1996
DOI: 10.1002/dme.1996.13.s6.59
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The Prevalence of Low Insulin Responders to Oral Glucose Load Among Groups with Various Patterns of Family History of Diabetes

Abstract: The prevalence of low insulin responders was assessed in non-diabetic subjects with various patterns of family history of diabetes. Subjects were divided into five groups: group A, without any family history of diabetes among all known relatives; group B, with diabetes among parents and/or siblings; group C, with one diabetic parent; group D, with two diabetic parents; and group E, non-diabetic co-twins of monozygotic twins with diabetes. Except twins, the type of diabetes in the family was not defined. They w… Show more

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Cited by 8 publications
(5 citation statements)
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“…These findings have important implications for genetic studies. Low insulin response to oral glucose has been suggested to have a genetic basis (53,54). Although the reduced ␤ cell mass in our study did not explain low insulin response in the offspring of probands with insulin deficient phenotype, other mechanisms, however, could be involved.…”
Section: Discussioncontrasting
confidence: 70%
“…These findings have important implications for genetic studies. Low insulin response to oral glucose has been suggested to have a genetic basis (53,54). Although the reduced ␤ cell mass in our study did not explain low insulin response in the offspring of probands with insulin deficient phenotype, other mechanisms, however, could be involved.…”
Section: Discussioncontrasting
confidence: 70%
“…For example, glucokinase defects (MODY 2) that have been shown to have a defective second-phase insulin secretion while ®rstphase insulin secretion is preserved [33] should show a normal or near normal DI arg and I GLP-1 . Furthermore, abnormalities of the insulin response to oral glucose, which is a sum effect of glucose and incretins, including GLP-1 [34], as secretagogues shows a strong genetic basis [35]. This would include defects resulting in abnormalities speci®c for incretin-stimulated insulin secretion that have yet to be de®ned.…”
Section: Discussionmentioning
confidence: 99%
“…[11] The IGI was calculated as follows: (30 minutes insulin [μU/mL] − fasting insulin [μU/ mL])/(30 minutes glucose [mg/dL] − fasting glucose [mg/dL]), and was used to estimate early phase insulin secretion. [16,17] We defined the remission of T2DM as HbA1c levels <6.0% without drug treatment, and patients satisfying this definition were classified into the remission group. [18,19] Data were presented as medians (interquartile range) for continuous variables and as numbers or percentages for categorical variables.…”
Section: Methodsmentioning
confidence: 99%