PMID- 23028137
OWN - NLM
STAT- MEDLINE
DCOM- 20130411
LR  - 20211021
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Print)
IS  - 0012-1797 (Linking)
VI  - 62
IP  - 2
DP  - 2013 Feb
TI  - Portal vein glucose entry triggers a coordinated cellular response that 
      potentiates hepatic glucose uptake and storage in normal but not 
      high-fat/high-fructose-fed dogs.
PG  - 392-400
LID - 10.2337/db12-0417 [doi]
AB  - The cellular events mediating the pleiotropic actions of portal vein glucose 
      (PoG) delivery on hepatic glucose disposition have not been clearly defined. 
      Likewise, the molecular defects associated with postprandial hyperglycemia and 
      impaired hepatic glucose uptake (HGU) following consumption of a high-fat, 
      high-fructose diet (HFFD) are unknown. Our goal was to identify hepatocellular 
      changes elicited by hyperinsulinemia, hyperglycemia, and PoG signaling in normal 
      chow-fed (CTR) and HFFD-fed dogs. In CTR dogs, we demonstrated that PoG infusion 
      in the presence of hyperinsulinemia and hyperglycemia triggered an increase in 
      the activity of hepatic glucokinase (GK) and glycogen synthase (GS), which 
      occurred in association with further augmentation in HGU and glycogen synthesis 
      (GSYN) in vivo. In contrast, 4 weeks of HFFD feeding markedly reduced GK protein 
      content and impaired the activation of GS in association with diminished HGU and 
      GSYN in vivo. Furthermore, the enzymatic changes associated with PoG sensing in 
      chow-fed animals were abolished in HFFD-fed animals, consistent with loss of the 
      stimulatory effects of PoG delivery. These data reveal new insight into the 
      molecular physiology of the portal glucose signaling mechanism under normal 
      conditions and to the pathophysiology of aberrant postprandial hepatic glucose 
      disposition evident under a diet-induced glucose-intolerant condition.
FAU - Coate, Katie C
AU  - Coate KC
AD  - Department of Molecular Physiology and Biophysics, Vanderbilt University School 
      of Medicine, Nashville, Tennessee, USA.
FAU - Kraft, Guillaume
AU  - Kraft G
FAU - Irimia, Jose M
AU  - Irimia JM
FAU - Smith, Marta S
AU  - Smith MS
FAU - Farmer, Ben
AU  - Farmer B
FAU - Neal, Doss W
AU  - Neal DW
FAU - Roach, Peter J
AU  - Roach PJ
FAU - Shiota, Masakazu
AU  - Shiota M
FAU - Cherrington, Alan D
AU  - Cherrington AD
LA  - eng
GR  - P60 DK020593/DK/NIDDK NIH HHS/United States
GR  - R01-DK-18243/DK/NIDDK NIH HHS/United States
GR  - DK-20593/DK/NIDDK NIH HHS/United States
GR  - P30 DK020593/DK/NIDDK NIH HHS/United States
GR  - R01 DK018243/DK/NIDDK NIH HHS/United States
GR  - R37-DK-27221/DK/NIDDK NIH HHS/United States
GR  - R37 DK027221/DK/NIDDK NIH HHS/United States
GR  - T32 DK007563/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20121001
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
RN  - 0 (Liver Glycogen)
RN  - 30237-26-4 (Fructose)
RN  - EC 2.4.1.11 (Glycogen Synthase)
RN  - EC 2.7.1.2 (Glucokinase)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Animals
MH  - Diet, High-Fat/*adverse effects
MH  - Dogs
MH  - Fructose/administration & dosage/*adverse effects
MH  - Glucokinase/analysis/metabolism
MH  - Glucose/administration & dosage/*metabolism
MH  - Glucose Intolerance/etiology
MH  - Glycogen Synthase/metabolism
MH  - Hyperglycemia/etiology/metabolism
MH  - Hyperinsulinism/etiology
MH  - Liver/enzymology/*metabolism
MH  - Liver Glycogen/biosynthesis
MH  - Male
MH  - Portal Vein/*physiology
MH  - Signal Transduction/physiology
PMC - PMC3554368
EDAT- 2012/10/03 06:00
MHDA- 2013/04/12 06:00
PMCR- 2014/02/01
CRDT- 2012/10/03 06:00
PHST- 2012/10/03 06:00 [entrez]
PHST- 2012/10/03 06:00 [pubmed]
PHST- 2013/04/12 06:00 [medline]
PHST- 2014/02/01 00:00 [pmc-release]
AID - db12-0417 [pii]
AID - 0417 [pii]
AID - 10.2337/db12-0417 [doi]
PST - ppublish
SO  - Diabetes. 2013 Feb;62(2):392-400. doi: 10.2337/db12-0417. Epub 2012 Oct 1.