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Normal secretion of the incretin hormones glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 during gestational diabetes mellitus.
Gynecol Endocrinol 2007; 23(1):58-62GE

Abstract

BACKGROUND AND AIM

Gestational diabetes mellitus (GDM) and type 2 diabetes mellitus (DM2) are suggested to be caused by the same metabolic disorder. Defects in gut hormone-dependent regulation of beta-cell function (entero-insular axis) have been proposed to contribute to the pathogenesis of DM2. The aim of study was to evaluate whether an impaired secretion of glucagon-like peptide-1 (GLP-1) and/or glucose-dependent insulinotropic polypeptide (GIP) could play a role in the development of carbohydrate disorders during pregnancy.

SUBJECTS AND METHODS

The study group (GDM) consisted of 13 gestational women with diabetes mellitus in whom GDM was diagnosed according to the World Health Organization criteria (75-g oral glucose tolerance test (OGTT)). The control group consisted of 13 pregnant women with normal glucose tolerance (NGT), matched according to age and duration of pregnancy. For all patients, plasma glucose, insulin, GLP-1 and GIP concentrations were evaluated after an OGTT, i.e. at 0, 30, 60, 90 and 120 min after glucose load.

RESULTS

Fasting plasma glucose concentrations were similar in both groups, but the 0-120 min area under the curve (AUC) for glucose was significantly greater in the GDM group than in the NGT group (p < 0.0005). Fasting insulin concentration was higher (p < 0.05) and the 2-h insulin response (AUCtotal) was significantly greater (p = 0.01) in the GDM group than in the NGT group. Insulin resistance was significantly higher in GDM compared with control women (homeostasis model assessment, p = 0.003). Fasting GLP-1 concentrations were higher in the GDM group (p = 0.05), but no differences were observed in GLP-1 response (AUC) between the studied groups. Fasting and stimulated GIP response did not differ between groups at any time of the study (p > 0.05). Positive correlations were observed between fasting GLP-1 and insulin concentration (r = 0.56, p < 0.004) and between fasting GLP-1 and insulin resistance (r = 0.43, p < 0.029).

CONCLUSION

An impaired secretion of GLP-1 and GIP does not seem to play a major role in the pathogenesis of GDM.

Authors+Show Affiliations

Department of Endocrinology and Metabolic Diseases, Medical University of Lodz, Polish Mother's Memorial Hospital Research Institute, Lodz, Poland. kcypryk@mp.plNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

17484514

Citation

Cypryk, Katarzyna, et al. "Normal Secretion of the Incretin Hormones Glucose-dependent Insulinotropic Polypeptide and Glucagon-like Peptide-1 During Gestational Diabetes Mellitus." Gynecological Endocrinology : the Official Journal of the International Society of Gynecological Endocrinology, vol. 23, no. 1, 2007, pp. 58-62.
Cypryk K, Vilsbøll T, Nadel I, et al. Normal secretion of the incretin hormones glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 during gestational diabetes mellitus. Gynecol Endocrinol. 2007;23(1):58-62.
Cypryk, K., Vilsbøll, T., Nadel, I., Smyczyńska, J., Holst, J. J., & Lewiński, A. (2007). Normal secretion of the incretin hormones glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 during gestational diabetes mellitus. Gynecological Endocrinology : the Official Journal of the International Society of Gynecological Endocrinology, 23(1), pp. 58-62.
Cypryk K, et al. Normal Secretion of the Incretin Hormones Glucose-dependent Insulinotropic Polypeptide and Glucagon-like Peptide-1 During Gestational Diabetes Mellitus. Gynecol Endocrinol. 2007;23(1):58-62. PubMed PMID: 17484514.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Normal secretion of the incretin hormones glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 during gestational diabetes mellitus. AU - Cypryk,Katarzyna, AU - Vilsbøll,Tina, AU - Nadel,Iwona, AU - Smyczyńska,Joanna, AU - Holst,Jens Juul, AU - Lewiński,Andrzej, PY - 2007/5/9/pubmed PY - 2007/6/1/medline PY - 2007/5/9/entrez SP - 58 EP - 62 JF - Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology JO - Gynecol. Endocrinol. VL - 23 IS - 1 N2 - BACKGROUND AND AIM: Gestational diabetes mellitus (GDM) and type 2 diabetes mellitus (DM2) are suggested to be caused by the same metabolic disorder. Defects in gut hormone-dependent regulation of beta-cell function (entero-insular axis) have been proposed to contribute to the pathogenesis of DM2. The aim of study was to evaluate whether an impaired secretion of glucagon-like peptide-1 (GLP-1) and/or glucose-dependent insulinotropic polypeptide (GIP) could play a role in the development of carbohydrate disorders during pregnancy. SUBJECTS AND METHODS: The study group (GDM) consisted of 13 gestational women with diabetes mellitus in whom GDM was diagnosed according to the World Health Organization criteria (75-g oral glucose tolerance test (OGTT)). The control group consisted of 13 pregnant women with normal glucose tolerance (NGT), matched according to age and duration of pregnancy. For all patients, plasma glucose, insulin, GLP-1 and GIP concentrations were evaluated after an OGTT, i.e. at 0, 30, 60, 90 and 120 min after glucose load. RESULTS: Fasting plasma glucose concentrations were similar in both groups, but the 0-120 min area under the curve (AUC) for glucose was significantly greater in the GDM group than in the NGT group (p < 0.0005). Fasting insulin concentration was higher (p < 0.05) and the 2-h insulin response (AUCtotal) was significantly greater (p = 0.01) in the GDM group than in the NGT group. Insulin resistance was significantly higher in GDM compared with control women (homeostasis model assessment, p = 0.003). Fasting GLP-1 concentrations were higher in the GDM group (p = 0.05), but no differences were observed in GLP-1 response (AUC) between the studied groups. Fasting and stimulated GIP response did not differ between groups at any time of the study (p > 0.05). Positive correlations were observed between fasting GLP-1 and insulin concentration (r = 0.56, p < 0.004) and between fasting GLP-1 and insulin resistance (r = 0.43, p < 0.029). CONCLUSION: An impaired secretion of GLP-1 and GIP does not seem to play a major role in the pathogenesis of GDM. SN - 0951-3590 UR - https://www.unboundmedicine.com/medline/citation/17484514/Normal_secretion_of_the_incretin_hormones_glucose_dependent_insulinotropic_polypeptide_and_glucagon_like_peptide_1_during_gestational_diabetes_mellitus_ L2 - http://www.tandfonline.com/doi/full/10.1080/09513590601137004 DB - PRIME DP - Unbound Medicine ER -