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Increased aortic stiffness and attenuated lysyl oxidase activity in obesity.

Arteriosclerosis, thrombosis, and vascular biology (2013-02-16)
Ju-Yi Chen, Pei-Jane Tsai, Haw-Chih Tai, Ruei-Lan Tsai, Yu-Tzu Chang, Mei-Chung Wang, Yu-Wei Chiou, Ming-Long Yeh, Ming-Jer Tang, Chen-Fuh Lam, Shu-Chu Shiesh, Yi-Heng Li, Wei-Chuan Tsai, Chang-Hua Chou, Li-Jen Lin, Hua-Lin Wu, Yau-Sheng Tsai

One potential mechanism through which obesity exerts adverse effects on the vascular system is by increasing aortic stiffness, a change known to be predictive of increased cardiovascular mortality. The aim of this study was to investigate the pathophysiology that links obesity to aortic stiffening. Obese (ob/ob) mice were used to examine physical, morphological, and molecular changes in the aorta in response to obesity. ob/ob mice had increased aortic pulse wave velocity and tissue rigidity. ob/ob aorta exhibited decreases of lysyl oxidase (LOX) activity and cross-linked elastin, and increases of elastin fragmentation and elastolytic activity. The aortas of ob/ob mice were surrounded by a significant amount of proinflammatory and pro-oxidative perivascular adipose tissue. In vitro studies revealed that the conditioned medium from differentiated adipocytes or the perivascular adipose tissue of ob/ob mice attenuated LOX activity. Furthermore, inhibition of LOX in wild-type lean mice caused elastin fragmentation and induced a significant increase in pulse wave velocity. Finally, we found that obese humans had stiffer arteries and lower serum LOX levels than do normal-weight humans. Our results demonstrated that obesity resulted in aortic stiffening in both humans and mice, and established a causal relationship between LOX downregulation and aortic stiffening in obesity.

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