ライフサイエンスコーパス: liver glycogen

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 In conclusion, liver glycogen accumulation caused a reduced food intake

6 Liver glycogen accumulation during period 2 was 21 +/- 1

7 were able to cause significant increases in liver glycogen accumulation in dose-dependent fashion.

8 ements of postprandial changes in muscle and liver glycogen and lipid content, and assessment of DNL

9 e derived from ingested carbohydrate, stored liver glycogen and newly synthesized glucose (gluconeoge

10 t in db/db mice, in association with reduced liver glycogen and reduced liver enzyme activity in seru

11 Feeding rats glucose elevated liver glycogen and significantly reduced hepatocellular

12 treated with AdCMV-GKL had 5.4 times as much liver glycogen as AdCMV-betaGAL-treated controls; no sig

13 In addition, we measured how enhancing liver glycogen by feeding glucose to the rat donors affe

14 od to improve the donor liver, but elevating liver glycogen by glucose supplementation is possible an

15 rved and characterized by depleted levels of liver glycogen, choline, taurine, trimethylamine N-oxide

16 After the liquid mixed meal, liver glycogen concentration rose from 207 +/- 22 to 316

17 enables in vivo assessments of muscle and/or liver glycogen concentrations.

18 The amount of liver glycogen consumed during exercise was similar for

19 109 +/- 28 mg/dl 6 days after injection) and liver glycogen content in STZ-injected rats.

20 Liver glycogen content was elevated, but the nitric oxid

21 In rats subjected to compound A treatment, liver glycogen content was increased.

22 ernight fast, PTG(OE) animals presented high liver glycogen content, lower liver triacylglycerol cont

23 counterregulatory axis that is responsive to liver glycogen content.

24 atory responses that resulted from increased liver glycogen content.

25 deficiency, and have a 95% reduction in fed liver glycogen content.

26 s indicated from serum metabolite levels and liver glycogen content.

27 compared to the control, whereas soleus and liver glycogen contents were less (P < 0.01 and P < 0.01

28 ob mice pretreated with 14C-glucose to label liver glycogen, CP-91149 administration reduced 14C-glyc

29 become markedly hypoglycemic as a result of liver glycogen depletion.

30 ce and excessive (210% of high-carbohydrate) liver glycogen deposition (from [14C]glucose) caused by

31 During the first 4 h of the study, liver glycogen deposition was stimulated by intraportal

32 The concomitant loss of liver glycogen impaired whole-body glucose homeostasis a

33 This study investigated how the lack of liver glycogen increases fat accumulation and the develo

34 Liver glycogen is important for the counterregulation of

35 y accessible method to noninvasively measure liver glycogen levels and their changes.

36 G(M)DeltaC-overexpressing rats lowered their liver glycogen levels by 57% (from 402 +/- 54 to 173 +/-

37 Liver glycogen levels were supercompensated (SCGly) in t

38 FAs, increased plasma lactate, and increased liver glycogen levels, relative to diabetic mice treated

39 These data indicate that liver glycogen loading impairs glycogen synthesis regard

40 of this study was to determine the effect of liver glycogen loading on net hepatic glycogen synthesis

41 testinal short chain fatty acids (SCFA), and liver glycogen of triplicate groups of 20 red hybrid til

42 lycogenolysis and gluconeogenesis, including liver glycogen phosphorylase (PYGL), phosphoenolpyruvate

43 An inhibitor of human liver glycogen phosphorylase a (HLGPa) has been identifi

44 the debilitating effects of diabetes, making liver glycogen phosphorylase a potential therapeutic tar

45 es of the active and inactive forms of human liver glycogen phosphorylase a.

46 performed using genetic markers flanking the liver glycogen phosphorylase gene ( PYGL ), which was su

47 vered a mutation in the catalytic subunit of liver glycogen phosphorylase kinase in a patient with Ma

48 Liver glycogen repletion was also brisk throughout the s

49 Liver glycogen represents an important physiological for

50 The liver glycogen reserve was found decreased in NQO1-/- mi

51 e, cholesterol and triglycerides, as well as liver glycogen, significantly increased.

52 Cell therapy was also found to improve liver glycogen storage and sera glucose level in mice ex

53 sion suggests that controlled stimulation of liver glycogen storage may be an effective mechanism for

54 d increase in insulin secretion and enhanced liver glycogen storage.

55 STZ-injected rats caused a large increase in liver glycogen stores but only a transient decrease in f

56 0 patients and highlights the importance of liver glycogen stores in whole body glucose homeostasis.

57 ociated with low circulating glucose and low liver glycogen stores.

58 nsulin sensitivity, accompanied by decreased liver glycogen stores.

59 Liver glycogen synthase (GYS2), a key enzyme in glycogen

60 The resulting LGSKO mice are viable, develop liver glycogen synthase deficiency, and have a 95% reduc

61 linked to the islet amyloid polypeptide and liver glycogen synthase genes showed no evidence for lin

62 liver-specific disruption of the Gys2 gene (liver glycogen synthase knock-out (LGSKO) mice), using L

63 (period 1 to period 2) in the active form of liver glycogen synthase was 0.7 +/- 0.4, 6.5 +/- 1.2, 2.

64 ues, and GYS2, primarily expressed in liver (liver glycogen synthase).

65 t artificial chromosome as the gene encoding liver glycogen synthase, another possible NIDDM suscepti

66 Expression of liver glycogen synthase, phosphoenolpyruvate carboxykina

67 GSK-3 inhibitor treatment increased liver glycogen synthesis about threefold independent of

68 Our results suggest that loss of liver glycogen synthesis diverts glucose toward fat synt

69 The reduction in liver glycogen synthesis in SCGly+INS was accompanied by

70 Net liver glycogen synthesis was similar between groups (eld

71 drate storage (estimating total, muscle, and liver glycogen synthesis) compared with GLU (+117 +/- 9

72 ibuted to an approximate twofold increase in liver glycogen synthesis.

73 oral glucose disposal, mostly by increasing liver glycogen synthesis.

74 fructose infusion caused a large increase in liver glycogen that markedly elevated the response of ep

75 e-body carbohydrate oxidation and muscle and liver glycogen utilization, and reduced whole-body fat o

76 Liver glycogen was nearly completely depleted in fasted

77 reated controls; no significant increases in liver glycogen were observed at either level of GK overe