ライフサイエンスコーパス: hepatic glycogen

1 e been attributed to reduced availability of hepatic glycogen.

2 t mice die soon after birth and have reduced hepatic glycogen.

3 actose for UDP-glucose flux and retention in hepatic glycogen.

4 critical for efficient storage of glucose as hepatic glycogen.

5 lar lipids (less than or equal to -31%), and hepatic glycogen (-20%); but muscle glycogen, VO(2max),

6 KK2 deficiency was associated with increased hepatic glycogen accumulation and decreased hepatic gluc

7 f the PTG gene in mice prevented HFD-induced hepatic glycogen accumulation.

8 ertriglyceridemia, hypercholesterolemia, and hepatic glycogen accumulation.

9 eceptors lowered blood glucose and increased hepatic glycogen after oral glucose loading and also sti

10 This effect is accompanied by hepatic glycogen and lipid deposition as well as up-regu

11 ors of glucose sensing for the regulation of hepatic glycogen and lipid metabolism.

12 riglyceride and fructose carbon storage into hepatic glycogen and lipids.

13 nstead fructose feeding caused a decrease in hepatic glycogen and plasma glucose levels.

14 Adult TG mice exhibited reduced hepatic glycogen and progressive liver injury, but maint

15 locus died as neonates due to the absence of hepatic glycogen and the resulting hypoglycemia.

16 s characterized by fasting hypoglycaemia and hepatic glycogen and triglyceride overaccumulation.

17 glycemic and hypoinsulinemic, depleted their hepatic glycogen, and developed fatty liver.

18 duces PEPCK mRNA, causes the mobilization of hepatic glycogen, and maintains normal glucose homeostas

19 regulation, hypoglycemia failed to stimulate hepatic glycogen breakdown or activation of EGP, factors

20 tic hormone secretion, ketone production, or hepatic glycogen breakdown.

21 loss of total body, lean, and fat masses and hepatic glycogen but resulted in enhanced insulin sensit

22 cerides, reduces white adipose, and depletes hepatic glycogen, but raises lactate.

23 These data indicate that increases in hepatic glycogen can generate a state of hepatic insulin

24 n(-1) compared with euglycemia, P = NS), and hepatic glycogen concentration did not change significan

25 In marked contrast, after an overnight fast, hepatic glycogen concentration in type 1 diabetic subjec

26 pectroscopy to measure sequential changes in hepatic glycogen concentration, a novel tracer approach

27 n; P < 0.001), causing a large difference in hepatic glycogen content (62 +/- 9 vs. 100 +/- 3 mg/g; P

28 -(13)C]glucose exhibited a large increase in hepatic glycogen content and a 70% increase in incorpora

29 Hepatic glycogen content and activities of the gluconeog

30 Therefore, we propose that hepatic glycogen content be considered a potential targe

31 of glycogenolysis was associated with lower hepatic glycogen content before the onset of exercise an

32 Net hepatic glycogen content declined progressively during h

33 Here, we examined the effect of varying hepatic glycogen content on the counterregulatory respon

34 Hepatic glycogen content was approximately 50% greater,

35 Hepatic glycogen content was higher in the transgenic mi

36 When hepatic glycogen content was lowered, glucagon and NHGO

37 c glycogen was significantly impaired, total hepatic glycogen content was substantially decreased, an

38 is study was to determine how increasing the hepatic glycogen content would affect the liver's abilit

39 Results show reduced blood glucose, hepatic glycogen content, and hepatic glucokinase (GK) a

40 ose intolerance, hyperinsulinemia, decreased hepatic glycogen content, and increased peripheral (musc

41 type 1a, UGRP(-/-) mice exhibit no change in hepatic glycogen content, blood glucose, or triglyceride

42 e turnover and glucose uptake, but decreased hepatic glycogen content.

43 n a reciprocal fashion; and (d) promotion of hepatic glycogen cycling may be the principal mechanism

44 ahepatic glucose disposal (2.02) and the net hepatic glycogen depletion rate was 0.93 (46%).

45 Likewise, myocardial necrosis and hepatic glycogen depletion with vacuolization were more

46 Overnight starvation led to complete hepatic glycogen depletion, associated hypoketotic hypog

47 yperglycemia, impaired glucose tolerance, or hepatic glycogen depletion.

48 tion (-44%) were reduced, whereas muscle and hepatic glycogen depletions were accelerated by 27-55%,

49 e after exercise, glucose incorporation into hepatic glycogen, determined using [3-3H]glucose, was no

50 feeding mice a high-fat diet (HFD) increases hepatic glycogen due to increased expression of the glyc

51 By the final 30 min of hypoglycemia, hepatic glycogen fell from 301 +/- 14 to 234 +/- 10 mmol

52 strain (LGSKO) that almost completely lacks hepatic glycogen, has impaired glucose disposal, and is

53 ibit hypoglycemia, nor did they show reduced hepatic glycogen in adult.

54 Furthermore, restoration of hepatic glycogen levels after AdHNF3beta and AdHNF6 coin

55 iver displayed only a transient reduction in hepatic glycogen levels and was associated with less sev

56 o reduced blood glucose levels but increases hepatic glycogen levels during the daytime or upon fasti

57 Hepatic glycogen levels were 2.1-2.4-fold greater in G(L

58 After hepatic glycogen levels were increased, animals underwen

59 v Ex9 infusion lowered insulin secretion and hepatic glycogen levels, whereas no effects of icv Ex4 w

60 Fasting significantly decreased hepatic glycogen levels.

61 lucose concentrations, and dysregulations in hepatic glycogen metabolism are linked to many diseases

62 e activity in vitro; however, its effects on hepatic glycogen metabolism in humans is unknown.

63 recovery of plasma glucose, abnormalities in hepatic glycogen metabolism per se could also play an im

64 uses hepatic insulin resistance selective to hepatic glycogen metabolism that is associated with elev

65 tute a mechanism for autocrine regulation of hepatic glycogen metabolism.

66 ction through the hormone's direct effect on hepatic glycogen metabolism.

67 They do not mobilize their hepatic glycogen or induce the cytosolic form of phospho

68 tion; and reduced ectopic fat deposition and hepatic glycogen overaccumulation.

69 o express the gene for PEPCK and to mobilize hepatic glycogen (phenotype B).

70 Increased hepatic glycogen reduced the percent of glucose taken up

71 rgeting metabolic pathway(s) associated with hepatic glycogen repletion.

72 -specific overexpression of Ppp1r3b enhanced hepatic glycogen storage above that of controls and, as

73 n order to maintain circadian homeostasis of hepatic glycogen storage and blood glucose levels.

74 d bilirubin levels and a complete absence of hepatic glycogen storage.

75 ferentiation of hepatocytes, accumulation of hepatic glycogen stores and generation of a hepatic epit

76 icate a major role for Ppp1r3b in regulating hepatic glycogen stores and whole-body glucose/energy ho

77 n is increased, and white adipose tissue and hepatic glycogen stores are depleted in stearate-fed Scd

78 ariables but leaves animals unable to reduce hepatic glycogen stores in response to fasting.

79 Furthermore, hepatic glycogen stores were diminished, and fasting pla

80 however, Gsk3beta phosphorylation (Ser9) and hepatic glycogen stores were nearly normal in all of the

81 iated with fetal growth restriction, reduced hepatic glycogen stores, and hypoglycemia.

82 ion and increased insulin secretion to favor hepatic glycogen stores, preparing efficiently for the n

83 gnificantly increased; 3) a reduction in the hepatic glycogen stores, which may contribute to the enh

84 ise performance, presumably because of lower hepatic glycogen stores.

85 detectable hepatic PEPCK mRNA and negligible hepatic glycogen stores.

86 Hepatic glycogen supercompensation (fructose infusion gr

87 ively; however, there were no differences in hepatic glycogen synthase activity or insulin signalling

88 in vivo resulted in significantly increased hepatic glycogen synthase activity.

89 pectroscopy was used to assess flux rates of hepatic glycogen synthase and phosphorylase in overnight

90 lted in a threefold increase in rates of net hepatic glycogen synthesis (0.54 +/- 0.12 mmol/l per min

91 Fructose infusion increased net hepatic glycogen synthesis (0.7 +/- 0.5 vs. 6.4 +/- 0.4

92 . control) without affecting the pathways of hepatic glycogen synthesis (direct pathway approximately

93 ed hepatic gluconeogenic genes and increased hepatic glycogen synthesis and glycogen content by a mec

94 pectroscopy to noninvasively assess rates of hepatic glycogen synthesis and glycogenolysis under eugl

95 In contrast, Zip14 KO mice exhibited greater hepatic glycogen synthesis and impaired gluconeogenesis

96 respective roles of insulin and glucagon for hepatic glycogen synthesis and turnover, hyperglycemic c

97 hypoglucagonemia (III) there was negligible hepatic glycogen synthesis and turnover.

98 of insulin and glucagon independently affect hepatic glycogen synthesis and turnover.

99 ed stimulation of hepatic glucose uptake and hepatic glycogen synthesis are reduced in people with ty

100 d type 1 and type 2 diabetes, stimulation of hepatic glycogen synthesis by this mechanism may be of p

101 of hepatic glucose production, and increased hepatic glycogen synthesis compared with WT controls dur

102 The contribution of the indirect pathway to hepatic glycogen synthesis did not differ in the diabeti

103 the effect of liver glycogen loading on net hepatic glycogen synthesis during hyperinsulinemia or he

104 infusion causes a threefold increase in net hepatic glycogen synthesis exclusively through stimulati

105 Because net hepatic glycogen synthesis has been shown to be diminish

106 The rates of hepatic glycogen synthesis in the ADM and control mouse

107 erlie the majority of these adaptations, net hepatic glycogen synthesis is sensitized.

108 , and acetaminophen to trace the pathways of hepatic glycogen synthesis to elucidate the homeostatic

109 ith a glucose load augmented NHGU, increased hepatic glycogen synthesis via the direct pathway, and a

110 l per min, respectively, and the rate of net hepatic glycogen synthesis was 0.14 +/- 0.05 mmol/l per

111 Hepatic glycogen synthesis was increased by elevated ins

112 to increased insulin action, the increase in hepatic glycogen synthesis was independent of it.

113 Net hepatic glycogen synthesis was markedly elevated (+360%)

114 Hepatic glycogen synthesis was reduced 20% in P versus N

115 the contribution of the indirect pathway to hepatic glycogen synthesis was similar between groups.

116 Relatively high rates of net hepatic glycogen synthesis were observed in protocol III

117 results in: (a) twofold increase in rate of hepatic glycogen synthesis, (b) reduction of glycogen tu

118 sly reported that splanchnic glucose uptake, hepatic glycogen synthesis, and hepatic glucokinase acti

119 tion of GS by glucose 6-phosphate, decreases hepatic glycogen synthesis, increases liver fat, causes

120 nous glucose production, and (iii) decreased hepatic glycogen synthesis.

121 reduced muscle glucose uptake and decreased hepatic glycogen synthesis.

122 of the mechanism by which insulin stimulates hepatic glycogen synthesis.

123 osphorylase can mimic insulin stimulation of hepatic glycogen synthesis.

124 in the mechanism by which insulin stimulates hepatic glycogen synthesis.

125 Notably, however, net hepatic glycogen synthetic rates were disproportionately

126 apid depletion of fuel substrates, including hepatic glycogen, to maintain core body temperature.

127 ared with age-matched Zucker (+/+) rats, and hepatic glycogen was dramatically higher among fa/fa ani

128 During the first 4 hours of each study, hepatic glycogen was increased by augmenting hepatic glu

129 Net incorporation of plasma glucose into hepatic glycogen was negligible.

130 As a consequence, glucose incorporation into hepatic glycogen was significantly impaired, total hepat

131 rect) contributions, and percent turnover of hepatic glycogen were assessed by in vivo 13C nuclear ma