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Original Article

Colostrum and mature breast milk analysis of serum irisin and sterol regulatory element-binding proteins-1c in gestational diabetes mellitus

ORCID Icon, , &
Pages 2993-2999 | Received 16 Oct 2017, Accepted 15 Mar 2018, Published online: 02 Apr 2018
 

Abstract

Background: We aimed to evaluate irisin and SREBP-1c levels in serum, colostrum and mature breast milk in women with and without gestational diabetes (GDM); and to relate them with maternal glucose, lipid profile and weight status of babies.

Methods: GDM positive women (n = 33) and normal glucose tolerant women (NGT) (n = 33) were recruited. Maternal blood samples were collected at 28th week of gestation and later at 6-week post-partum while breast milk samples of the lactating mothers were collected within 72 hours of birth (colostrum) and at 6 weeks post-partum (mature milk). Irisin and SREBP-1c levels were analyzed by commercially available ELISA kits for all maternal samples.

Results: Lower levels of irisin were seen in serum, colostrum and mature breast milk of GDM females (p < .01). SREBP-1c profile showed a similar trend of low serum levels in GDM, however, they were undetectable in colostrum and mature breast milk. Weak to moderate correlations of serum irisin with BMI (r = 0.439; p < .001), GTT 0 hours (r = 0.403; p = .01), HbA1c (r = −0.312; p = .011), Fasting blood glucose (r = 0.992; p = .008), and baby weight at birth (r = 0.486; p < .001). Colostrum and mature breast milk irisin showed positive associations with baby weight at 6 weeks (r = 0.325; p = .017; r = 0.296; p = .022, respectively). Serum SREBP-1c at 6 weeks correlated with random blood glucose (r = 0.318; p = .009), and HbA1c (r= −0.292; p = .011). All correlations were lost once we adjusted for maternal BMI.

Conclusions: Low irisin and SREBP1-c levels may favor development of GDM in pregnant subjects. Further, low mature breast milk levels may act as a continued stressor from fetal to infant life as long as breast-feeding is continued. Further studies are required to identify the mechanistic relationship between these biomarkers and GDM.

Disclosure statement

The authors declare that they have no conflict of interest.

Additional information

Funding

This work was supported by Department of Biological and Biomedical Sciences and AKU – Seed Money Funds.

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