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Relationships among Serum Resistin Levels,Insulin Resistance and Pancreatic Beta-Cell Functions in Obese Children

Chunlin Wang

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Abstract

Objective To study the relationships of serum resistin levels,insulin resistance (IR) and pancreatic beta-cell functions in obese children with different degrees and normal children.Methods Thirty normal and 113 obese children were enrolled in this study and were divided into 3 groups based on body mass index (BMI). Obese group 1 was defined as 23 ≤BMI30, obese group 2 was defined as BMI≥30, while control group were defined as BMI22. An oral glucose tolerance test was done and the level of serum fasting resistin was measured in all subjects. Homeostasis model assessment (HOMA) was applied to assess the basic status of insulin resistance (HOMA-IR) and function o f pancreatic beta-cell (HOMA-β). Whole body insulin sensitivity index (WBISI) and the ratio of the increment of insulin to that of plasma glucose of the initial 30 minutes(△I_ 30/△G_ 30) were used to evaluate postprandial insulin sensitivity and pancreatic beta-cell function.Results In these obese children, 6 cases (5.3%) with impaired glucose tolerance and 2 cases (1.8%) with type 2 diabetes were found. With the increase of BMI, the levels of fasting insulin (FINS), area under the curve of insulin (AUCi), postprandial 2 hours glucose (2 h PG),area under the curve of glucose (AUCg), HOMA-IR were significantly increased (all P0.05), WBISI was declined (P0.001). HOMA-β and △I_ 30/△G_ 30 in two obese groups were higher than those of control group (P0.05 on an average), but no difference between themselves was found (P0.05). The levels of fasting serum resistin had no statistic differences among 3 groups (P0.05). The mean resistin levels in 8 cases with abnormal glucose tole rance were higher than those of control group, but no significant difference was found(P0.05). There were positive correlations between BMI and 2 h PG,FINS,HOMA- IR,HOMA-β,△I_ 30/△G_ 30(all P0.05).WBISI was significantly negatively correlated with BMI(P0.001). Serum resistin levels did not correlate with any index above (all P0.05).Conclusions Obese children are usually complicated with IR,higher postprandial plasma glucose and increasing pancreatic beta-cell functions.Severe obese children have lower insulin sensitivity while their pancreatic beta-cell functions have not increased accordingly. Circulating resistin is unlikely to play a major role in obesity,or IR in children.The function of resistin needs further study.

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Objective To study the relationships of serum resistin levels,insulin resistance (IR) and pancreatic beta-cell functions in obese children with different degrees and normal children.Methods Thirty normal and 113 obese children were enrolled in this study and were divided into 3 groups based on body mass index (BMI). Obese group 1 was defined as 23 ≤BMI30, obese group 2 was defined as BMI≥30, while control group were defined as BMI22. An oral glucose tolerance test was done and the level of serum fasting resistin was measured in all subjects. Homeostasis model assessment (HOMA) was applied to assess the basic status of insulin resistance (HOMA-IR) and function o f pancreatic beta-cell (HOMA-β). Whole body insulin sensitivity index (WBISI) and the ratio of the increment of insulin to that of plasma glucose of the initial 30 minutes(△I_ 30/△G_ 30) were used to evaluate postprandial insulin sensitivity and pancreatic beta-cell function.Results In these obese children, 6 cases (5.3%) with impaired glucose tolerance and 2 cases (1.8%) with type 2 diabetes were found. With the increase of BMI, the levels of fasting insulin (FINS), area under the curve of insulin (AUCi), postprandial 2 hours glucose (2 h PG),area under the curve of glucose (AUCg), HOMA-IR were significantly increased (all P0.05), WBISI was declined (P0.001). HOMA-β and △I_ 30/△G_ 30 in two obese groups were higher than those of control group (P0.05 on an average), but no difference between themselves was found (P0.05). The levels of fasting serum resistin had no statistic differences among 3 groups (P0.05). The mean resistin levels in 8 cases with abnormal glucose tole rance were higher than those of control group, but no significant difference was found(P0.05). There were positive correlations between BMI and 2 h PG,FINS,HOMA- IR,HOMA-β,△I_ 30/△G_ 30(all P0.05).WBISI was significantly negatively correlated with BMI(P0.001). Serum resistin levels did not correlate with any index above (all P0.05).Conclusions Obese children are usually complicated with IR,higher postprandial plasma glucose and increasing pancreatic beta-cell functions.Severe obese children have lower insulin sensitivity while their pancreatic beta-cell functions have not increased accordingly. Circulating resistin is unlikely to play a major role in obesity,or IR in children.The function of resistin needs further study.

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Available abstract

Objective To study the relationships of serum resistin levels,insulin resistance (IR) and pancreatic beta-cell functions in obese children with different degrees and normal children.Methods Thirty normal and 113 obese children were enrolled in this study and were divided into 3 groups based on body mass index (BMI). Obese group 1 was defined as 23 ≤BMI30, obese group 2 was defined as BMI≥30, while control group were defined as BMI22. An oral glucose tolerance test was done and the level of serum fasting resistin was measured in all subjects. Homeostasis model assessment (HOMA) was applied to assess the basic status of insulin resistance (HOMA-IR) and function o f pancreatic beta-cell (HOMA-β). Whole body insulin sensitivity index (WBISI) and the ratio of the increment of insulin to that of plasma glucose of the initial 30 minutes(△I_ 30/△G_ 30) were used to evaluate postprandial insulin sensitivity and pancreatic beta-cell function.Results In these obese children, 6 cases (5.3%) with impaired glucose tolerance and 2 cases (1.8%) with type 2 diabetes were found. With the increase of BMI, the levels of fasting insulin (FINS), area under the curve of insulin (AUCi), postprandial 2 hours glucose (2 h PG),area under the curve of glucose (AUCg), HOMA-IR were significantly increased (all P0.05), WBISI was declined (P0.001). HOMA-β and △I_ 30/△G_ 30 in two obese groups were higher than those of control group (P0.05 on an average), but no difference between themselves was found (P0.05). The levels of fasting serum resistin had no statistic differences among 3 groups (P0.05). The mean resistin levels in 8 cases with abnormal glucose tole rance were higher than those of control group, but no significant difference was found(P0.05). There were positive correlations between BMI and 2 h PG,FINS,HOMA- IR,HOMA-β,△I_ 30/△G_ 30(all P0.05).WBISI was significantly negatively correlated with BMI(P0.001). Serum resistin levels did not correlate with any index above (all P0.05).Conclusions Obese children are usually complicated with IR,higher postprandial plasma glucose and increasing pancreatic beta-cell functions.Severe obese children have lower insulin sensitivity while their pancreatic beta-cell functions have not increased accordingly. Circulating resistin is unlikely to play a major role in obesity,or IR in children.The function of resistin needs further study.

Key concepts: Internal medicine, Insulin resistance, Postprandial, Endocrinology, Resistin, Medicine, Insulin, Body mass index

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Relationships among Serum Resistin Levels,Insulin Resistance and Pancreatic Beta-Cell Functions in Obese Children — Research Paper | ScholarLens