PMID- 22067319
OWN - NLM
STAT- MEDLINE
DCOM- 20120305
LR  - 20111223
IS  - 1945-7170 (Electronic)
IS  - 0013-7227 (Linking)
VI  - 153
IP  - 1
DP  - 2012 Jan
TI  - Role of IGFBP-3 in the regulation of beta-cell mass during obesity: adipose 
      tissue/beta-cell cross talk.
PG  - 177-87
LID - 10.1210/en.2011-0181 [doi]
AB  - In obesity an increase in beta-cell mass occurs to cope with the rise in insulin 
      demand. This beta-cell plasticity is essential to avoid the onset of hyperglycemia, 
      although the molecular mechanisms that regulate this process remain unclear. This 
      study analyzed the role of adipose tissue in the control of beta-cell replication. 
      Using a diet-induced model of obesity, we obtained conditioned media from three 
      different white adipose tissue depots. Only in the adipose tissue depot 
      surrounding the pancreas did the diet induce changes that led to an increase in 
      INS1E cells and the islet replication rate. To identify the factors responsible 
      for this proliferative effect, adipose tissue gene expression analysis was 
      conducted by microarrays and quantitative RT-PCR. Of all the differentially 
      expressed proteins, only the secreted ones were studied. IGF binding protein 3 
      (Igfbp3) was identified as the candidate for this effect. Furthermore, in the 
      conditioned media, although the blockage of IGFBP3 led to an increase in the 
      proliferation rate, the blockage of IGF-I receptor decreased it. Taken together, 
      these data show that obesity induces specific changes in the expression profile 
      of the adipose tissue depot surrounding the pancreas, leading to a decrease in 
      IGFBP3 secretion. This decrease acts in a paracrine manner, stimulating the 
      beta-cell proliferation rate, probably through an IGF-I-dependent mechanism. This 
      cross talk between the visceral-pancreatic adipose tissue and beta-cells is a novel 
      mechanism that participates in the control of beta-cell plasticity.
FAU - Palau, Nuria
AU  - Palau N
AD  - Diabetes and Obesity Laboratory, Institut d'Investigations Biomediques August Pi 
      i Sunyer, Rossello 149-153, E-08036 Barcelona, Spain.
FAU - Rebuffat, Sandra A
AU  - Rebuffat SA
FAU - Altirriba, Jordi
AU  - Altirriba J
FAU - Piquer, Sandra
AU  - Piquer S
FAU - Hanzu, Felicia A
AU  - Hanzu FA
FAU - Gomis, Ramon
AU  - Gomis R
FAU - Barbera, Albert
AU  - Barbera A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20111108
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Culture Media, Conditioned)
RN  - 0 (Insulin-Like Growth Factor Binding Protein 3)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Adipose Tissue/pathology/*physiopathology
MH  - Animals
MH  - Base Sequence
MH  - Cell Count
MH  - Cell Line
MH  - Cell Proliferation
MH  - Culture Media, Conditioned
MH  - Diet/adverse effects
MH  - Disease Models, Animal
MH  - Insulin-Like Growth Factor Binding Protein 3/genetics/*physiology
MH  - Insulin-Secreting Cells/*pathology/*physiology
MH  - Male
MH  - Obesity/etiology/genetics/*pathology/*physiopathology
MH  - RNA, Messenger/genetics/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Receptor Cross-Talk/physiology
EDAT- 2011/11/10 06:00
MHDA- 2012/03/06 06:00
CRDT- 2011/11/10 06:00
PHST- 2011/11/10 06:00 [entrez]
PHST- 2011/11/10 06:00 [pubmed]
PHST- 2012/03/06 06:00 [medline]
AID - en.2011-0181 [pii]
AID - 10.1210/en.2011-0181 [doi]
PST - ppublish
SO  - Endocrinology. 2012 Jan;153(1):177-87. doi: 10.1210/en.2011-0181. Epub 2011 Nov 
      8.