We hypothesized a sweet potato intervention would prevent high-fat (HF) diet−induced aortic stiffness, which would be associated with decreased arterial oxidative stress and increased mitochondrial uncoupling. Young (8-week old) C57BL/6J mice were randomly divided into 4 groups: low fat (LF; 10% fat), HF (60% fat), low-fat sweet potato (LFSP; 10% fat containing 260.3 μg/kcal sweet potato), or high-fat sweet potato diet (HFSP; 60% fat containing 260.3 μg/kcal sweet potato) for 16 weeks. Compared with LF and LFSP, HF- and HFSP-fed mice had increased body mass and percent fat mass with lower percent lean mass (all, P < 0.05). Sweet potato intervention did not influence body composition (all, P > 0.05). Arterial stiffness, assessed by aortic pulse wave velocity and ex vivo mechanical testing of the elastin region elastic modulus (EEM) was greater in HF compared with LF and HFSP animals (all, P < 0.05). Advanced glycation end products and nitrotyrosine abundance were greater in aortic segments from HF mice compared with LF and HFSP animals (all, P < 0.05). Aortic elastin and uncoupling protein 2 expressions, however, were reduced in HF compared with LF and HFSP mice (all, P < 0.05). Aortic segments cultured with 2,4-dinitrophenol (DNP), a mitochondrial uncoupler, for 72 h reduced the EEM of HF arteries compared with nontreated HF segments (P < 0.05). DNP had no effect on the EEM of aortic segments from HFSP mice. In conclusion, sweet potato attenuates diet-induced aortic stiffness independent of body mass and composition, which is associated with a normalization of arterial oxidative stress possibly due to mitochondrial uncoupling.
Efficacy of Sweet Potato Powder and Added Water as Fat Replacer on the Quality Attributes of Low-fat Pork Patties