PMID- 26549348
OWN - NLM
STAT- MEDLINE
DCOM- 20160908
LR  - 20220408
IS  - 1872-9452 (Electronic)
IS  - 0098-2997 (Print)
IS  - 0098-2997 (Linking)
VI  - 46
DP  - 2015 Dec
TI  - Molecular pathophysiology of hepatic glucose production.
PG  - 21-33
LID - S0098-2997(15)30005-4 [pii]
LID - 10.1016/j.mam.2015.09.003 [doi]
AB  - Maintaining blood glucose concentration within a relatively narrow range through 
      periods of fasting or excess nutrient availability is essential to the survival 
      of the organism. This is achieved through an intricate balance between glucose 
      uptake and endogenous glucose production to maintain constant glucose 
      concentrations. The liver plays a major role in maintaining normal whole body 
      glucose levels by regulating the processes of de novo glucose production 
      (gluconeogenesis) and glycogen breakdown (glycogenolysis), thus controlling the 
      levels of hepatic glucose release. Aberrant regulation of hepatic glucose 
      production (HGP) can result in deleterious clinical outcomes, and excessive HGP 
      is a major contributor to the hyperglycemia observed in Type 2 diabetes mellitus 
      (T2DM). Indeed, adjusting glycemia as close as possible to a non-diabetic range 
      is the foremost objective in the medical treatment of patients with T2DM and is 
      currently achieved in the clinic primarily through suppression of HGP. Here, we 
      review the molecular mechanisms controlling HGP in response to nutritional and 
      hormonal signals and discuss how these signals are altered in T2DM.
CI  - Copyright (c) 2015 Elsevier Ltd. All rights reserved.
FAU - Sharabi, Kfir
AU  - Sharabi K
AD  - Department of Cancer Biology, Department of Cell Biology, Dana-Farber Cancer 
      Institute, Harvard Medical School, Boston, MA 02115, USA.
FAU - Tavares, Clint D J
AU  - Tavares CD
AD  - Department of Cancer Biology, Department of Cell Biology, Dana-Farber Cancer 
      Institute, Harvard Medical School, Boston, MA 02115, USA.
FAU - Rines, Amy K
AU  - Rines AK
AD  - Department of Cancer Biology, Department of Cell Biology, Dana-Farber Cancer 
      Institute, Harvard Medical School, Boston, MA 02115, USA.
FAU - Puigserver, Pere
AU  - Puigserver P
AD  - Department of Cancer Biology, Department of Cell Biology, Dana-Farber Cancer 
      Institute, Harvard Medical School, Boston, MA 02115, USA. Electronic address: 
      pere_puigserver@dfci.harvard.edu.
LA  - eng
GR  - F32 DK102293/DK/NIDDK NIH HHS/United States
GR  - F32DK102293-01/DK/NIDDK NIH HHS/United States
GR  - R24 DK080261/DK/NIDDK NIH HHS/United States
GR  - R01 DK081418/DK/NIDDK NIH HHS/United States
GR  - R01 DK089883/DK/NIDDK NIH HHS/United States
GR  - R01 DK069966/DK/NIDDK NIH HHS/United States
GR  - R24 DK080261-06/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20151105
PL  - England
TA  - Mol Aspects Med
JT  - Molecular aspects of medicine
JID - 7603128
RN  - 0 (Blood Glucose)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Blood Glucose/*metabolism
MH  - Diabetes Mellitus, Type 2/blood/metabolism/pathology
MH  - Fasting/metabolism
MH  - Gluconeogenesis/physiology
MH  - Glucose/*metabolism
MH  - Humans
MH  - Hyperglycemia/metabolism/pathology
MH  - Liver/*metabolism/pathology
PMC - PMC4674831
MID - NIHMS735842
OTO - NOTNLM
OT  - glucagon
OT  - gluconeogenesis
OT  - glucose
OT  - insulin
OT  - liver
EDAT- 2015/11/10 06:00
MHDA- 2016/09/09 06:00
PMCR- 2016/12/01
CRDT- 2015/11/10 06:00
PHST- 2015/09/09 00:00 [received]
PHST- 2015/09/09 00:00 [accepted]
PHST- 2015/11/10 06:00 [entrez]
PHST- 2015/11/10 06:00 [pubmed]
PHST- 2016/09/09 06:00 [medline]
PHST- 2016/12/01 00:00 [pmc-release]
AID - S0098-2997(15)30005-4 [pii]
AID - 10.1016/j.mam.2015.09.003 [doi]
PST - ppublish
SO  - Mol Aspects Med. 2015 Dec;46:21-33. doi: 10.1016/j.mam.2015.09.003. Epub 2015 Nov 
      5.