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Obese children experienced dyslipemia, hyperinsulinemia after meal high in saturated fat

Dyslipemia, hyperinsulinemia and altered expression of lipoprotein occurred in obese children with and without nonalcoholic fatty liver disease after consuming a meal high in saturated fat in a recent study.

Researchers evaluated blood samples collected from children before and after consumption of a meal high in saturated fat (SFA, 18.8%) and low in long-chain polyunsaturated fatty acids (LCPUFA, 21.7:1). The cohort included 11 obese children with nonalcoholic fatty liver disease (NAFLD), nine age-and-sex-matched obese children without NAFLD and 11 age-matched lean children. Blood samples were collected at baseline after an overnight fast, and at 1, 3 and 6 hours after eating.

Children with NAFLD had higher levels of ALT and AST at baseline than both control groups (P<.001). They also had higher baseline levels of insulin, nonesterified fatty acids (NEFA), triglycerides, C-reactive protein and insulin resistance, plus lower levels of high-density lipoprotein (HDL) and inflammatory marker IL-10, than lean (P.05) but not obese controls.

Obese children, regardless of NAFLD, experienced hyperinsulinemia and hypertriglyceridemia after eating compared with lean controls (P<.05). Concentrations of HDL were significantly lower before and after the meal among obese participants, while apolipoprotein-B100 was significantly higher (P<.001). No significant difference was observed in these values between obese children with or without NAFLD.

One hour after consumption, patients with NAFLD experienced marked hyperinsulinemia (P<.001 vs. other groups) and a decrease to NEFA 6 hours afterward (P<.05). Prolonged increases to apolipoprotein-B48 also occurred among NAFLD patients compared with controls (P<.001), and these participants had significantly higher concentrations of tumor necrosis factor-alpha than both control groups at all time points (P<.001).

“Children with NAFLD experience postprandial lipemia, hyperinsulinemia and some alterations in lipoprotein expression that are suggestive of an altered balance of fat across the liver when compared with obese and lean children,” the researchers wrote. “How this may contribute to fat accumulation in the liver is unclear. … Studies examining hepatic partitioning of dietary fat, particularly the SFA and LCPUFA, using stable isotope tracers are necessary to elucidate these mechanisms.”

Disclosure: See the study for a full list of relevant disclosures.