TITLE

The study of soluble intercellular adhesion molecule-1 and ghrelin in adolescents with family history of type 2 diabetes

AUTHOR(S)
Liu, Bo-Wei; Lu, Qiang; Ma, Chun-Ming; Liu, Jun-Ru; Lou, Dong-Hui; Liu, Xiao-Li; Yin, Fu-Zai
PUB. DATE
December 2012
SOURCE
Endocrine (1355008X);Dec2012, Vol. 42 Issue 3, p599
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
The purpose of this study was to observe both the changes of soluble intercellular adhesion molecule-1 (sICAM-1) and ghrelin in adolescents with family history of type 2 diabetes (FHD) and the relationship between sICAM-1 and ghrelin. This case-control study included 63 adolescents (boys/girls 29/34, age 14.1 ± 0.7 years) without FHD (FHD−) and 67 adolescents (boys/girls 33/34, age 14.0 ± 0.8 years) with FHD (FHD+). Anthropometric measurements, including height, weight, waist circumference (WC), and blood pressure, were obtained. Blood samples were collected, and fasting plasma glucose (FPG), serum lipids, true insulin, sICAM-1, and ghrelin were assayed. The results showed that the age and gender were similar in two groups ( P > 0.05). Body mass index (BMI), WC, FPG, fasting insulin, HOMA-IR, and sICAM-1 were all significantly higher in the FHD+ group than in the FHD− group ( P < 0.05). Ghrelin was significantly lower in the FHD+ group than in the FHD− group ( P < 0.05). sICAM-1 was positively correlated with WC ( r = 0.178, P = 0.043), fasting insulin ( r = 0.195, P = 0.026), HOMA-IR ( r = 0.197, P = 0.024), and ghrelin ( r = 0.290, P = 0.001). After multivariate analysis, the ghrelin ( β = 0.788, 95 % CI: 0.416-1.159, P = 0.000) and HOMA-IR ( β = 0.106, 95 % CI: 0.045-0.167, P = 0.001) maintained an independent association with sICAM-1. These findings led to the conclusion that endothelial dysfunction and decline of ghrelin were found in adolescents with family history of diabetes. The decline of ghrelin maybe a protection mechanism for endothelial function in adolescents with family history of diabetes and should be examined in future studies.
ACCESSION #
83709715

 

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