<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Cohen CC</submitter><funding>National Center for Advancing Translational Sciences</funding><funding>Nutrition Science Initiative</funding><funding>NCATS NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>National Institute of Diabetes and Digestive and Kidney Diseases</funding><funding>NIH Office of the Director</funding><funding>NINR NIH HHS</funding><pagination>e150996</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8670836</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>131(24)</volume><pubmed_abstract>BACKGROUNDHepatic de novo lipogenesis (DNL) is elevated in nonalcoholic fatty liver disease (NAFLD). Improvements in hepatic fat by dietary sugar reduction may be mediated by reduced DNL, but data are limited, especially in children. We examined the effects of 8 weeks of dietary sugar restriction on hepatic DNL in adolescents with NAFLD and correlations between DNL and other metabolic outcomes.METHODSAdolescent boys with NAFLD (n = 29) participated in an 8-week, randomized controlled trial comparing a diet low in free sugars versus their usual diet. Hepatic DNL was measured as percentage contribution to plasma triglyceride palmitate using a 7-day metabolic labeling protocol with heavy water. Hepatic fat was measured by magnetic resonance imaging-proton density fat fraction.RESULTSHepatic D</pubmed_abstract><journal>The Journal of clinical investigation</journal><pubmed_title>Dietary sugar restriction reduces hepatic de novo lipogenesis in adolescent boys with fatty liver disease.</pubmed_title><pmcid>PMC8670836</pmcid><funding_grant_id>R01 NR019083</funding_grant_id><funding_grant_id>n/a</funding_grant_id><funding_grant_id>T32-DK07658</funding_grant_id><funding_grant_id>UL1TR001442</funding_grant_id><funding_grant_id>UL1 TR002378</funding_grant_id><funding_grant_id>UL1 TR001442</funding_grant_id><funding_grant_id>UL1TR002378</funding_grant_id><funding_grant_id>R01 DK125701</funding_grant_id><funding_grant_id>T32 DK007658</funding_grant_id><pubmed_authors>Newton KP</pubmed_authors><pubmed_authors>Carrier CA</pubmed_authors><pubmed_authors>Cohen CC</pubmed_authors><pubmed_authors>Beysen C</pubmed_authors><pubmed_authors>Vos MB</pubmed_authors><pubmed_authors>Nyangau EM</pubmed_authors><pubmed_authors>Welsh JA</pubmed_authors><pubmed_authors>Li KW</pubmed_authors><pubmed_authors>Alazraki AL</pubmed_authors><pubmed_authors>Ugalde-Nicalo PA</pubmed_authors><pubmed_authors>Cleeton RL</pubmed_authors><pubmed_authors>Schwimmer JB</pubmed_authors><pubmed_authors>Knight-Scott J</pubmed_authors><pubmed_authors>Figueroa J</pubmed_authors><pubmed_authors>Knott CJ</pubmed_authors><pubmed_authors>Dandan M</pubmed_authors><pubmed_authors>Sirlin CB</pubmed_authors><pubmed_authors>Hellerstein MK</pubmed_authors></additional><is_claimable>false</is_claimable><name>Dietary sugar restriction reduces hepatic de novo lipogenesis in adolescent boys with fatty liver disease.</name><description>BACKGROUNDHepatic de novo lipogenesis (DNL) is elevated in nonalcoholic fatty liver disease (NAFLD). Improvements in hepatic fat by dietary sugar reduction may be mediated by reduced DNL, but data are limited, especially in children. We examined the effects of 8 weeks of dietary sugar restriction on hepatic DNL in adolescents with NAFLD and correlations between DNL and other metabolic outcomes.METHODSAdolescent boys with NAFLD (n = 29) participated in an 8-week, randomized controlled trial comparing a diet low in free sugars versus their usual diet. Hepatic DNL was measured as percentage contribution to plasma triglyceride palmitate using a 7-day metabolic labeling protocol with heavy water. Hepatic fat was measured by magnetic resonance imaging-proton density fat fraction.RESULTSHepatic D</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Dec</publication><modification>2026-05-31T01:03:45.557Z</modification><creation>2025-04-04T11:31:34.292Z</creation></dates><accession>S-EPMC8670836</accession><cross_references><pubmed>34907907</pubmed><doi>10.1172/JCI150996</doi><doi>10.1172/jci150996</doi></cross_references></HashMap>