Effect of ARB on expression of CD68 and MCP-1 in adipose tissue of rats on long-term high fat diet.
In adipose tissue of rats on long-term high fat diet, the inflammatory changes the roles of angiotensin receptor blocker (ARB) in pimelitis and insulin resistance (IR) were observed. IR rat model was established by feeding high calorie and high fat diet. The change in insulin sensitivity was detected by euglycemic-hyperinsulinemic clamp technique 8 weeks after intervention by valsartan. The expression levels of CD68 and MCP-1 mRNA and proteins in adipose tissue were examined by RT-PCR and immunohistochemistry respectively. The parameters of blood glucose, insulin and blood lipid were analyzed. The results showed that in high fat diet group intra-abdominal obesity developed, the content of visceral fat and the number of inflammatory cells in local adipose tissue were significantly increased (P<0.01), the levels of serum triglyceride, free fatty acids and fasting serum insulin were markedly increased, the insulin sensitivity was significantly lowered (P<0.01), and the expression of CD68 and MCP-1 was significantly increased as compared with control group (P<0.01). In ARB interventional group, the content of visceral fat, the number of inflammatory cells and the expression of CD68 and MCP-1 in local adipose tissue were significantly reduced (all P<0.01), but the insulin sensitivity was significantly enhanced (P<0.01) as compared with high fat diet group. There were pimelitis and IR in rats with obesity induced by long-term high calorie and high fat diet. The ARB can significantly inhibit the infiltration of macrophages and the expression of MCP-1 in adipose tissue, thereby attenuating the inflammation and improving IR in rats.
Guo
Caihong
C
Department of Endocrinology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Yuan
Li
L
Liu
Xiaoling
X
Du
Aimin
A
Huang
Yan
Y
Zhang
Lili
L
D000273:Adipose Tissue / Q000378:metabolism*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology*; D057911:Angiotensin Receptor Antagonists; D000818:Animals; D015703:Antigens, CD / Q000096:biosynthesis*; D015214:Antigens, Differentiation, Myelomonocytic / Q000096:biosynthesis*; D000959:Antihypertensive Agents / Q000494:pharmacology; D018932:Chemokine CCL2 / Q000096:biosynthesis*; D004041:Dietary Fats / Q000378:metabolism*; D007249:Inflammation; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance; D008264:Macrophages / Q000378:metabolism; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D000097382:CD68 Molecule
D047228:Angiotensin II Type 1 Receptor Blockers; D057911:Angiotensin Receptor Antagonists; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000959:Antihypertensive Agents; D018932:Chemokine CCL2; D004041:Dietary Fats; D007328:Insulin; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C491766:Ccl2 protein, rat