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Racial Disparity in Glucagon-Like Peptide 1 and Inflammation Markers Among Severely Obese Adolescents
Oleh:
Velásquez-Mieyer, Pedro A.
;
Cowan, Patricia A.
;
Pérez-Faustinelli, Sylvia
;
Nieto-Martínez, Ramfis
;
Villegas-Barreto, Cesar
;
and Others
Jenis:
Article from Journal - ilmiah internasional
Dalam koleksi:
Diabetes Care vol. 31 no. 04 (Apr. 2008)
,
page 770.
Topik:
AUC
;
area under the curve
;
CVD
;
cardiovascular disease
;
CISI
;
composite insulin sensitivity index
;
CRPhs
;
high-sensitivity C-reactive protein
;
DPP-IV
;
dipeptidyl peptidase IV
;
EIA
;
enteroinsular axis
;
GLP-1
;
glucagon-like peptide 1
;
I30/G30
;
insulinogenic index
;
IGM
;
impaired glucose metabolism
;
IFG
;
impaired fasting glucose
;
IGT
;
impaired glucose tolerance
;
INF+
;
inflammation positive
;
NGT
;
normal glucose tolerance
;
OGTT
;
oral glucose tolerance test
;
RBMI
;
relative BMI
;
RIA
;
radioimmunoassay
Ketersediaan
Perpustakaan FK
Nomor Panggil:
D05.K.2008.02
Non-tandon:
1 (dapat dipinjam: 0)
Tandon:
tidak ada
Lihat Detail Induk
Isi artikel
OBJECTIVE—Compared with Caucasians, obese African-American adolescents have a higher risk for type 2 diabetes. Subclinical inflammation and reduced glucagon-like peptide 1 (GLP-1) concentration are linked to the pathogenesis of the disease. We determined the relationship between insulin resistance, ß-cell activity, and subclinical inflammation with GLP-1 concentrations and whether racial disparities in GLP-1 response were present in 49 obese adolescents (14 ± 3 years; 76% African American; 71% female). RESEARCH DESIGN AND METHODS—Subjects underwent physical examination and an oral glucose tolerance test. We measured levels of high-sensitivity CRP (CRPhs), fibrinogen, glucose, GLP-1total, GLP-1active, and insulin. Insulin and glucose area under the curve (AUC), insulinogenic index (I30/G30), and composite insulin sensitivity index (CISI) were computed. Subjects were categorized by race and as inflammation positive (INF+) if CRPhs or fibrinogen were elevated. RESULTS—No racial differences were seen in mean or relative BMI. Thirty-five percent of subjects had altered fasting or 2-h glucose levels (African American vs. Caucasian, NS), and 75% were INF+ (African American vs. Caucasian, P = 0.046). Glucose and insulin, CISI, and I30/G30 values were similar; African Americans had lower GLP-1total AUC (P = 0.01), GLP-1active at 15 min (P = 0.03), and GLP-1active AUC (P = 0.06) and higher fibrinogen (P = 0.01) and CRPhs (NS) compared with Caucasians. CONCLUSIONS—African Americans exhibited lower GLP-1 concentrations and increased inflammatory response. Both mechanisms may act synergistically to enhance the predisposition of obese African Americans to type 2 diabetes. Our findings might be relevant to effective deployment of emerging GLP-1–based treatments across ethnicities.
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