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Insulin resistance and impaired pancreatic β-cell function in adult offspring of women with diabetes in pregnancy.

Abstract

CONTEXT

Offspring of women with diabetes during pregnancy have an increased risk of glucose intolerance in adulthood, but the underlying mechanisms are unknown.

OBJECTIVE

We aimed to investigate the effects of intrauterine hyperglycemia on insulin secretion and action in adult offspring of mothers with diabetes.

DESIGN, SETTING, AND PARTICIPANTS

A cohort of 587 Caucasian offspring, without known diabetes, was followed up at the age of 18-27 years. We included 2 groups exposed to maternal diabetes in utero: offspring of women with gestational diabetes mellitus (n = 167) or type 1 diabetes (n = 153). Two reference groups were included: offspring of women with risk factors for gestational diabetes mellitus but normoglycemia during pregnancy (n = 139) and offspring from the background population (n = 128).

MAIN OUTCOME MEASURES

Indices of insulin sensitivity and insulin release were calculated using insulin and glucose values from a standard oral glucose tolerance test (120 minutes, 75 g glucose). Pancreatic β-cell function taking the prevailing insulin sensitivity into account was estimated by disposition indices.

RESULTS

Both groups of offspring exposed during pregnancy to either maternal gestational diabetes or type 1 diabetes had reduced insulin sensitivity compared with offspring from the background population (both P < .005). We did not find any significant difference in absolute measures of insulin release. However, the disposition index was significantly reduced in both the diabetes-exposed groups (both P < .005).

CONCLUSION

Reduced insulin sensitivity as well as impaired pancreatic β-cell function may contribute to the increased risk of glucose intolerance among adult offspring born to women with diabetes during pregnancy.

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  • Authors+Show Affiliations

    ,

    Center for Pregnant Women with Diabetes, Department of Obstetrics, Research Unit 7821, Rigshospitalet, Copenhagen University Hospital, Blegdamsvej 9, DK-2100 Copenhagen, Denmark. louisekelstrup@dadlnet.dk

    , , , , ,

    Source

    MeSH

    Adolescent
    Adult
    Adult Children
    Child of Impaired Parents
    Diabetes Mellitus, Type 1
    Diabetes, Gestational
    Female
    Glucose Tolerance Test
    Humans
    Insulin Resistance
    Insulin-Secreting Cells
    Male
    Pancreas
    Pregnancy
    Pregnancy in Diabetics
    Risk Factors

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    23796568

    Citation

    Kelstrup, Louise, et al. "Insulin Resistance and Impaired Pancreatic Β-cell Function in Adult Offspring of Women With Diabetes in Pregnancy." The Journal of Clinical Endocrinology and Metabolism, vol. 98, no. 9, 2013, pp. 3793-801.
    Kelstrup L, Damm P, Mathiesen ER, et al. Insulin resistance and impaired pancreatic β-cell function in adult offspring of women with diabetes in pregnancy. J Clin Endocrinol Metab. 2013;98(9):3793-801.
    Kelstrup, L., Damm, P., Mathiesen, E. R., Hansen, T., Vaag, A. A., Pedersen, O., & Clausen, T. D. (2013). Insulin resistance and impaired pancreatic β-cell function in adult offspring of women with diabetes in pregnancy. The Journal of Clinical Endocrinology and Metabolism, 98(9), pp. 3793-801. doi:10.1210/jc.2013-1536.
    Kelstrup L, et al. Insulin Resistance and Impaired Pancreatic Β-cell Function in Adult Offspring of Women With Diabetes in Pregnancy. J Clin Endocrinol Metab. 2013;98(9):3793-801. PubMed PMID: 23796568.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Insulin resistance and impaired pancreatic β-cell function in adult offspring of women with diabetes in pregnancy. AU - Kelstrup,Louise, AU - Damm,Peter, AU - Mathiesen,Elisabeth R, AU - Hansen,Torben, AU - Vaag,Allan A, AU - Pedersen,Oluf, AU - Clausen,Tine D, Y1 - 2013/06/24/ PY - 2013/6/26/entrez PY - 2013/6/26/pubmed PY - 2013/11/10/medline SP - 3793 EP - 801 JF - The Journal of clinical endocrinology and metabolism JO - J. Clin. Endocrinol. Metab. VL - 98 IS - 9 N2 - CONTEXT: Offspring of women with diabetes during pregnancy have an increased risk of glucose intolerance in adulthood, but the underlying mechanisms are unknown. OBJECTIVE: We aimed to investigate the effects of intrauterine hyperglycemia on insulin secretion and action in adult offspring of mothers with diabetes. DESIGN, SETTING, AND PARTICIPANTS: A cohort of 587 Caucasian offspring, without known diabetes, was followed up at the age of 18-27 years. We included 2 groups exposed to maternal diabetes in utero: offspring of women with gestational diabetes mellitus (n = 167) or type 1 diabetes (n = 153). Two reference groups were included: offspring of women with risk factors for gestational diabetes mellitus but normoglycemia during pregnancy (n = 139) and offspring from the background population (n = 128). MAIN OUTCOME MEASURES: Indices of insulin sensitivity and insulin release were calculated using insulin and glucose values from a standard oral glucose tolerance test (120 minutes, 75 g glucose). Pancreatic β-cell function taking the prevailing insulin sensitivity into account was estimated by disposition indices. RESULTS: Both groups of offspring exposed during pregnancy to either maternal gestational diabetes or type 1 diabetes had reduced insulin sensitivity compared with offspring from the background population (both P < .005). We did not find any significant difference in absolute measures of insulin release. However, the disposition index was significantly reduced in both the diabetes-exposed groups (both P < .005). CONCLUSION: Reduced insulin sensitivity as well as impaired pancreatic β-cell function may contribute to the increased risk of glucose intolerance among adult offspring born to women with diabetes during pregnancy. SN - 1945-7197 UR - https://www.unboundmedicine.com/medline/citation/23796568/Insulin_resistance_and_impaired_pancreatic_β_cell_function_in_adult_offspring_of_women_with_diabetes_in_pregnancy_ L2 - https://academic.oup.com/jcem/article-lookup/doi/10.1210/jc.2013-1536 DB - PRIME DP - Unbound Medicine ER -