[Renin-angiotensin system in mesenteric adipose tissues in rats with metabolic syndrome].
OBJECTIVE
To investigate the renin-angiotensin system (RAS) in mesenteric adipose tissues and effect of angiotensin II on adipocyte differentiation.


METHODS
Thirty normal 8-week-old male Wistar rats were divided into groups on normal diet and high-fat diet. The rats on high-fat diet for 24 weeks developed the metabolic syndrome respectively. The mRNA and protein expression of mesenteric adipose tissue were measured by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. Lipid drop in 3T3-L1 preadipocytes and mature adipocytes were observed using oil-red O staining. The fluorescence microscope was used to detect cytosolic-free calcium in 3T3-L1 preadipocytes and mature adipocytes.


RESULTS
The expressions of angiotensinogen, angiotensin converting enzyme, angiotensin II receptor type 1 in mesenteric adipose tissue were significantly increased in rats with metabolic syndrome compared with those in rats on normal diet (P <0. 05, P <0. 01). After administration of angiotensin II , no lipid droplet in 3T3 -L1 preadipocytes and adipocytes were observed, however, intensive lipid droplet in adipocyte was found after administration of captopril and candesartan. Angiotensin II increased the intracellular-free calcium concentration in preadipocytes (P < 0. 01 ) , which was blocked by captopril and candesartan; in contrast, angiotensin II effect was blunt in mature adipocyte. Captopril and candesartan partially recovered the angiotensin II -mediated increase of cytosolic-free calcium.


CONCLUSIONS
RAS in the mesenteric adipose tissues is active in rats with metabolic syndrome, and antagonization of RAS can recover the lipogenesis of adipocyte.
Ma
Li-qun
LQ
Department of Hypertension and Endocrinology, Daping Hospital, Third Military Medical University, Chongqing 400042, China.
Zhang
Li-li
LL
Zhang
Ya-ping
YP
Wang
Li-juan
LJ
Li
Zhi-bing
ZB
Cao
Ting-bing
TB
Liu
Dao-yan
DY
Zhu
Zhi-ming
ZM
D017667:Adipocytes / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism*; D000804:Angiotensin II / Q000494:pharmacology; D000808:Angiotensinogen / Q000096:biosynthesis; D000818:Animals; D001562:Benzimidazoles / Q000494:pharmacology; D001713:Biphenyl Compounds; D002118:Calcium / Q000378:metabolism; D002216:Captopril / Q000494:pharmacology; D002478:Cells, Cultured; D008297:Male; D024821:Metabolic Syndrome / Q000503:physiopathology*; D007703:Peptidyl-Dipeptidase A / Q000096:biosynthesis; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017208:Rats, Wistar; D044139:Receptor, Angiotensin, Type 2 / Q000096:biosynthesis; D012084:Renin-Angiotensin System / Q000502:physiology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013777:Tetrazoles / Q000494:pharmacology
D001562:Benzimidazoles; D001713:Biphenyl Compounds; D012333:RNA, Messenger; D044139:Receptor, Angiotensin, Type 2; D013777:Tetrazoles; D000808:Angiotensinogen; D000804:Angiotensin II; D002216:Captopril; D007703:Peptidyl-Dipeptidase A; C081643:candesartan; D002118:Calcium