<HashMap><database>biostudies-literature</database><scores/><additional><submitter>De Leon ER</submitter><funding>U.S. Department of Health &amp;amp;amp; Human Services | National Institutes of Health</funding><funding>BLRD VA</funding><funding>NIDDK NIH HHS</funding><funding>NIA NIH HHS</funding><funding>American Diabetes Association</funding><funding>U.S. Department of Health &amp;amp; Human Services | National Institutes of Health (NIH)</funding><funding>American Diabetes Association (ADA)</funding><pagination>17814</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6292902</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>8(1)</volume><pubmed_abstract>Type 2 diabetes is an age-and-obesity associated disease driven by impairments in glucose homeostasis that ultimately result in defective insulin secretion from pancreatic β-cells. To deconvolve the effects of age and obesity in an experimental model of prediabetes, we fed young and aged mice either chow or a short-term high-fat/high-sucrose Western diet (WD) and examined how weight, glucose tolerance, and β-cell function were affected. Although WD induced a similar degree of weight gain in young and aged mice, a high degree of heterogeneity was found exclusively in aged mice. Weight gain in WD-fed aged mice was well-correlated with glucose intolerance, fasting insulin, and in vivo glucose-stimulated insulin secretion, relationships that were not observed in young animals. Although β-cell </pubmed_abstract><journal>Scientific reports</journal><pubmed_title>Age-Dependent Protection of Insulin Secretion in Diet Induced Obese Mice.</pubmed_title><pmcid>PMC6292902</pmcid><funding_grant_id>1-16-IBS-212</funding_grant_id><funding_grant_id>R21 AG051974</funding_grant_id><funding_grant_id>F31 DK109698</funding_grant_id><funding_grant_id>AG051974</funding_grant_id><funding_grant_id>R21 AG050135</funding_grant_id><funding_grant_id>DK113103</funding_grant_id><funding_grant_id>R00 AG041765</funding_grant_id><funding_grant_id>R01 DK113103</funding_grant_id><funding_grant_id>R01 AG056771</funding_grant_id><funding_grant_id>AG041765</funding_grant_id><funding_grant_id>DK102598</funding_grant_id><funding_grant_id>R01 DK102598</funding_grant_id><funding_grant_id>AG056771</funding_grant_id><funding_grant_id>DK101683</funding_grant_id><funding_grant_id>I01 BX004031</funding_grant_id><funding_grant_id>T32GM008349</funding_grant_id><funding_grant_id>T32 AG000213</funding_grant_id><funding_grant_id>AG050135</funding_grant_id><funding_grant_id>K01 DK101683</funding_grant_id><pubmed_authors>Fenske RJ</pubmed_authors><pubmed_authors>Schmidt BA</pubmed_authors><pubmed_authors>Kimple ME</pubmed_authors><pubmed_authors>Brinkman JA</pubmed_authors><pubmed_authors>Sherman DS</pubmed_authors><pubmed_authors>Merrins MJ</pubmed_authors><pubmed_authors>Cummings NE</pubmed_authors><pubmed_authors>Peter DC</pubmed_authors><pubmed_authors>Lamming DW</pubmed_authors><pubmed_authors>Gregg T</pubmed_authors><pubmed_authors>De Leon ER</pubmed_authors></additional><is_claimable>false</is_claimable><name>Age-Dependent Protection of Insulin Secretion in Diet Induced Obese Mice.</name><description>Type 2 diabetes is an age-and-obesity associated disease driven by impairments in glucose homeostasis that ultimately result in defective insulin secretion from pancreatic β-cells. To deconvolve the effects of age and obesity in an experimental model of prediabetes, we fed young and aged mice either chow or a short-term high-fat/high-sucrose Western diet (WD) and examined how weight, glucose tolerance, and β-cell function were affected. Although WD induced a similar degree of weight gain in young and aged mice, a high degree of heterogeneity was found exclusively in aged mice. Weight gain in WD-fed aged mice was well-correlated with glucose intolerance, fasting insulin, and in vivo glucose-stimulated insulin secretion, relationships that were not observed in young animals. Although β-cell </description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Dec</publication><modification>2026-07-16T16:44:15.38Z</modification><creation>2019-03-27T00:13:13Z</creation></dates><accession>S-EPMC6292902</accession><cross_references><pubmed>30546031</pubmed><doi>10.1038/s41598-018-36289-0</doi></cross_references></HashMap>