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(OR21-04-26) De Novo Lipogenesis Is Increased in Adolescents With Obesity and Metabolic Dysfunction-Associated Steatotic Liver Disease

Monday, July 27, 2026
3:06 PM - 3:18 PM ET
Location: Maryland Ballroom C

    Presenting Author(s)

  • KS

    Kevin R. Short, PhD

    Professor
    University of Oklahoma Health Campus
    Oklahoma City, Oklahoma, United States

    Disclosure(s): No relevant financial relationship(s) with ineligible companies to disclose.

    • Co-Author(s)

  • SP

    Sirish K. Palle, MD

    University of Oklahoma Health Campus
    Oklahoma City, Oklahoma, United States

  • Jessica G. George, BHS

    Doctoral Candidate
    University of Missouri
    Columbia, Missouri, United States

  • YK

    Youngsil Kim

    University of Oklahoma Health Campus
    Oklahoma City, Oklahoma, United States

  • JF

    Jacob E. Friedman, PhD

    University of Oklahoma Health Campus
    Oklahoma City, Oklahoma, United States

  • EP

    Elizabeth J. Parks

    University of Missouri, United States

Disclosure(s):
Kevin R. Short, PhD: No relevant financial relationship(s) with ineligible companies to disclose.
Jessica G. George, BHS: No relevant financial relationship(s) with ineligible companies to disclose.
Objectives: In adults with metabolic dysfunction-associated steatotic liver disease (MASLD), de novo lipogenesis (DNL) is increased and contributes to disease pathology. MASLD is present in nearly 40% of adolescents with obesity, but the role of DNL in this population is not established.  Disease progression is faster in adolescents than adults and there are differences in liver histology, supporting the need for studies in young people so that age-appropriate treatment strategies can be developed.  We tested the hypothesis that DNL is increased in adolescents with biopsy-confirmed MASLD compared to peers with either obesity (Ob) or normal weight (NW) without MASLD.

Methods: Boys and girls, 10-19y (n = 28 MASLD, n = 18 Ob, n = 23 NW) consumed oral 2H2O.  2H incorporation into triglyceride (TG)-rich lipoprotein palmitate (i.e., DNL) was assessed while fasting and for 4 hours after consuming 75g glucose + 25g fructose (oral sugars tolerance test, OSTT).

Results: Most MASLD participants (82%) had steatohepatitis (MASH) or borderline MASH (14%).  The MASLD and Ob groups had similar body fat and were higher than the NW group (47 ± 5, 44 ± 8, & 28 ± 9%, p< 0.01).  Insulin resistance (iHOMA2-IR) differed among all groups (MASLD: 3.4 ± 2.3;  Ob: 1.9 ± 0.9; NW: 0.8 ± 0.5 units, p< 0.001).  Fractional DNL while fasting was lower in the NW group than the Ob and MASLD groups (4.8 ± 3.1, 11.5 ± 7.6, 9.8 ± 3.7%, p< 0.01) and did not significantly change from fasting in response to the OSTT.  Fractional DNL was positively correlated with body fat and trunk fat (r = 0.45 & 0.46), fasting insulin (r = 0.36), and fasting TG (r = 0.36, all p < 0.01), but did not vary with liver histology scores for steatosis or other features.  Absolute DNL was also lowest in the NW group throughout the study, with the Ob and MASLD groups not differing (fasting: 7.9 ± 9.9, 24.5 ± 30.9 & 26.9 ± 23.1 µmol/l, p< 0.01).  Compared to fasting, absolute DNL increased ~40% in the MASLD group by 3.5 hours post-OSTT (p < 0.01) but was not significantly changed in the other two groups.

Conclusions: DNL is increased in adolescents with obesity and not significantly further increased in those with MASLD, as it is in adults. However, pediatric patients with MASLD appear to direct more dietary sugars to DNL than their healthier peers, which may contribute to their condition.

Funding Sources: NIH R01DK129656 and Oklahoma Children’s Health Foundation