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The Impact of Serum Leptin, Leptin Receptor and Insulin on Maternal Obesity


Affiliations
1 Department of Chemistry, College of Science, Mustansiriyah University, Baghdad, Iraq
2 College of Medicine, Mustansiriyah University, Baghdad, Iraq
3 College of Biotechnology, Al-Nahrain University, Baghdad, Iraq
     

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The prevalence of overweight and obesity is rising worldwide, particularly, among women of reproductive age. Obesity during pregnancy can result in adverse outcomes for both mothers and fetuses. The current study was carried out to investigate whether the leptin (LEP), leptin receptor (LEPR) and insulin have a role in obesity development among Iraqi pregnant women. A case-control study included 90 pregnant women recruited at term for a scheduled cesarean delivery and classified equally according to body mass index (BMI) into three groups; control, overweight, and obese. Insulin, LEP, and LEPR were measured by enzyme-linked immunosorbent assay (ELISA). Obese group showed a significant increase in serum LEP (P<0.001), LEPR (p<0.05) and fasting insulin (P<0.05) concentrations compared with control group. Meanwhile, overweight females showed a significant (P<0.05) increase only in serum LEP and LEP/LEPR ratio (P<0.001,) compared to control group. Furthermore, maternal BMI was positively associated with, LEPR (adjusted r = 0.276, β: 0.104, P<0.01), LEP (adjusted r = 0.471, β: 0.256, P<0.001), and insulin (adjusted r = 0.439, β: 0.363, P<0.001) among entire data set. Similarly, BMI was positively associated with LEP (adjusted r = 0.297, β: 0.161, P<0.05), LEPR (adjusted r=0.444, β: 0.133, P<0.001) and insulin (adjusted r = 0.432, β: 0.266, P<0.001) among overweight/obese females. In Conclusion both of LEP and insulin are the strongest predictor for maternal BMI after age adjustment, while among overweight/obese females, LEPR has greatest impact on maternal obesity and insulin comes in second place.

Keywords

Maternal Obesity, Body Mass Index, Leptin, Leptin Receptor, Insulin, Lipid Profile, Insulin Resistance.
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  • The Impact of Serum Leptin, Leptin Receptor and Insulin on Maternal Obesity

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Authors

Shahla O. Al-Ogaidi
Department of Chemistry, College of Science, Mustansiriyah University, Baghdad, Iraq
Sura A. Abdulsattar
College of Medicine, Mustansiriyah University, Baghdad, Iraq
Hameed M. J. Al-Dulaimi
College of Biotechnology, Al-Nahrain University, Baghdad, Iraq

Abstract


The prevalence of overweight and obesity is rising worldwide, particularly, among women of reproductive age. Obesity during pregnancy can result in adverse outcomes for both mothers and fetuses. The current study was carried out to investigate whether the leptin (LEP), leptin receptor (LEPR) and insulin have a role in obesity development among Iraqi pregnant women. A case-control study included 90 pregnant women recruited at term for a scheduled cesarean delivery and classified equally according to body mass index (BMI) into three groups; control, overweight, and obese. Insulin, LEP, and LEPR were measured by enzyme-linked immunosorbent assay (ELISA). Obese group showed a significant increase in serum LEP (P<0.001), LEPR (p<0.05) and fasting insulin (P<0.05) concentrations compared with control group. Meanwhile, overweight females showed a significant (P<0.05) increase only in serum LEP and LEP/LEPR ratio (P<0.001,) compared to control group. Furthermore, maternal BMI was positively associated with, LEPR (adjusted r = 0.276, β: 0.104, P<0.01), LEP (adjusted r = 0.471, β: 0.256, P<0.001), and insulin (adjusted r = 0.439, β: 0.363, P<0.001) among entire data set. Similarly, BMI was positively associated with LEP (adjusted r = 0.297, β: 0.161, P<0.05), LEPR (adjusted r=0.444, β: 0.133, P<0.001) and insulin (adjusted r = 0.432, β: 0.266, P<0.001) among overweight/obese females. In Conclusion both of LEP and insulin are the strongest predictor for maternal BMI after age adjustment, while among overweight/obese females, LEPR has greatest impact on maternal obesity and insulin comes in second place.

Keywords


Maternal Obesity, Body Mass Index, Leptin, Leptin Receptor, Insulin, Lipid Profile, Insulin Resistance.

References