{'fraction_non_alphanumeric': 0.031027795733678087, 'fraction_numerical': 0.007110536522301228, 'mean_word_length': 6.267605633802817, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Inflammation, but not oxidative stress or apoptosis, predominates in atherosclerosis‐associated endothelial dysfunction in juvenile Ossabaw pigs with metabolic syndrome

Mechanisms underlying premature atherosclerosis‐associated endothelial dysfunction in childhood obesity have not been clearly established. We hypothesized that inflammation, but not oxidative stress or apoptosis, contributes to endothelial dysfunction in obese juvenile Ossabaw pigs. To test this hypothesis, female Ossabaw pigs at 8‐weeks of age were fed with either a normal diet (lean control) or a high‐fat/high‐fructose diet (obese) for 18‐weeks. Bradykinin‐induced endothelium‐dependent vasorelaxation of the left anterior descending artery (LAD) was impaired in obese pigs, but endothelium‐independent vasorelaxation to sodium nitroprusside was preserved. Incubating the LAD with the superoxide scavenger TEMPOL did not ameliorate endothelial dysfunction in obese pigs. Nitrotyrosine protein expression, p38 phosphorylation, p53 protein expression, and DNA degradation were not increased in LAD of obese pigs. However, expression of lectin‐like oxLDL receptor 1 (LOX‐1) and suppressor of cytokine signaling 1 (SOCS‐1), key regulators of atherogenesis, as well as the inflammatory cytokine tumor necrosis factor‐alpha (TNFa) were higher in LAD of obese pigs. The data support an increased inflammatory response, as opposed to oxidative stress or vascular apoptosis, being the major factor in impaired endothelial function in juvenile Ossabaw pigs with metabolic syndrome.