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Family history of diabetes impacts on interactions between minimal model estimates of insulin sensitivity and glucose effectiveness
Author(s) -
Lopez X.,
Bouché C.,
Tatro E.,
Goldfine A. B.
Publication year - 2009
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/j.1463-1326.2008.00913.x
Subject(s) - insulin resistance , medicine , family history , impaired glucose tolerance , endocrinology , diabetes mellitus , type 2 diabetes , insulin , body mass index , offspring , glucose tolerance test , glucose homeostasis , biology , pregnancy , genetics
Aims/hypothesis: Insulin resistance and glucose effectiveness (S G ) are major determinants of glucose tolerance and independently predict the development of type 2 diabetes in individuals with a family history of disease. We examined the inter‐relationship between insulin sensitivity (S I ) and S G in offspring of two parents with type 2 diabetes and in individuals with no family history of diabetes. Methods: Fifty non‐diabetic individuals, including 26 offspring of two type 2 diabetic parents (family history, FH+) and 24 with no family history of diabetes (FH−) similar in gender, age, ethnicity and body mass index (BMI) were studied. Each subject underwent a 100‐g oral glucose tolerance test (OGTT) and insulin modified frequently sampled intravenous glucose tolerance, analysed using the Bergman’s minimal model (MINMOD). Results: Thirteen subjects of the FH+ group and nine of the FH− group had impaired glucose tolerance (IGT). S I and S G were independent variables in the FH+ group, while they correlated highly with each other in the FH− group (r = 0.69, p = 0.0002). The relationship between S I and S G persisted when analysing the IGT and normal glucose tolerance subgroups separately, demonstrating that these associations were not because of differences in glycaemia. Consistently, S G strongly correlated with additional measures of insulin resistance only in the FH− group, including fasting insulin (r = 0.56, p = 0.004), homeostasis model assessment of insulin resistance (r = 0.57 p = 0.003) and BMI (r = 0.66, p = 0.0004). Conclusions: These results demonstrate that familial factors impart important physiological differences in the inter‐relationship between insulin‐dependent and insulin‐independent glucose disposal, which may be important in modulating risk for development of disease.