In Angiotensin II-infused mice, obesity (ob/ob genotype) significantly increased the incidence of abdominal aortic aneurysms compared to lean controls (76% vs 32%, P<0.05).
Does obesity promote Angiotensin II-induced abdominal aortic aneurysm formation in mice?
Obesity promotes macrophage accumulation in periaortic adipose tissue and enhances Angiotensin II-induced abdominal aortic aneurysm formation in a mouse model.
Absolute Event Rate: 76% vs 32%
p-value: p=<0.05
OBJECTIVE: Obesity promotes macrophage infiltration into adipose tissue and is associated with increases in several cardiovascular diseases. Infusion of angiotensin II (AngII) to mice induces formation of abdominal aortic aneurysms (AAAs) with profound medial and adventitial macrophage infiltration. We sought to determine whether obesity promotes macrophage infiltration and proinflammatory cytokines in periaortic adipose tissue surrounding abdominal aortas and increases AngII-induced AAAs. METHODS AND RESULTS: Hypertrophied white adipocytes surrounded abdominal aortas, whereas brown adipocytes surrounded thoracic aortas of obese mice. mRNA abundance of macrophage proinflammatory chemokines and their receptors were elevated with obesity to a greater extent in abdominal compared to thoracic periaortic adipose tissue. Periaortic adipose tissue explants surrounding abdominal aortas of obese mice released greater concentrations of MCP-1 and promoted more macrophage migration than explants from thoracic aortas. Male C57BL/6 mice were fed a high-fat (HF) diet for 1, 2, or 4 months and then infused with AngII (1000 ng/kg/min) for 28 days. AAA incidence increased progressively with the duration of HF feeding (18%, 36%,and 60%, respectively). Similarly, AngII-infused ob/ob mice exhibited increased AAAs compared to lean controls (76% compared to 32%, respectively, P<0.05). Infusion of AngII to obese mice promoted further macrophage infiltration into periaortic and visceral adipose tissue, and obese mice exhibiting AAAs had greater macrophage content in visceral adipose tissue than mice not developing AAAs. CONCLUSIONS: Increased macrophage accumulation in periaortic adipose tissue surrounding abdominal aortas of AngII-infused obese mice is associated with enhanced AAA formation.
Police et al. (Fri,) conducted a other in Abdominal aortic aneurysm. Obesity (high-fat diet or ob/ob genotype) with Angiotensin II infusion vs. Lean controls was evaluated on Abdominal aortic aneurysm (AAA) incidence (p=<0.05). In Angiotensin II-infused mice, obesity (ob/ob genotype) significantly increased the incidence of abdominal aortic aneurysms compared to lean controls (76% vs 32%, P<0.05).