ライフサイエンスコーパス: hepatic glycogen

1 critical for efficient storage of glucose as hepatic glycogen.

2 e been attributed to reduced availability of hepatic glycogen.

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

4 glucagon, which is known to rapidly deplete hepatic glycogen.

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

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

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

8 ced hepatic glucose production and increased hepatic glycogen accumulation.

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

10 ertriglyceridemia, hypercholesterolemia, and hepatic glycogen accumulation.

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

12 reased glycolytic flux, leading to increased hepatic glycogen and fat content.

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

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

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

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

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

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

19 Hepatic glycogen and triglyceride concentrations were me

20 s show that fenofibrate can rapidly decrease hepatic glycogen and triglyceride levels and renal trigl

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

22 s with GSD Ia, there is over-accumulation of hepatic glycogen and triglycerides that can lead to stea

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

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

25 These results identify hepatic glycogen as a key regulator of endurance capacit

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

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

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

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

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

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

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

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

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

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

36 Hepatic glycogen content and activities of the gluconeog

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

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

39 Net hepatic glycogen content declined progressively during h

40 ith altered glycogen metabolism and elevated hepatic glycogen content during unfed state.

41 transporter type 1 (Glut1) and a decrease in hepatic glycogen content in the RRE-treated T2DM rats.

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

43 the S + T co-treatment led to an increase in hepatic glycogen content that coincides with heavier liv

44 Hepatic glycogen content was approximately 50% greater,

45 Hepatic glycogen content was higher in the transgenic mi

46 When hepatic glycogen content was lowered, glucagon and NHGO

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

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

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

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

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

52 n receptor substrate 2 and maintained normal hepatic glycogen content, effects that were IL-10-depend

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

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

55 althy_follow-up: -6.9 +/- 4.6; P = 0.17] and hepatic glycogen (Deltaglycogen_baseline: 64.4 +/- 14.1

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

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

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

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

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

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

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

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

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

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

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

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

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

69 elevated hepatic and renal triglyceride and hepatic glycogen levels found in control G6pc -/- mice.

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

71 After hepatic glycogen levels were increased, animals underwen

72 th E. piscicida led to significantly reduced hepatic glycogen levels, indicating a stress response re

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

74 Fasting significantly decreased hepatic glycogen levels.

75 ith the depletion and loss of rhythmicity in hepatic glycogen levels.

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

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

78 Hepatic glycogen metabolism is impaired in diabetes.

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

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

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

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

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

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

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

86 Increased hepatic glycogen reduced the percent of glucose taken up

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

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

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

90 g glycogen depleting exercise, the idea that hepatic glycogen storage and hepatic de novo lipogenesis

91 As expected, impaired hepatic glycogen storage and increased ectopic lipid sto

92 that fructose has the capacity to upregulate hepatic glycogen storage, and replenish these stores mor

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

94 ion of hepatic insulin signaling and reduced hepatic glycogen storage.

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

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

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

98 ses to fructose ingestion, and saturation of hepatic glycogen stores could exacerbate the negative me

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

100 We propose that hepatic glycogen stores may be a key factor in determini

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

102 Hepatic glycogen stores were evaluated using periodic ac

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

104 se homeostasis, balancing the degradation of hepatic glycogen stores, and gluconeogenesis (GNG).

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

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

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

108 detectable hepatic PEPCK mRNA and negligible hepatic glycogen stores.

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

110 Hepatic glycogen supercompensation (fructose infusion gr

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

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

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

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

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

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

117 otein kinase B phosphorylation and increased hepatic glycogen synthesis after an oral glucose challen

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

134 In response to a meal, insulin drives hepatic glycogen synthesis to help regulate systemic glu

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

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

137 Hepatic glycogen synthesis was increased by elevated ins

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

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

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

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

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

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

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

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

146 esultant hepatic insulin resistance prevents hepatic glycogen synthesis, preserving glucose for gluco

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

148 and the subsequent induction of postprandial hepatic glycogen synthesis.

149 reduced muscle glucose uptake and decreased hepatic glycogen synthesis.

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

151 osphorylase can mimic insulin stimulation of hepatic glycogen synthesis.

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

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

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

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

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

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

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

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