Location: Children's Nutrition Research CenterTitle: Differences in beta-cell function and insulin secretion in Black vs. White obese adolescents: Do incretin hormones play a role? Author
|Michaliszyn, Sara - Youngstown State University|
|Lee, So - University Of Pittsburgh Medical Center|
|Bacha, Fida - Children'S Nutrition Research Center (CNRC)|
|Tfayli, Hala - American University Of Beirut|
|Farchoukh, Lama - University Of Pittsburgh Medical Center|
|Mari, Andrea - Cnr Institute Of Biomedical Engineering|
|Ferrannini, Ele - University Of Pisa|
|Arslanian, Silva - University Of Pittsburgh Medical Center|
Submitted to: Pediatric Diabetes
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/22/2015
Publication Date: 3/1/2017
Citation: Michaliszyn, S.F., Lee, S.J., Bacha, F., Tfayli, H., Farchoukh, L., Mari, A., Ferrannini, E., Arslanian, S. 2017. Differences in beta-cell function and insulin secretion in Black vs. White obese adolescents: Do incretin hormones play a role? Pediatric Diabetes. 18(2):143-151.
Interpretive Summary: Black children have higher risk for diabetes despite higher insulin responses to intravenous glucose than white children. We tested if this holds true in response to oral glucose challenge and whether there are racial differences in hormones that regulate insulin production called glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). We found that black obese youth had a heightened early insulin secretion together with greater sensitivity in their beta cells to glucose, with no differences in GLP-1, GIP and glucagon concentrations. In conclusion, during an oral glucose challenge, black obese youth with normal glucose tolerance demonstrate a pronounced early insulin secretion with increased beta-cell glucose sensitivity. Therefore, the racial disparities in T2D are unlikely to be attributed to these hormones that regulate insulin secretion and need to be investigated further.
Technical Abstract: Black youth are at higher risk for type 2 diabetes (T2D) than their White peers. Previously we demonstrated that for the same degree of insulin sensitivity, Black youth have an upregulated beta-cell function and insulin hypersecretion, in response to intravenous (IV) glucose, compared with Whites. To investigate if the same holds true during an oral glucose challenge and because of the important role of glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) in augmenting insulin secretion, we examined beta-cell function and incretin hormones in 85 Black and 78 White obese adolescents, with normal glucose tolerance (NGT), during a 2-h oral glucose tolerance test (OGTT) with mathematical modeling of plasma glucose and C-peptide concentrations to assess beta-cell glucose sensitivity (betaCGS), rate sensitivity, potentiation factor, and insulin sensitivity. Incretin, pancreatic polypeptide, and glucagon concentrations were measured during the OGTT. Black obese youth had a heightened early insulin secretion together with significantly greater betaCGS, rate sensitivity, and potentiation factor compared with Whites, with no differences in incretin and glucagon concentrations. Basal and stimulated insulin clearance was lower (p=0.001) in Black vs. White youth. In conclusion, during an OGTT Black obese youth with NGT demonstrate a pronounced early insulin secretion jointly with heightened beta-cell glucose sensitivity, rate sensitivity, and potentiation factor. These racial disparities in beta-cell function and the pathophysiological components of T2D are unlikely to be attributed to incretin hormones and remain to be investigated further to explain the metabolic basis for the enhanced risk of T2D in back youth.