Endothelial function worsens in adolescents with obesity, NAFLD
Hispanic adolescents with obesity and nonalcoholic fatty liver disease have greater arterial stiffness and worse overall endothelial function compared with adolescents with obesity without nonalcoholic fatty liver disease, according to researchers.
Fida Bacha, MD, of the Children’s Nutrition Research Center at Baylor College of Medicine, and colleagues evaluated 36 Hispanic adolescents with obesity (20 boys; mean age, 15.3 years; 20 with prediabetes; 16 with type 2 diabetes) to determine whether nonalcoholic fatty liver disease (NAFLD) contributes to the risk for endothelial dysfunction.
NAFLD was diagnosed in 23 participants and confirmed as an elevated hepatic fat fraction greater than 5.5% on magnetic resonance spectroscopy; non-NAFLD (n = 13) was defined as liver transaminases less than 40 U/L and hepatic fat fractions less than 5.5% on magnetic resonance spectroscopy. Augmentation index was used as a measure of arterial stiffness.
Participants with NAFLD had significantly higher total, LDL and HDL cholesterol levels and circulating inflammatory markers, including high-sensitivity C-reactive protein (hs-CRP), intercellular adhesion molecule, vascular adhesion molecule and e-selectin. Reactive hyperemia index was lower (P = .001) and augmentation index (P = .002) and augmentation index-75 (P = .03) were greater (worse) in participants with NAFLD compared with those without NAFLD. Among participants with prediabetes, those with NAFLD had lower reactive hyperemia index (P = .04) and greater augmentation index (P = .009) compared with those without NAFLD. Among participants with type 2 diabetes, those with NAFLD also had lower reactive hyperemia index (P = .03) and greater augmentation index (P = .03) compared with those without NAFLD.
There were no significant differences between participants with and without NAFLD for fasting glucose or hepatic glucose production. Participants with NAFLD had higher glycerol Ra and fasting insulin levels and lower hepatic insulin sensitivity, adipose tissue insulin sensitivity, peripheral skeletal muscle glucose disposal rate and insulin sensitivity compared with participants without NAFLD.
Alanine aminotransferase (ALT; P = .002), aspartate aminotransferase (AST; P = .02), total cholesterol (P = .04) and non-HDL cholesterol (P = .004) were all positively related to hepatic fat content. Reactive hyperemia index (P = .002) was inversely associated with hepatic fat content, whereas hepatic fat content was positively associated with augmentation index (P = .006), augmentation index-75 (P = .04) and vascular adhesion molecule-1 (P = .01). Reactive hyperemia index was inversely associated with ALT (P = .006) and AST (P = .005), whereas ALT and AST were positively associated with augmentation index-75 and hs-CRP. Reactive hyperemia index was inversely associated with vascular molecule-1 (P = .046) and e-selectin (P = .04). Augmentation index-75 was positively related to reactive hyperemia index (P = .02) and inversely associated with hepatic insulin sensitivity (P = .01) and adipose tissue insulin sensitivity (P = .001).
“NAFLD and the associated hepatic and adipose tissue insulin resistance are related to the impairment of vascular reactivity and increased vascular stiffness in [Hispanic adolescents with obesity] with dysglycemia,” the researchers wrote. “In the high-risk group of Hispanic youth with dysglycemia, the presence of NAFLD is an important risk factor for subclinical atherosclerosis. This supports the importance of surveillance for liver disease in these high-risk children, as an indicator of increased risk for early atherogenesis.” – by Amber Cox
Disclosures: The researchers report no relevant financial disclosures.