PMID- 22953992
OWN - NLM
STAT- MEDLINE
DCOM- 20130226
LR  - 20190328
IS  - 1557-9077 (Electronic)
IS  - 1050-7256 (Linking)
VI  - 22
IP  - 10
DP  - 2012 Oct
TI  - AMP-activated protein kinase upregulates glucose uptake in thyroid PCCL3 cells 
      independent of thyrotropin.
PG  - 1063-8
LID - 10.1089/thy.2012.0041 [doi]
AB  - BACKGROUND: Glucose is transported into cells by specific glucose transporter 
      proteins (GLUTs) that are widely expressed in a tissue-specific manner. The 
      mechanisms that regulate glucose uptake and metabolism in thyroid cells are 
      poorly defined. Recently, our group showed that AMP-activated protein kinase 
      (AMPK) plays a pivotal role in the rat thyroid gland, downregulating iodide 
      uptake by thyroid cells even in the presence of its main stimulator thyrotropin 
      (TSH). Since AMPK increases glucose uptake in different tissues, and taken into 
      consideration that in pathophysiological conditions such as thyroid cancer a 
      negative correlation between iodide and glucose uptake occurs, we hypothesized 
      that AMPK might modulate glucose uptake in thyroid cells. METHODS: Rat follicular 
      thyroid PCCL3 cells cultivated in Ham's F-12 supplemented with 5% calf serum and 
      hormones were exposed to the AMPK pharmacological activator 5-aminoimidazole-4 
      carboxamide ribonucleoside (AICAR) or AMPK antagonist compound C for 24 hours 
      either in the presence or absence of TSH. Glucose uptake was assessed in vitro 
      using 2-deoxy-D-[(3)H]glucose. RESULTS: AMPK activation by AICAR induced a 
      significant increase in glucose uptake by PCCL3 cells, an effect that was 
      completely reversed by the AMPK inhibitor compound C. Also, the AICAR mediated 
      increase in glucose uptake was detected either in the presence or absence of TSH. 
      The mechanism by which AICAR increases glucose uptake is related to higher levels 
      of GLUT 1 protein content and hexokinase (HK) activity in thyroid cells. 
      CONCLUSION: Our results show that AMPK activation significantly upregulates GLUT 
      1 content and glucose uptake, and it also stimulates hexokinase activity, the 
      first step of glycolysis.
FAU - Andrade, Bruno M
AU  - Andrade BM
AD  - Laboratory of Endocrine Physiology, Carlos Chagas Filho Institute of Biophysics, 
      Federal University of Rio de Janeiro, Rio de Janeiro, Brazil. 
      brunoma@biof.ufrj.br
FAU - Cazarin, Juliana
AU  - Cazarin J
FAU - Zancan, Patricia
AU  - Zancan P
FAU - Carvalho, Denise P
AU  - Carvalho DP
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120906
PL  - United States
TA  - Thyroid
JT  - Thyroid : official journal of the American Thyroid Association
JID - 9104317
RN  - 0 (Glucose Transporter Type 1)
RN  - 0 (Pyrazoles)
RN  - 0 (Pyrimidines)
RN  - 0 (Ribonucleotides)
RN  - 0 (Slc2a1 protein, rat)
RN  - 10K52CIC1Z (dorsomorphin)
RN  - 360-97-4 (Aminoimidazole Carboxamide)
RN  - 9002-71-5 (Thyrotropin)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
RN  - F0X88YW0YK (AICA ribonucleotide)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - AMP-Activated Protein Kinases/antagonists & inhibitors/*physiology
MH  - Aminoimidazole Carboxamide/analogs & derivatives/pharmacology
MH  - Animals
MH  - Cells, Cultured
MH  - Glucose/*metabolism
MH  - Glucose Transporter Type 1/biosynthesis
MH  - Pyrazoles/pharmacology
MH  - Pyrimidines/pharmacology
MH  - Rats
MH  - Ribonucleotides/pharmacology
MH  - Thyroid Gland/drug effects/*metabolism
MH  - Thyrotropin/*physiology
MH  - Up-Regulation
EDAT- 2012/09/08 06:00
MHDA- 2013/02/27 06:00
CRDT- 2012/09/08 06:00
PHST- 2012/09/08 06:00 [entrez]
PHST- 2012/09/08 06:00 [pubmed]
PHST- 2013/02/27 06:00 [medline]
AID - 10.1089/thy.2012.0041 [doi]
PST - ppublish
SO  - Thyroid. 2012 Oct;22(10):1063-8. doi: 10.1089/thy.2012.0041. Epub 2012 Sep 6.