<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Jastreboff AM</submitter><funding>NCATS NIH HHS</funding><funding>NIDCR NIH HHS</funding><funding>National Institute of Diabetes and Digestive and Kidney Diseases</funding><funding>NIDDK NIH HHS</funding><funding>NIDA NIH HHS</funding><funding>NCRR NIH HHS</funding><funding>NIH</funding><pagination>1929-39</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5384636</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>65(7)</volume><pubmed_abstract>Increased sugar-sweetened beverage consumption has been linked to higher rates of obesity. Using functional MRI, we assessed brain perfusion responses to drinking two commonly consumed monosaccharides, glucose and fructose, in obese and lean adolescents. Marked differences were observed. In response to drinking glucose, obese adolescents exhibited decreased brain perfusion in brain regions involved in executive function (prefrontal cortex [PFC]) and increased perfusion in homeostatic appetite regions of the brain (hypothalamus). Conversely, in response to drinking glucose, lean adolescents demonstrated increased PFC brain perfusion and no change in perfusion in the hypothalamus. In addition, obese adolescents demonstrated attenuated suppression of serum acyl-ghrelin and increased circulating insulin level after glucose ingestion; furthermore, the change in acyl-ghrelin and insulin levels after both glucose and fructose ingestion was associated with increased hypothalamic, thalamic, and hippocampal blood flow in obese relative to lean adolescents. Additionally, in all subjects there was greater perfusion in the ventral striatum with fructose relative to glucose ingestion. Finally, reduced connectivity between executive, homeostatic, and hedonic brain regions was observed in obese adolescents. These data demonstrate that obese adolescents have impaired prefrontal executive control responses to drinking glucose and fructose, while their homeostatic and hedonic responses appear to be heightened. Thus, obesity-related brain adaptations to glucose and fructose consumption in obese adolescents may contribute to excessive consumption of glucose and fructose, thereby promoting further weight gain.</pubmed_abstract><journal>Diabetes</journal><pubmed_title>Altered Brain Response to Drinking Glucose and Fructose in Obese Adolescents.</pubmed_title><pmcid>PMC5384636</pmcid><funding_grant_id>UL1-RR024139</funding_grant_id><funding_grant_id>UL1 TR000142</funding_grant_id><funding_grant_id>R01 DK085577</funding_grant_id><funding_grant_id>UL1-DE019586</funding_grant_id><funding_grant_id>P30 DK045735</funding_grant_id><funding_grant_id>R01-DK-099039</funding_grant_id><funding_grant_id>R37-DK-20495</funding_grant_id><funding_grant_id>1K23-DK-101694</funding_grant_id><funding_grant_id>1R01-DK-085577-01</funding_grant_id><funding_grant_id>P30-DK-045735</funding_grant_id><funding_grant_id>UL1 DE019586</funding_grant_id><funding_grant_id>R01 DK099039</funding_grant_id><funding_grant_id>K12 DK094714</funding_grant_id><funding_grant_id>UL1 RR024139</funding_grant_id><funding_grant_id>K23 DK101694</funding_grant_id><funding_grant_id>PL1 DA024859</funding_grant_id><funding_grant_id>PL1-DA024859</funding_grant_id><funding_grant_id>5K12-DK-094714</funding_grant_id><funding_grant_id>R37 DK020495</funding_grant_id><funding_grant_id>R01 DK020495</funding_grant_id><pubmed_authors>Van Name MA</pubmed_authors><pubmed_authors>Sherwin RS</pubmed_authors><pubmed_authors>Malik S</pubmed_authors><pubmed_authors>Jastreboff AM</pubmed_authors><pubmed_authors>Duran EJ</pubmed_authors><pubmed_authors>Savoye M</pubmed_authors><pubmed_authors>Constable RT</pubmed_authors><pubmed_authors>Sinha R</pubmed_authors><pubmed_authors>Santoro N</pubmed_authors><pubmed_authors>Cline G</pubmed_authors><pubmed_authors>Giannini C</pubmed_authors><pubmed_authors>Kubat J</pubmed_authors><pubmed_authors>Caprio S</pubmed_authors><pubmed_authors>Arora J</pubmed_authors><pubmed_authors>Pierpont B</pubmed_authors></additional><is_claimable>false</is_claimable><name>Altered Brain Response to Drinking Glucose and Fructose in Obese Adolescents.</name><description>Increased sugar-sweetened beverage consumption has been linked to higher rates of obesity. Using functional MRI, we assessed brain perfusion responses to drinking two commonly consumed monosaccharides, glucose and fructose, in obese and lean adolescents. Marked differences were observed. In response to drinking glucose, obese adolescents exhibited decreased brain perfusion in brain regions involved in executive function (prefrontal cortex [PFC]) and increased perfusion in homeostatic appetite regions of the brain (hypothalamus). Conversely, in response to drinking glucose, lean adolescents demonstrated increased PFC brain perfusion and no change in perfusion in the hypothalamus. In addition, obese adolescents demonstrated attenuated suppression of serum acyl-ghrelin and increased circulating insulin level after glucose ingestion; furthermore, the change in acyl-ghrelin and insulin levels after both glucose and fructose ingestion was associated with increased hypothalamic, thalamic, and hippocampal blood flow in obese relative to lean adolescents. Additionally, in all subjects there was greater perfusion in the ventral striatum with fructose relative to glucose ingestion. Finally, reduced connectivity between executive, homeostatic, and hedonic brain regions was observed in obese adolescents. These data demonstrate that obese adolescents have impaired prefrontal executive control responses to drinking glucose and fructose, while their homeostatic and hedonic responses appear to be heightened. Thus, obesity-related brain adaptations to glucose and fructose consumption in obese adolescents may contribute to excessive consumption of glucose and fructose, thereby promoting further weight gain.</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Jul</publication><modification>2024-11-19T20:33:08.198Z</modification><creation>2019-03-27T02:40:44Z</creation></dates><accession>S-EPMC5384636</accession><cross_references><pubmed>27207544</pubmed><doi>10.2337/db15-1216</doi></cross_references></HashMap>