title: Captopril intake decreases body weight gain via angiotensin-(1-7).
abstract: Angiotensin-(1-7) [Ang-(1-7)] plays a beneficial role in cardiovascular physiology by providing a counterbalance to the function of angiotensin II (Ang II). Although Ang II has been shown to be an adipokine secreted by adipocyte and affect lipid metabolism, the role of Ang-(1-7) in adipose tissue remains to be clarified. The aim of the present study was to investigate whether Ang-(1-7) affects lipid metabolism in adipose tissue. Ang-(1-7) increased glycerol release from primary adipocytes in a dose-dependent manner. A lipolytic effect of Ang-(1-7) was attenuated by pretreatment with A-779, a Mas receptor blocker and with an inhibitor of phosphoinositol 3-kinase (PI3K), or eNOS. However, losartan and PD123319 did not cause any change in Ang-(1-7)-induced lipolysis. Ang-(1-7)-induced lipolysis had an addictive effect with isoproterenol. In normal rats, chronic intake of captopril for 4 wks decreased body weight gain and the amount of adipose tissue and increased plasma Ang-(1-7) level. These effects were attenuated by administration of A-779. The levels of Mas receptor and phosphorylation of hormone-sensitive lipase (p-HSL) were significantly increased by treatment with captopril and these captopril-mediated effects were attenuated by the administration of A-779. There was no difference in diameter of adipocytes among sham, captopril- and captopril+A-779-treated groups. The similar effects of captopril on body weight, expression of Mas receptor, and p-HSL were observed in Ang-(1-7)-treated rats. These results suggest that captopril intake decreased body weight gain partly through Ang-(1-7)/Mas receptor/PI3K pathway.
authors: Department of Physiology, Diabetic Research Center, Chonbuk National University Medical School, Jeonju, Republic of Korea.
authors: Young-Bin
authors: YB
authors: Oh
authors: Jong Hun
authors: JH
authors: Kim
authors: Byung Mun
authors: BM
authors: Park
authors: Byung Hyun
authors: BH
authors: Park
authors: Suhn Hee
authors: SH
authors: Kim
mesh_terms: D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism; D000273:Adipose Tissue / Q000187:drug effects / Q000473:pathology; D050154:Adiposity / Q000187:drug effects; D000803:Angiotensin I / Q000494:pharmacology / Q000502:physiology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage*; D000818:Animals; D002216:Captopril / Q000008:administration & dosage*; D048429:Cell Size / Q000187:drug effects; D002478:Cells, Cultured; D004822:Epididymis / Q000187:drug effects / Q000473:pathology; D005990:Glycerol / Q000378:metabolism; D008066:Lipolysis / Q000187:drug effects; D008297:Male; D010446:Peptide Fragments / Q000494:pharmacology / Q000502:physiology*; D061251:Primary Cell Culture; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism; D002787:Sterol Esterase / Q000378:metabolism; D015430:Weight Gain / Q000187:drug effects*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D010446:Peptide Fragments; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins; D043562:Receptors, G-Protein-Coupled; D000803:Angiotensin I; D002216:Captopril; D002787:Sterol Esterase; C118790:angiotensin I (1-7); D005990:Glycerol