scholarly journals Placental Endocrine Activity: Adaptation and Disruption of Maternal Glucose Metabolism in Pregnancy and the Influence of Fetal Sex

2021 ◽  
Vol 22 (23) ◽  
pp. 12722
Author(s):  
Christina Stern ◽  
Sarah Schwarz ◽  
Gerit Moser ◽  
Silvija Cvitic ◽  
Evelyn Jantscher-Krenn ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Sex Differences ◽  
Glucose Metabolism ◽  
Cell Mass ◽  
Maternal Blood ◽  
Endocrine Function ◽  
Endocrine Activity ◽  
Glucose Levels ◽  
Fetal Organ ◽  
Maternal Glucose

The placenta is an endocrine fetal organ, which secretes a plethora of steroid- and proteo-hormones, metabolic proteins, growth factors, and cytokines in order to adapt maternal physiology to pregnancy. Central to the growth of the fetus is the supply with nutrients, foremost with glucose. Therefore, during pregnancy, maternal insulin resistance arises, which elevates maternal blood glucose levels, and consequently ensures an adequate glucose supply for the developing fetus. At the same time, maternal β-cell mass and function increase to compensate for the higher insulin demand. These adaptations are also regulated by the endocrine function of the placenta. Excessive insulin resistance or the inability to increase insulin production accordingly disrupts physiological modulation of pregnancy mediated glucose metabolism and may cause maternal gestational diabetes (GDM). A growing body of evidence suggests that this adaptation of maternal glucose metabolism differs between pregnancies carrying a girl vs. pregnancies carrying a boy. Moreover, the risk of developing GDM differs depending on the sex of the fetus. Sex differences in placenta derived hormones and bioactive proteins, which adapt and modulate maternal glucose metabolism, are likely to contribute to this sexual dimorphism. This review provides an overview on the adaptation and maladaptation of maternal glucose metabolism by placenta-derived factors, and highlights sex differences in this regulatory network.

scholarly journals Maternal carbohydrate intake and pregnancy outcome

2002 ◽  
Vol 61 (1) ◽  
pp. 45-50 ◽  
Author(s):  
James F. Clapp III
Keyword(s):  
Insulin Resistance ◽  
Weight Gain ◽  
Postprandial Glucose ◽  
Maternal Blood ◽  
Metabolic Efficiency ◽  
Maternal Weight Gain ◽  
Maternal Weight ◽  
Glucose Levels ◽  
Energy Retention ◽  
Pregnant State

Experimental evidence indicates that the primary maternal environmental factor that regulates feto–placental growth is substrate delivery to the placental site, which is the product of maternal substrate levels and the rate of placental-bed blood flow. Thus, maternal factors which change either substrate level or flow alter feto–placental growth rate. The best-studied substrate in human pregnancy is glucose, and there is a direct relationship between maternal blood glucose levels and size at birth. Altering the type of carbohydrate eaten (high- v. low-glycaemic sources) changes postprandial glucose and insulin responses in both pregnant and non-pregnant women, and a consistent change in the type of carbohydrate eaten during pregnancy influences both the rate of feto–placental growth and maternal weight gain. Eating primarily high-glycaemic carbohydrate results in feto–placental overgrowth and excessive maternal weight gain, while intake of low-glycaemic carbohydrate produces infants with birth weights between the 25th and the 50th percentile and normal maternal weight gain. The calculated difference in energy retention with similar total energy intakes is of the order of 80 000 kJ. Preliminary information from subsequent metabolic studies indicates that the mechanisms involved include changes in: daily digestible energy requirements (i.e. metabolic efficiency), substrate utilization (glucose oxidation v. lipid oxidation), and insulin resistance and sensitivity. Thus, altering the source of maternal dietary carbohydrate may prove to be a valuable tool in the management of pregnancies at risk for anomalous feto–placental growth and for the prevention and/or treatment of obesity and insulin resistance in the non-pregnant state.

No associations of prenatal maternal psychosocial stress with fasting glucose metabolism in offspring at 5–6 years of age

2014 ◽  
Vol 5 (5) ◽  
pp. 361-369 ◽  
Author(s):  
A. E. van Dijk ◽  
M. van Eijsden ◽  
K. Stronks ◽  
R. J. B. J. Gemke ◽  
T. G. M. Vrijkotte
Keyword(s):  
Insulin Resistance ◽  
Sex Differences ◽  
Glucose Metabolism ◽  
Psychosocial Stress ◽  
Job Strain ◽  
Fasting Glucose ◽  
Stress Hormones ◽  
Daily Hassles ◽  
C Peptide ◽  
Cumulative Score

Highly prevalent maternal psychosocial complaints are accompanied by increases in glucocorticoid stress hormones, which may predispose the offspring for type 2 diabetes and cardiovascular disease later in adulthood. The aim of the current research is to study whether prenatal maternal psychosocial stress is associated with parameters of blood glucose metabolism in their children aged 5–6 years. The study design was a prospective birth cohort (the Amsterdam Born Children and their Development study, the Netherlands). Depressive symptoms, pregnancy-related anxiety, parenting daily hassles and job strain were recorded by questionnaire (gestational week 16). A cumulative score was also calculated. Possible sex differences in the associations were considered. The subjects were 1952 mother–child pairs. Outcome measures were fasting glucose (n=1952), C-peptide and insulin resistance (HOMA2-IR) (n=1478) in the children at the age of 5–6 years. The stress scales, single and cumulative, were not associated with glucose/C-peptide/insulin resistance (allP>0.05). We did not find evidence for sex differences. In conclusion, we did not find evidence for an association between psychosocial stress during early pregnancy and parameters of glucose metabolism in offspring at the age of 5–6 years. Differences emerging later in life or in response to a metabolic challenge should not be ruled out.

scholarly journals Adverse Effects of Bisphenol A Exposure on Glucose Metabolism Regulation

2016 ◽  
Vol 10 (1) ◽  
pp. 122-130 ◽  
Author(s):  
Ciro Menale ◽  
Damiano G. Mita ◽  
Nadia Diano ◽  
Sabrina Diano
Keyword(s):  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Adverse Effects ◽  
Bisphenol A ◽  
Estrogenic Activity ◽  
Endocrine Function ◽  
Peripheral Tissues ◽  
Metabolism Regulation

Bisphenol A (BPA) is used as basic chemical compound in the production of polycarbonate food containers or epoxy resins coating metallic cans for food and beverages conservation. Its xeno-estrogenic activity alters endocrine-metabolic pathways modulating glucose metabolism and increasing the risk of developing diabetes, insulin resistance, and obesity. Based on in vitro and in vivo experimental research, here we report some of the major BPA adverse effects on tissues that play a key role in the regulation on the whole body’s metabolism. Evidences have shown that BPA is able to exert its endocrine disrupting action altering glucose metabolism and contributing to the onset of metabolic disorders, acting on liver functions and affecting insulin production by the pancreas. Exposure to BPA has been reported also to modulate glucose utilization in muscles, as well as to interfere with adipose tissue endocrine function. In addition, to peripheral tissues, recent studies have shown that BPA by acting in the Central Nervous System affects neuroendocrine regulation of glucose metabolism, promoting glucose metabolism dysfunction such as glucose intolerance and insulin resistance. Thus, exposure to BPA seems to be an important risk factor in the onset of obesity and metabolic syndrome. However, its mechanisms of action need to be further investigated to provide a major evaluation of risk assessment.

Low-carbohydrate-diet and maternal glucose metabolism in Chinese pregnant women

2020 ◽  
pp. 1-22
Author(s):  
Qian Chen ◽  
Yajun Chen ◽  
Weijia Wu ◽  
Nu Tang ◽  
Dongyu Wang ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Pregnant Women ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Dietary Intakes ◽  
Glucose Levels ◽  
Low Carbohydrate Diet ◽  
Low Carbohydrate ◽  
Mixed Regression ◽  
Maternal Glucose

Abstract Few studies have suggested that long-term adherence to low-carbohydrate diets (LCD) may affect maternal glucose metabolism in western countries. We aimed to investigate the association between LCD during pregnancy and glucose metabolism in Chinese population. A total of 1,018 women in mid-pregnancy were recruited in 2017-2018. Participants underwent a 75g oral glucose tolerance test (OGTT). Daily dietary intakes over the past month were accessed using a validated food frequency questionnaire. The overall, animal, and vegetable LCD scores which represent adherence to different low-carbohydrate dietary patterns were calculated. Mixed linear regression and generalized linear mixed regression were conducted to evaluate the associations between LCD scores and maternal glucose metabolism. Of the 1,018 subjects, 194 (19.1%) was diagnosed with gestational diabetes mellitus (GDM). The overall LCD score (β: 0.024, standard error (SE): 0.008, PFDR=0.02) and animal LCD score (β: 0.023, SE: 0.008, PFDR=0.02) was positively associated with OGTT 1-h glucose. No significant associations were found between the three different LCD scores with fasting plasma glucose (FPG), OGTT 2-h glucose, or insulin resistance, respectively. Compared with the lowest quartile, the crude odds ratios of GDM for the highest quartile were 1.84 (95% CI: 1.14, 2.95) for overall LCD score (P for trend = 0.02) and 1.56 (1.00, 2.45) for animal LCD score (P for trend = 0.02). However, these associations became nonsignificant after adjustment for covariates. In conclusion, a low-carbohydrate dietary pattern with high animal protein and fat is associated with higher postprandial 1-h glucose levels in Chinese pregnant women.

scholarly journals Acute psychological stress results in the rapid development of insulin resistance

2013 ◽  
Vol 217 (2) ◽  
pp. 175-184 ◽  
Author(s):  
Li Li ◽  
Xiaohua Li ◽  
Wenjun Zhou ◽  
Joseph L Messina
Keyword(s):  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Insulin Receptor ◽  
Psychological Stress ◽  
Insulin Signaling ◽  
Rapid Development ◽  
Whole Body ◽  
Glucose Levels ◽  
Insulin Tolerance ◽  
Acute Psychological Stress

In recent years, the roles of chronic stress and depression as independent risk factors for decreased insulin sensitivity and the development of diabetes have been increasingly recognized. However, an understanding of the mechanisms linking insulin resistance and acute psychological stress are very limited. We hypothesized that acute psychological stress may cause the development of insulin resistance, which may be a risk factor in developing type 2 diabetes. We tested the hypothesis in a well-established mouse model using 180 episodes of inescapable foot shock (IES) followed by a behavioral escape test. In this study, mice that received IES treatment were tested for acute insulin resistance by measuring glucose metabolism and insulin signaling. When compared with normal and sham mice, mice that were exposed to IES resulting in escape failure (defined as IES with behavioral escape failure) displayed elevated blood glucose levels in both glucose tolerance and insulin tolerance tests. Furthermore, mice with IES exposure and behavioral escape failure exhibited impaired hepatic insulin signaling via the insulin-induced insulin receptor/insulin receptor substrate 1/Akt pathway, without affecting similar pathways in skeletal muscle, adipose tissue, and brain. Additionally, a rise in the murine growth-related oncogene KC/GRO was associated with impaired glucose metabolism in IES mice, suggesting a mechanism by which psychological stress by IES may influence glucose metabolism. The present results indicate that psychological stress induced by IES can acutely alter hepatic responsiveness to insulin and affect whole-body glucose metabolism.

High doses of dexamethasone induce increased β-cell proliferation in pancreatic rat islets

2009 ◽  
Vol 296 (4) ◽  
pp. E681-E689 ◽  
Author(s):  
Alex Rafacho ◽  
Tânia M. Cestari ◽  
Sebastião R. Taboga ◽  
Antonio C. Boschero ◽  
José R. Bosqueiro
Keyword(s):  
Insulin Resistance ◽  
Cell Proliferation ◽  
Cell Mass ◽  
Fold Increase ◽  
Insulin Requirement ◽  
Β Cell ◽  
Cell Hyperplasia ◽  
Glucose Levels ◽  
Cell Alterations ◽  
High Doses

Activation of insulin signaling and cell cycle intermediates is required for adult β-cell proliferation. Here, we report a model to study β-cell proliferation in living rats by administering three different doses of dexamethasone (0.1, 0.5, and 1.0 mg/kg ip, DEX 0.1, DEX 0.5, and DEX 1.0, respectively) for 5 days. Insulin sensitivity, insulin secretion, and histomorphometric data were investigated. Western blotting was used to analyze the levels of proteins related to the control of β-cell growth. DEX 1.0 rats, which present moderate hyperglycemia and marked hyperinsulinemia, exhibited a 5.1-fold increase in β-cell proliferation and an increase (17%) in β-cell size, with significant increase in β-cell mass, compared with control rats. The hyperinsulinemic but euglycemic DEX 0.5 rats also showed a significant 3.6-fold increase in β-cell proliferation. However, DEX 0.1 rats, which exhibited the lowest degree of insulin resistance, compensate for insulin demand by improving only islet function. Activation of the insulin receptor substrate 2/phosphatidylinositol 3-kinase/serine-threonine kinase/ribosomal protein S6 kinase pathway, as well as protein retinoblastoma in islets from DEX 1.0 and DEX 0.5, but not in DEX 0.1, rats was also observed. Therefore, increasing doses of dexamethasone induce three different degrees of insulin requirement in living rats, serving as a model to investigate compensatory β-cell alterations. Augmented β-cell mass involves β-cell hyperplasia and, to a lower extent, β-cell hypertrophy. We suggest that alterations in circulating insulin and, to a lesser extent, glucose levels could be the major stimuli for β-cell proliferation in the dexamethasone-induced insulin resistance.

scholarly journals Association between the serum estrone-to-estradiol ratio and parameters related to glucose metabolism and insulin resistance in women with polycystic ovary syndrome

2021 ◽  
Vol 48 (4) ◽  
pp. 374-379
Author(s):  
Nayoung Kim ◽  
Sungwook Chun
Keyword(s):  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Postprandial Glucose ◽  
Serum Glucose ◽  
Clinical Variable ◽  
Fasting Insulin ◽  
Ovary Syndrome ◽  
Glucose Levels

Objective: We aimed to evaluate associations between the ratio of serum estrone (E1) to estradiol (E2) and parameters related to serum glucose metabolism and insulin resistance in women with polycystic ovary syndrome (PCOS). Methods: In total, 133 women between the ages of 18 and 33 diagnosed with PCOS were enrolled in this study. All participants with PCOS underwent blood tests to determine hormonal and biochemical metabolic parameters and a standard 2-hour 75-g oral glucose tolerance test. They were divided into two groups according to the serum E1-to-E2 ratio: group 1 (E1/E2 ratio <2.0) and group 2 (E1/E2 ratio ≥2.0). Results: In the comparative analysis, the waist-to-hip ratio (WHR) was the only clinical variable that was significantly different between the two groups. Patients with a higher E1/E2 ratio showed higher fasting insulin levels, homeostasis model for insulin resistance, and postprandial glucose levels at 2 hours (PPG2). In a correlation analysis, only PPG2 was significantly related to the serum E1/E2 ratio. However, after controlling for the confounding effects of body mass index (BMI) and WHR, fasting glucose was also significantly correlated with the serum E1/E2 ratio. Conclusion: Women with PCOS with a higher serum E1/E2 ratio were found to be more likely to show higher fasting insulin and postprandial glucose levels. Significant correlations were found between the serum E1/E2 ratio and both fasting and postprandial serum glucose levels after adjusting for BMI and WHR in women with PCOS.

Increased Aβ production prompts the onset of glucose intolerance and insulin resistance

2012 ◽  
Vol 302 (11) ◽  
pp. E1373-E1380 ◽  
Author(s):  
Margarita Jiménez-Palomares ◽  
Juan José Ramos-Rodríguez ◽  
José Francisco López-Acosta ◽  
Mar Pacheco-Herrero ◽  
Alfonso M. Lechuga-Sancho ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Glucose Metabolism ◽  
Glucose Intolerance ◽  
Cell Mass ◽  
Phenotypic Characterization ◽  
Β Cell ◽  
Altered Glucose ◽  
Islet Volume ◽  
Aβ Production

Type 2 diabetes (T2D) mellitus and Alzheimer's disease (AD) are two prevalent diseases with comparable pathophysiological features and genetic predisposition. Patients with AD are more susceptible to develop T2D. However, the molecular mechanism linking AD and T2D remains elusive. In this study, we have generated a new mouse model to test the hypothesis that AD would prompt the onset of T2D in mice. To test our hypothesis, we crossed Alzheimer APPswe/PS1dE9 (APP/PS1) transgenic mice with mice partially deficient in leptin signaling ( db/+). Body weight, plasma glucose, and insulin levels were monitored. Phenotypic characterization of glucose metabolism was performed using glucose and insulin tolerance tests. β-Cell mass, islet volume, and islet number were analyzed by histomorphometry. APP/PS1 coexpression in mice with intact leptin receptor signaling did not show any metabolic perturbations in glucose metabolism or insulin sensitivity. In contrast, APP/PS1 coexpression in db/+ mice resulted in nonfasting hyperglycemia, hyperinsulinemia, and hypercholesterolemia without changes in body weight. Conversely, fasting blood glucose and cholesterol levels remained unchanged. Coinciding with altered glucose metabolism, APP/PS1 coexpression in db/+ mice resulted in glucose intolerance, insulin resistance, and impaired insulin signaling. In addition, histomorphometric analysis of pancreata revealed augmented β-cell mass. Taken together, these findings provide experimental evidence to support the notion that aberrant Aβ production might be a mechanistic link underlying the pathology of insulin resistance and T2D in AD.

scholarly journals Association between maternal triglycerides and disturbed glucose metabolism in pregnancy

2021 ◽  
Author(s):  
Daniel Eppel ◽  
Michael Feichtinger ◽  
Tina Lindner ◽  
Grammata Kotzaeridi ◽  
Ingo Rosicky ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Gestational Diabetes ◽  
Pregnant Women ◽  
Early Pregnancy ◽  
Early Gestation ◽  
Glucose Levels ◽  
Increased Risk ◽  
Mean Glucose ◽  
In Pregnancy

Abstract Aims Dyslipidemia in pregnancy is associated with adverse pregnancy outcomes as elevated triglycerides might be considered as a risk factor for hyperglycemia and gestational diabetes. As only a few studies have addressed the association between maternal triglycerides and glucose metabolism, we aimed to explore the pathophysiologic associations of moderate hypertriglyceridemia and maternal glucose metabolism in pregnancy. Methods Sixty-seven pregnant women received a detailed metabolic characterization at 12+0–22+6 weeks of gestation by an extended 2h-75g OGTT (oral glucose tolerance test); with measurements of glucose, insulin and C-peptide at fasting and every 30 min after ingestion and assessment of triglycerides at fasting state. All examinations were repeated at 24+0–27+6 weeks of gestation. Results Elevated triglycerides in early gestation were associated with insulin resistance and β-cell dysfunction. Mean glucose concentrations during the OGTT in early pregnancy were already higher in women with hypertriglyceridemia as compared to women with triglycerides in the normal range. A higher degree of insulin resistance and increased OGTT glucose levels were also observed when metabolic assessments were repeated between 24 and 28 weeks of gestation. Of note, elevated triglycerides at early gestation were associated with development of gestational diabetes by logistic regression (odds ratio: 1.16, 95%CI: 1.03–1.34, p=0.022 for an increase of 10 mg/dl). Conclusions Hypertriglyceridemia at the start of pregnancy is closely related to impaired insulin action and β-cell function. Women with hypertriglyceridemia have higher mean glucose levels in early- and mid-gestation. Pregnant women with elevated triglycerides in early pregnancy are at increased risk of developing gestational diabetes.

scholarly journals Sex differences in glucose metabolism of streptozotocin-induced diabetes inbred mice (C57BL/6J)

2020 ◽  
Vol 63 (1) ◽  
Author(s):  
Boyoung Kim ◽  
Yoo Yeon Kim ◽  
Phuong Thi-Thanh Nguyen ◽  
Hajin Nam ◽  
Jun Gyo Suh
Keyword(s):  
Insulin Resistance ◽  
Sex Differences ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Inbred Mice ◽  
Glycosylated Hemoglobin ◽  
Fasting Blood Glucose ◽  
Oral Glucose ◽  
Model Assessment ◽  
Female Mice

Abstract Considering that sex differences in glucose metabolism are observed in mice, researchers unconsciously use male mice to reduce variations by an estrogen cycle in female mice. In this study, we investigated the sex differences in glucose homeostasis in streptozotocin (STZ)-induced diabetes inbred mice (C57BL/6J). The C57BL/6J male and female mice were injected with or without STZ (40 mg/kg) for 5 consecutive days. Levels of fasting blood glucose (FBG), glycosylated hemoglobin (HbA1C), lipid profiles, oral glucose tolerance, and insulin resistance were measured at 3 and 6 weeks after STZ treatment. The FBG level in the STZ-induced male (M-STZ) group was significantly higher than that in the STZ-induced female (F-STZ) group during the entire experimental period. Furthermore, HbA1C and glucose tolerance levels in the M-STZ group were significantly higher than those in the F-STZ group at 3 and 6 weeks after STZ treatment. The glucagon/insulin ratio in the M-STZ group was significantly higher than that in the F-STZ group. Values of the homeostatic model assessment-insulin resistance, an indicator of β-cell function and insulin resistance, significantly increased in both the M-STZ and F-STZ groups at 3 weeks after STZ treatment. However, insulin resistance was observed in the M-STZ group, but not in the F-STZ group, at 6 weeks after STZ treatment. Taken together, our results indicate that glucose metabolism in the M-STZ group was worse than that in the F-STZ group, indicating that estrogen may have an important role in glucose metabolism by STZ treatment.

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