Relationship between basal metabolic rate and cortisol secretion throughout pregnancy

Abstract

The role of cortisol in mediating basal metabolic rate (BMR) changes that accompany the adjustment of maternal body weight (BW) and body composition during pregnancy is unknown. We tested whether increase in BMR during pregnancy is explained by variations in cortisol secretion. Longitudinal changes in BW, fat mass (FM), fat-free mass (FFM), BMR, hormonal, and metabolic parameters in 31 parous Caucasian women at gestational weeks 12, 26, and 36 were examined. Individual differences (Delta) between the last and the first measurement occasions for each variable were calculated. By gestational week 36, BW and BMR increased while both FFM/FM and BMR/BW ratio decreased (P < 0.001 for all) suggesting higher proportion of FM accretion. Cortisol, leptin, and insulin-like growth factor-1 (IGF-1) concentration rose, whereas non-placental growth hormone (GH) and thyroid hormones declined (P < 0.001 for all). Insulin resistance changed; basal glucose (P < 0.001) and ghrelin (P < 0.014) declined, whereas insulin (P < 0.001), homeostatic model index (HOMA-IR) (P = 0.041), and free fatty acid (FFA) concentration (P = 0.007) increased. The elevation in BMR showed inverse correlations with DeltaBW (r = 0.37, P = 0.047) and Deltacortisol (r = -0.53, P = 0.004). Significant portion (51.6%) of the variation in BMR change was explained by increases of cortisol (27.1%), FFA (13.4%), and free triiodothyronine (11.1%). In conclusion, the changes in maternal cortisol concentration are in relationship with changes in BMR and BW, further suggesting that increased cortisol secretion during pregnancy could be linked with the maintenance of maternal BW and body composition.

The effects of childhood sexual abuse on cortisol trajectories in pregnancy are moderated by current family functioning

“…Women were also excluded from participating for a variety of medical conditions and medications that could impact maternal cortisol output. Therefore, results from this study may not generalize to high-risk pregnancies and may underestimate the effects of CSA and family functioning on maternal cortisol during pregnancy, given that women with chronic health conditions in pregnancy or medication use may exhibit altered cortisol profiles during gestation (Damjanovic, et al, 2009; McKenna, Wittber, Nagaraja, & Samuels, 2000; Salustiano, De Pinho, Provost, Ruano, & Zugaib, 2013; Shea et al, 2007). …”

“…Past studies suggest that elevated cortisol in pregnancy may place women at increased risk for health problems during pregnancy including pre-eclampsia, gestational diabetes, and increased weight gain (Damjanovic et al, 2009; Keller-Wood et al, 2014; Redman & Sacks, 1999). Women may also be at elevated risk for disorders in the postpartum period such as thyroiditis and rheumatoid arthritis (Elenkov et al, 2001; Mastorakos & Ilias, 2000) and postpartum mood disorders (Mastorakos & Ilias, 2000; A Nierop, Bratsikas, Zimmerman, & Ehlert, 2006).…”

Pattern of maternal circulating CRH in laboratory‐housed squirrel and owl monkeys

“…Cortisol serves to drive the maternal-placental-fetal adrenal axis through a positive feed-back system [Robinson et al, 1988] which results in increasing estrogen production over gestation [Lockwood, 2004; Rainey et al, 2004]. Maternal cortisol also is likely involved in many of the metabolic adjustments necessary for successful pregnancy, such as the increase in maternal metabolic rate and insulin resistance [Damjanovic et al, 2009]. Circulating cortisol in the fetus serves to mature fetal organs.…”

The Association between a Medical History of Depression and Gestational Diabetes in a Large Multi‐ethnic Cohort in the United States

“…Prolonged exposure to cortisol can, therefore, lead to visceral adiposity, insulin resistance, dyslipidemia and hypertension, each implicated in the pathology of GDM. During the course of pregnancy, urinary cortisol levels increase along with the upregulation of the maternal HPA axis, and may in fact regulate metabolic changes, such as increases in body weight and metabolic rate, that lead to insulin resistance in pregnancy . Exacerbating these high cortisol levels could, in turn, increase the metabolic consequences that contribute to GDM pathogenesis.…”

“…During the course of pregnancy, urinary cortisol levels increase along with the upregulation of the maternal HPA axis, 22 and may in fact regulate metabolic changes, such as increases in body weight and metabolic rate, that lead to insulin resistance in pregnancy. 23 Exacerbating these high cortisol levels could, in turn, increase the metabolic consequences that contribute to GDM pathogenesis. Additional pathways include catecholamine release due to an enhanced sympathetic nervous system response or an inflammatory response, which also contributes to insulin resistance.…”