**4. Conclusions**

These values are not markedly different from those obtained in the other study [167]. In this study, there are statistically significant differences in HOMA-S% between the NGT and GDM groups (Р = 0.002). It is found a reverse correlation between HOMA-S% and BMI in the both NGT and GDM patient groups (r = −0.467 and r = −0.679, respectively). The authors' hypothesis is that as higher is a BMI, stronger is its influence on insulin sensitivity, expressed by HOMA-S% index [167]. The current studies confirm that GDM is associated with increased insulin resistance and β-cell dysfunction, as well as reduced insulin sensitivity and secretion. BMI, glucose, and insulin sensitivity are interrelated and alter maternal metabolism. A novel aspect of studies is identification of metabolic signatures uniquely associated with maternal BMI and glycemia, including differences in metabolites most strongly associated with these phenotypes [218]. The association of several plasma metabolites with maternal prepregnancy BMI across gestation in a cohort of 167 non-Hispanic and Hispanic ancestry women was reported [219]. Some of these metabolites have been found to have a role in aspects of metabolism such as insulin sensitivity and pancreatic β-cell function. A limited number of GDM metabolomics studies have been performed, evidence suggests that the metabolic signatures of T2D and GDM overlap [220]. Metabolomic studies of maternal metabolism during pregnancy are focused largely on normal pregnancy and GDM [221–227]. It is important to examine the associations of maternal BMI on the maternal metabolome, to consider estimated maternal insulin sensitivity as a predictor of the maternal metabolome. Furthermore, maternal BMI and insulin sensitivity impact a broad array of metabolites and have shared indepen-

dent associations with the maternal metabolome [228].

**(HOMA-IR)**

30 Body-mass Index and Health

**3.4. The effect of BMI on homeostasis model assessment of insulin resistance** 

Insulin resistance is, by definition, a disorder in the signal transduction of several known hormones [229]. Insulin resistance in peripheral tissues in women with GDM is exacerbated, but few studies have examined the extent of insulin resistance in placenta in this disease. It is possible that this insulin resistance could contribute to alter the placental transport of nutrients [230–232]. The degree of maternal insulin resistance manifested during pregnancy is theoretically associated with the degree of glucose flux from mother to fetus. Excessive insulin resistance during pregnancy is also observed in obese subjects without abnormal glucose tolerance [10]. Different studies found HOMA-IR values in the GDM group are significantly higher than in NGT patients, which indicated a significant insulin resistance [167, 215, 233–239]. Some studies report controversial results. They found that the HOMA-IR values are similar in GDM patients and healthy NGT controls [240–243]. Women with GDM in early pregnancy had significantly higher HOMA-IR values than those with GDM in later pregnancy or those with NGT [244] and results are similar to other from prior work [245]. Probably, higher BMIs among women with early-onset GDM are detected to at least partially explain this phenomenon [246]. An important goal is to identifying women with GDM during early pregnancy to minimize maternal and neonatal morbidity. One study reported that first trimester HOMA-IR values are independent predictors for the development of GDM in logistic regression analysis, and the HOMA-IR value is found to be a better marker (AUC ¼ 0.75; 95% CI, 0.67e0.83) than the other factors [247]. Another study detects borderline significance for risk of subsequent GDM for increased HOMA-IR values at gestational weeks 16–18, independent of other variables that

Undoubtedly, in recent years, the frequency of GDM is increasing in tandem with the dramatic increase in the prevalence of overweight and obesity in women of childbearing age, assessing by BMI. Another risk factor for GDM is the excessive weight gain during the pregnancy, assessing by use of BMI. The optimal weight increase in pregnancy is well established on the base of studies, and is different depending on BMI prior to pregnancy. Some studies show, that excessive weight gain is a significant risk factor for GDM in all categories of BMI, but the relationship is more stringent in obese individuals. Most of studies observed that higher BMI decreases the insulin sensitivity, increases the IR and contributes to development of GDM. New guidelines into the mechanisms underlying maternal metabolism during pregnancy are being gained through the use of new technologies. Future studies on the base of integrated data from multiple technologies will allow a systems biology approach to maternal metabolism during pregnancy.

[5] Damn P. Gestational diabetes mellitus and subsequent development of overt diabetes

Body Mass Index and Insulin Sensitivity/Resistance: Cross Talks in Gestational Diabetes, Normal…

http://dx.doi.org/10.5772/intechopen.78363

33

[6] Homko C, Sivan E, Chen X, Reece EA, Boden G. Insulin secretion during and after pregnancy in patients with gestational diabetes mellitus. The Journal of Clinical

[7] Buchanan TA, Xiang A. Gestational diabetes mellitus. The Journal of Clinical Inves-

[8] Basu R, Breda E, Oberg A, Powell C, Man CD, Basu A, et al. Mechanisms of age-associated determination in glucose tolerance, contribution of alterations in insulin secretion, action and clearance. Diabetes. 2003;**52**:1738-1748. DOI: 10.2337/diabetes.52.7.1738

[9] Reyes-Lopez R, Perez-Luque E, Malacara JM. Metabolic, hormonal characteristics and genetic variants of TCF7L2 associated with development of gestational diabetes mellitus in Mexican women. Diabetes/Metabolism Research and Reviews. 2014;**30**(8):701-706.

[10] Catalano P, Huston L, Amini SB, Kalhan SC. Longitudinal changes in glucose metabolism during pregnancy in obese women with normal glucose tolerance and gestational diabetes mellitus. American Journal of Obstetrics and Gynecology. 1999;**180**(4):903-916.

[11] Barbour LA, CataMcCurdy CE, Hernandez TL, Kirwan JP, Catalano PM, Friedman JE. Cellular mechanisms for insulin resistance in normal pregnancy and gestational dia-

[12] Ryan EA, O'Sullivan MJ, Skyler J. Insulin action during pregnancy. Studies with the euglycemic clamp technique. Diabetes. 1985;**34**(4):380-389. DOI: 10.2337/diab.34.4.380

[13] Buchanan TA, Xiang AH, Page KA. Gestational diabetes mellitus: Risks and management during and after pregnancy. Nature Reviews. Endocrinology. 2012;**8**(11):639-649.

[14] Kim C. Mint: Maternal outcomes and follow-up after gestational diabetes mellitus.

[15] Bellamy L, Casas JP, Hingorani AD, Williams D. Type 2 diabetes mellitus after gestational diabetes: A systematic review and meta-analysis. Lancet. 2009;**373**(9677):1773-

[16] Ferrara A, Kahn HS, Quesenberry CP, Riley C, Hedderson MM. An increase in the incidence of gestational diabetes mellitus: Northern California, 1991-2000. Obstetrics and

[17] Getahun D, Nath C, Ananth CV, Chavez MR, Smulian JC. Gestational diabetes in the United States: Temporal trends 1989 through 2004. American Journal of Obstetrics and

Gynecology. 2004;**103**(3):526-533. DOI: 10.1097/01.AOG.0000113623.18286.20

Gynecology. 2008;**198**(5):525.e1-525.e5. DOI: 10.1016/j.ajog.2007.11.017

Diabetic Medicine. 2014;**31**(3):292-301. DOI: 10.1111/dme.12382

betes. Diabetes Care. 2007;**30**(Suppl. 2):S112-S119. DOI: 10.2337/dc07-s202

Endocrinology and Metabolism. 2001;**86**:568-573. DOI: 10.1210/jcem.86.2.7137

mellitus. Danish Medical Bulletin. 1998;**45**:495-509

tigation. 2005;**115**(3):485-491. DOI: 10.1172/JCI200524531

DOI: 10.1002/dmrr.2538

DOI: 10.1016/S0002-9378(99)70662-9

DOI: 10.1038/nrendo.2012.96

1779. DOI: 10.1016/S0140-6736(09)60731-5
