{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Davidson WS"],"funding":["NCATS NIH HHS","NIDDK NIH HHS","NHLBI NIH HHS","Cincinnati Children’s Hospital Medical Center","The Central Society for Clinical and Translational Research","National Institutes of Health"],"pagination":["1916-1923"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5580903"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["58(9)"],"pubmed_abstract":["We aimed to determine the risk factors associated with the depletion of large HDL particles and enrichment of small HDL particles observed in adolescents with T2D. Four groups of adolescents were recruited: <i>1</i>) lean insulin-sensitive (L-IS), normal BMI and no insulin resistance; <i>2</i>) lean insulin-resistant (L-IR), normal BMI but insulin resistance (fasting insulin levels ≥ 25 mU/ml and homeostatic model assessment of insulin resistance ≥ 6); <i>3</i>) obese insulin-sensitive (O-IS), BMI ≥ 95th percentile and no insulin resistance; and <i>4</i>) obese insulin-resistant (O-IR), BMI ≥ 95th percentile and insulin resistance. Plasma was separated by using gel-filtration chromatography to assess the HDL subspecies profile and compared with that of obese adolescents with T2D (O-T2D). Large HDL subspecies were significantly lower across groups from L-IS > L-IR > O-IS > O-IR > O-T2D (<i>P</i> < 0.0001); small HDL particles were higher from L-IS to O-T2D (<i>P</i> < 0.0001); and medium-sized particles did not differ across groups. The contributions of obesity, insulin resistance, and diabetes to HDL subspecies profile were between 23% and 28%, 1% and 10%, and 4% and 9%, respectively. Obesity is the major risk factor associated with the altered HDL subspecies profile previously reported in adolescents with T2D, with smaller contributions from insulin resistance and diabetes."],"journal":["Journal of lipid research"],"pubmed_title":["Obesity is associated with an altered HDL subspecies profile among adolescents with metabolic disease."],"pmcid":["PMC5580903"],"funding_grant_id":["UL1TR000077","R01 HL067093","R21 HL104136","UL1 TR000077","DK59183","R01 DK059183","K23HL118132","R01HL67093","R01HL104136","K23 HL118132"],"pubmed_authors":["Khoury J","Shah AS","Gordon SM","Geh E","Otvos JD","Elder DA","Davidson WS","Dolan LM","Melchior JT","Sexmith H","Heink A"],"additional_accession":[]},"is_claimable":false,"name":"Obesity is associated with an altered HDL subspecies profile among adolescents with metabolic disease.","description":"We aimed to determine the risk factors associated with the depletion of large HDL particles and enrichment of small HDL particles observed in adolescents with T2D. Four groups of adolescents were recruited: <i>1</i>) lean insulin-sensitive (L-IS), normal BMI and no insulin resistance; <i>2</i>) lean insulin-resistant (L-IR), normal BMI but insulin resistance (fasting insulin levels ≥ 25 mU/ml and homeostatic model assessment of insulin resistance ≥ 6); <i>3</i>) obese insulin-sensitive (O-IS), BMI ≥ 95th percentile and no insulin resistance; and <i>4</i>) obese insulin-resistant (O-IR), BMI ≥ 95th percentile and insulin resistance. Plasma was separated by using gel-filtration chromatography to assess the HDL subspecies profile and compared with that of obese adolescents with T2D (O-T2D). Large HDL subspecies were significantly lower across groups from L-IS > L-IR > O-IS > O-IR > O-T2D (<i>P</i> < 0.0001); small HDL particles were higher from L-IS to O-T2D (<i>P</i> < 0.0001); and medium-sized particles did not differ across groups. The contributions of obesity, insulin resistance, and diabetes to HDL subspecies profile were between 23% and 28%, 1% and 10%, and 4% and 9%, respectively. Obesity is the major risk factor associated with the altered HDL subspecies profile previously reported in adolescents with T2D, with smaller contributions from insulin resistance and diabetes.","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Sep","modification":"2025-04-19T22:15:56.004Z","creation":"2019-03-26T23:53:08Z"},"accession":"S-EPMC5580903","cross_references":{"pubmed":["28743729"],"doi":["10.1194/jlr.m078667","10.1194/jlr.M078667"]}}