Suppression of lipoprotein lipase expression in 3T3-L1 cells by inhibition of adipogenic differentiation through activation of the renin-angiotensin system.
The renin-angiotensin system (RAS) may inhibit adipogenic differentiation by down-regulating peroxisome proliferator-activated receptor gamma gene expression in adipocytes, and adipocytes express all components of the RAS, including angiotensinogen. Expression of lipoprotein lipase (LPL), which is expressed mainly in adipocytes, is considered to be affected by adipogenic differentiation. We studied whether LPL expression in mouse 3T3-L1 cells is suppressed by inhibition of adipogenic differentiation through activation of RAS by the cells. The mean 3T3-L1 cell size increased and peroxisome proliferator-activated receptor gamma messenger RNA (mRNA) expression in the cells measured by reverse transcriptase polymerase chain reaction (RT-PCR) was enhanced with increase in incubation time. The LPL activity, LPL protein expression (Western blot), and mRNA expression (RT-PCR) in 3T3-L1 cells increased transiently followed by a decline during long-term incubation. Angiotensin II suppressed adipogenic differentiation, LPL activity, protein expression, and mRNA expression in 3T3-L1 cells. On the other hand, the selective angiotensin type 1 receptor blocker valsartan enhanced adipogenic differentiation and LPL activity in 3T3-L1 cells. Angiotensinogen mRNA expression in 3T3-L1 cells measured by RT-PCR was enhanced with increase in incubation time. These results suggest that LPL expression may be suppressed by inhibition of adipogenic differentiation through activation of endogenous RAS in 3T3-L1 cells angiotensin type 1 receptor.
Saiki
Atsuhito
A
Center of Diabetes, Endocrine and Metabolism, Toho University Sakura Medical Center, Chiba 285-8741, Japan.
Koide
Nobukiyo
N
Watanabe
Fusako
F
Murano
Takeyoshi
T
Miyashita
Yoh
Y
Shirai
Kohji
K
D041721:3T3-L1 Cells; D017667:Adipocytes / Q000166:cytology* / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D000804:Angiotensin II / Q000494:pharmacology*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D000808:Angiotensinogen / Q000096:biosynthesis / Q000235:genetics; D000818:Animals; D001391:Azo Compounds / Q000737:chemistry; D015153:Blotting, Western; D002454:Cell Differentiation / Q000187:drug effects / Q000502:physiology*; D008071:Lipoprotein Lipase / Q000096:biosynthesis* / Q000235:genetics; D051379:Mice; D008858:Microscopy, Phase-Contrast; D047495:PPAR gamma / Q000096:biosynthesis / Q000235:genetics; D000077205:Pioglitazone; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013777:Tetrazoles / Q000494:pharmacology; D045162:Thiazolidinediones / Q000494:pharmacology; D014633:Valine / Q000031:analogs & derivatives / Q000494:pharmacology; D000068756:Valsartan
D047228:Angiotensin II Type 1 Receptor Blockers; D001391:Azo Compounds; D047495:PPAR gamma; D012333:RNA, Messenger; D013777:Tetrazoles; D045162:Thiazolidinediones; D000808:Angiotensinogen; D000804:Angiotensin II; D000068756:Valsartan; D008071:Lipoprotein Lipase; C011049:oil red O; D014633:Valine; D000077205:Pioglitazone