PMID- 21852089
OWN - NLM
STAT- MEDLINE
DCOM- 20121207
LR  - 20211020
IS  - 1873-4847 (Electronic)
IS  - 0955-2863 (Linking)
VI  - 23
IP  - 8
DP  - 2012 Aug
TI  - Caloric restriction increases adiponectin expression by adipose tissue and 
      prevents the inhibitory effect of insulin on circulating adiponectin in rats.
PG  - 867-74
LID - 10.1016/j.jnutbio.2011.04.011 [doi]
AB  - Aging is associated with redistribution of body fat and the development of 
      insulin resistance. White adipose tissue emerges as an important organ in 
      controlling life span. Caloric restriction (CR) delays the rate of aging possibly 
      modulated partly by altering the amount and function of adipose tissue. 
      Adiponectin is a major adipose-derived adipokine that has anti-inflammatory and 
      insulin-sensitizing properties. This study examined the effects of CR on 
      adiposity and gene expression of adiponectin, its receptors (AdipoR1 and AdipoR2) 
      in adipose tissue and in isolated adipocytes of Brown Norway rats that had 
      undergone CR for 4 months or fed ad libitum. The study also determined plasma 
      concentrations of adiponectin and insulin in these animals and whether insulin 
      infusion for 7 days affects adiponectin expression and its circulating 
      concentrations under CR conditions. CR markedly reduced body weight as 
      anticipated, epididymal fat mass and adipocyte size. CR led to an increase in 
      plasma free fatty acid and glycerol (both twofold), and adipose triglyceride 
      lipase messenger RNA (mRNA) in adipose tissue and isolated adipocytes (both 
      >2-fold). Adiponectin mRNA levels were elevated in adipose tissue and adipocytes 
      (both >2-fold) as was plasma adiponectin concentration (2.8-fold) in CR rats. 
      However, CR did not alter tissue or cellular AdipoR1 and AdipoR2 expression. 
      Seven days of insulin infusion decreased adiponectin mRNA in adipose tissue but 
      did not reverse the CR-induced up-regulation of circulating adiponectin levels. 
      Our results suggest that the benefits of CR could be, at least in part, dependent 
      on enhanced expression and secretion of adiponectin by adipocytes.
CI  - Copyright (c) 2012 Elsevier Inc. All rights reserved.
FAU - Ding, Qi
AU  - Ding Q
AD  - Department of Obesity and Endocrinology, Institute of Ageing and Chronic 
      Diseases, University of Liverpool, Liverpool, UK.
FAU - Ash, Catherine
AU  - Ash C
FAU - Mracek, Tomas
AU  - Mracek T
FAU - Merry, Brian
AU  - Merry B
FAU - Bing, Chen
AU  - Bing C
LA  - eng
GR  - BB/E015379/1/BB_/Biotechnology and Biological Sciences Research Council/United 
      Kingdom
GR  - BBE015379/BB_/Biotechnology and Biological Sciences Research Council/United 
      Kingdom
GR  - BBSSN200411555/BB_/Biotechnology and Biological Sciences Research Council/United 
      Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110817
PL  - United States
TA  - J Nutr Biochem
JT  - The Journal of nutritional biochemistry
JID - 9010081
RN  - 0 (Adiponectin)
RN  - 0 (Insulin)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Adiponectin)
RN  - 0 (adiponectin receptor 1, rat)
RN  - 0 (adiponectin receptor 2, rat)
SB  - IM
MH  - Adiponectin/*blood/*metabolism
MH  - Adipose Tissue/*metabolism
MH  - Adiposity/genetics
MH  - Animals
MH  - *Caloric Restriction
MH  - Insulin/*metabolism
MH  - Insulin Resistance
MH  - Male
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Receptors, Adiponectin/genetics/metabolism
EDAT- 2011/08/20 06:00
MHDA- 2012/12/12 06:00
CRDT- 2011/08/20 06:00
PHST- 2010/10/05 00:00 [received]
PHST- 2011/04/14 00:00 [revised]
PHST- 2011/04/14 00:00 [accepted]
PHST- 2011/08/20 06:00 [entrez]
PHST- 2011/08/20 06:00 [pubmed]
PHST- 2012/12/12 06:00 [medline]
AID - S0955-2863(11)00138-0 [pii]
AID - 10.1016/j.jnutbio.2011.04.011 [doi]
PST - ppublish
SO  - J Nutr Biochem. 2012 Aug;23(8):867-74. doi: 10.1016/j.jnutbio.2011.04.011. Epub 
      2011 Aug 17.