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Low adiponectin concentration during pregnancy predicts postpartum insulin resistance, beta cell dysfunction and fasting glycaemia.
Diabetologia. 2010 Feb; 53(2):268-76.D

Abstract

AIMS/HYPOTHESIS

The postpartum phase following gestational diabetes (GDM) is characterised by subtle metabolic defects, including the beta cell dysfunction that is believed to mediate the increased future risk of type 2 diabetes in this patient population. Low circulating levels of adiponectin and increased leptin and C-reactive protein (CRP) have recently emerged as novel diabetic risk factors, although their relevance to GDM and subsequent diabetes has not been characterised. Thus, we sought to determine whether adiponectin, leptin and CRP levels during pregnancy relate to the postpartum metabolic defects linking GDM with type 2 diabetes.

METHODS

Metabolic characterisation, including oral glucose tolerance testing, was undertaken in 487 women during pregnancy and at 3 months postpartum. Based on the antepartum OGTT, there were 137 women with GDM, 91 with gestational impaired glucose tolerance and 259 with normal glucose tolerance.

RESULTS

Adiponectin levels were lowest (p < 0.0001) and CRP levels highest (p = 0.0008) in women with GDM. Leptin did not differ between the glucose tolerance groups (p = 0.4483). Adiponectin (r = 0.41, p < 0.0001), leptin (r = -0.36, p < 0.0001) and CRP (r = -0.30, p < 0.0001) during pregnancy were all associated with postpartum insulin sensitivity (determined using the insulin sensitivity index of Matsuda and DeFronzo [IS(OGTT)]). Intriguingly, adiponectin levels were also related to postpartum beta cell function (insulinogenic index/HOMA of insulin resistance; r = 0.16, p = 0.0009). Indeed, on multiple linear regression analyses, adiponectin levels during pregnancy independently predicted both postpartum insulin sensitivity (t = 3.97, p < 0.0001) and beta cell function (t = 2.37, p = 0.0181), even after adjustment for GDM. Furthermore, adiponectin emerged as a significant negative independent determinant of postpartum fasting glucose (t = -3.01, p = 0.0027).

CONCLUSIONS/INTERPRETATION

Hypoadiponectinaemia during pregnancy predicts postpartum insulin resistance, beta cell dysfunction and fasting glycaemia, and hence may be relevant to the pathophysiology relating GDM with type 2 diabetes.

Authors+Show Affiliations

Leadership Sinai Centre for Diabetes, Mount Sinai Hospital, 60 Murray Street, Suite-L5-039, Mailbox-21, Toronto, ON, Canada. rretnakaran@mtsinai.on.caNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

19937225

Citation

Retnakaran, R, et al. "Low Adiponectin Concentration During Pregnancy Predicts Postpartum Insulin Resistance, Beta Cell Dysfunction and Fasting Glycaemia." Diabetologia, vol. 53, no. 2, 2010, pp. 268-76.
Retnakaran R, Qi Y, Connelly PW, et al. Low adiponectin concentration during pregnancy predicts postpartum insulin resistance, beta cell dysfunction and fasting glycaemia. Diabetologia. 2010;53(2):268-76.
Retnakaran, R., Qi, Y., Connelly, P. W., Sermer, M., Hanley, A. J., & Zinman, B. (2010). Low adiponectin concentration during pregnancy predicts postpartum insulin resistance, beta cell dysfunction and fasting glycaemia. Diabetologia, 53(2), 268-76. https://doi.org/10.1007/s00125-009-1600-8
Retnakaran R, et al. Low Adiponectin Concentration During Pregnancy Predicts Postpartum Insulin Resistance, Beta Cell Dysfunction and Fasting Glycaemia. Diabetologia. 2010;53(2):268-76. PubMed PMID: 19937225.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Low adiponectin concentration during pregnancy predicts postpartum insulin resistance, beta cell dysfunction and fasting glycaemia. AU - Retnakaran,R, AU - Qi,Y, AU - Connelly,P W, AU - Sermer,M, AU - Hanley,A J, AU - Zinman,B, Y1 - 2009/11/24/ PY - 2009/07/14/received PY - 2009/10/07/accepted PY - 2009/11/26/entrez PY - 2009/11/26/pubmed PY - 2010/4/27/medline SP - 268 EP - 76 JF - Diabetologia JO - Diabetologia VL - 53 IS - 2 N2 - AIMS/HYPOTHESIS: The postpartum phase following gestational diabetes (GDM) is characterised by subtle metabolic defects, including the beta cell dysfunction that is believed to mediate the increased future risk of type 2 diabetes in this patient population. Low circulating levels of adiponectin and increased leptin and C-reactive protein (CRP) have recently emerged as novel diabetic risk factors, although their relevance to GDM and subsequent diabetes has not been characterised. Thus, we sought to determine whether adiponectin, leptin and CRP levels during pregnancy relate to the postpartum metabolic defects linking GDM with type 2 diabetes. METHODS: Metabolic characterisation, including oral glucose tolerance testing, was undertaken in 487 women during pregnancy and at 3 months postpartum. Based on the antepartum OGTT, there were 137 women with GDM, 91 with gestational impaired glucose tolerance and 259 with normal glucose tolerance. RESULTS: Adiponectin levels were lowest (p < 0.0001) and CRP levels highest (p = 0.0008) in women with GDM. Leptin did not differ between the glucose tolerance groups (p = 0.4483). Adiponectin (r = 0.41, p < 0.0001), leptin (r = -0.36, p < 0.0001) and CRP (r = -0.30, p < 0.0001) during pregnancy were all associated with postpartum insulin sensitivity (determined using the insulin sensitivity index of Matsuda and DeFronzo [IS(OGTT)]). Intriguingly, adiponectin levels were also related to postpartum beta cell function (insulinogenic index/HOMA of insulin resistance; r = 0.16, p = 0.0009). Indeed, on multiple linear regression analyses, adiponectin levels during pregnancy independently predicted both postpartum insulin sensitivity (t = 3.97, p < 0.0001) and beta cell function (t = 2.37, p = 0.0181), even after adjustment for GDM. Furthermore, adiponectin emerged as a significant negative independent determinant of postpartum fasting glucose (t = -3.01, p = 0.0027). CONCLUSIONS/INTERPRETATION: Hypoadiponectinaemia during pregnancy predicts postpartum insulin resistance, beta cell dysfunction and fasting glycaemia, and hence may be relevant to the pathophysiology relating GDM with type 2 diabetes. SN - 1432-0428 UR - https://www.unboundmedicine.com/medline/citation/19937225/Low_adiponectin_concentration_during_pregnancy_predicts_postpartum_insulin_resistance_beta_cell_dysfunction_and_fasting_glycaemia_ L2 - https://doi.org/10.1007/s00125-009-1600-8 DB - PRIME DP - Unbound Medicine ER -