ce and excessive (210% of high-carbohydrate) liver glycogen deposition (from [14C]glucose) caused by
46           During the first 4 h of the study, liver glycogen deposition was stimulated by intraportal
47                      The concomitant loss of liver glycogen impaired whole-body glucose homeostasis a
48 xamining the long-term effects of increasing liver glycogen in an animal model of insulin-deficient a
49                                  Reduced pup liver glycogen, increased liver weights and reduced thyr
50      This study investigated how the lack of liver glycogen increases fat accumulation and the develo
51                                              Liver glycogen is important for the counterregulation of
52                                              Liver glycogen is liberated to glucose, glycerol and (gl
53 ation caused markedly increased postprandial liver glycogen levels (in a HNF4alpha-dependent fashion)
54  that these daytime effects mostly relate to liver glycogen levels and correspond to the animals' fee
55 y accessible method to noninvasively measure liver glycogen levels and their changes.
56 G(M)DeltaC-overexpressing rats lowered their liver glycogen levels by 57% (from 402 +/- 54 to 173 +/-
57    Without carbohydrate ingestion muscle and liver glycogen levels remain depleted.
58                                              Liver glycogen levels were supercompensated (SCGly) in t
59 ver-specific deletion of p53 in mice reduces liver glycogen levels, and we implicate the transcriptio
60           Hyperglycemia also correlates with liver glycogen levels, but there is no evidence of subst
61  daytime-dependent manner through changes in liver glycogen levels, likely due to their effect on ani
62 FAs, increased plasma lactate, and increased liver glycogen levels, relative to diabetic mice treated
63 se tolerance test (GTT) and normalization of liver glycogen levels.
64                     These data indicate that liver glycogen loading impairs glycogen synthesis regard
65 of this study was to determine the effect of liver glycogen loading on net hepatic glycogen synthesis
66 testinal short chain fatty acids (SCFA), and liver glycogen of triplicate groups of 20 red hybrid til
67 eover, G6PC or another glycogenolysis enzyme-liver glycogen phosphorylase (PYGL) deficiency in both h
68 lycogenolysis and gluconeogenesis, including liver glycogen phosphorylase (PYGL), phosphoenolpyruvate
69                        An inhibitor of human liver glycogen phosphorylase a (HLGPa) has been identifi
70 the debilitating effects of diabetes, making liver glycogen phosphorylase a potential therapeutic tar
71 es of the active and inactive forms of human liver glycogen phosphorylase a.
72 performed using genetic markers flanking the liver glycogen phosphorylase gene ( PYGL ), which was su
73 vered a mutation in the catalytic subunit of liver glycogen phosphorylase kinase in a patient with Ma
74 Kinetic studies with rabbit muscle and human liver glycogen phosphorylases showed that the (R)-imidaz
75                                              Liver glycogen repletion was also brisk throughout the s
76 ratio of maltodextrin and fructose) enhances liver glycogen repletion when compared with maltodextrin
77 ingestion can also accelerate post-exercise (liver) glycogen repletion rates, which may be relevant w
78 rcise sessions and accelerate post-exercise (liver) glycogen repletion.
79                                              Liver glycogen represents an important physiological for
80                                          The liver glycogen reserve was found decreased in NQO1-/- mi
81  fructose) does not compromise post-exercise liver glycogen resynthesis, allowing for increased amino
82 amino acid availability without compromising liver glycogen resynthesis, despite enhanced glucagonaem
83 e, cholesterol and triglycerides, as well as liver glycogen, significantly increased.
84       Cell therapy was also found to improve liver glycogen storage and sera glucose level in mice ex
85 sion suggests that controlled stimulation of liver glycogen storage may be an effective mechanism for
86 d increase in insulin secretion and enhanced liver glycogen storage.
87 ngestion is required to replenish muscle and liver glycogen stores after a strenuous bout of exercise
88 ver glycogen contents increase rapidly, with liver glycogen stores being fully repleted within 6 h.
89 STZ-injected rats caused a large increase in liver glycogen stores but only a transient decrease in f
90  0 patients and highlights the importance of liver glycogen stores in whole body glucose homeostasis.
91                              After exercise, liver glycogen stores were totally depleted in control m
92 liver damage, with overexpression increasing liver glycogen stores, while deletion resulted in higher
93 ociated with low circulating glucose and low liver glycogen stores.
94 nsulin sensitivity, accompanied by decreased liver glycogen stores.
95                                              Liver glycogen synthase (GYS2), a key enzyme in glycogen
96 The resulting LGSKO mice are viable, develop liver glycogen synthase deficiency, and have a 95% reduc
97  linked to the islet amyloid polypeptide and liver glycogen synthase genes showed no evidence for lin
98  liver-specific disruption of the Gys2 gene (liver glycogen synthase knock-out (LGSKO) mice), using L
99 (period 1 to period 2) in the active form of liver glycogen synthase was 0.7 +/- 0.4, 6.5 +/- 1.2, 2.
100 ues, and GYS2, primarily expressed in liver (liver glycogen synthase).
101 t artificial chromosome as the gene encoding liver glycogen synthase, another possible NIDDM suscepti
102                                Expression of liver glycogen synthase, phosphoenolpyruvate carboxykina
103          GSK-3 inhibitor treatment increased liver glycogen synthesis about threefold independent of
104 e, encoding PPP1R3B protein, is critical for liver glycogen synthesis and maintaining blood glucose l
105             Our results suggest that loss of liver glycogen synthesis diverts glucose toward fat synt
106                             The reduction in liver glycogen synthesis in SCGly+INS was accompanied by
107                                          Net liver glycogen synthesis was similar between groups (eld
108 drate storage (estimating total, muscle, and liver glycogen synthesis) compared with GLU (+117 +/- 9
109 ibuted to an approximate twofold increase in liver glycogen synthesis.
110  oral glucose disposal, mostly by increasing liver glycogen synthesis.
111 fructose infusion caused a large increase in liver glycogen that markedly elevated the response of ep
112 w studies have addressed the contribution of liver glycogen to exercise performance.
113 e-body carbohydrate oxidation and muscle and liver glycogen utilization, and reduced whole-body fat o
114                                              Liver glycogen was nearly completely depleted in fasted
115 reated controls; no significant increases in liver glycogen were observed at either level of GK overe

 
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