The insulin response to glucose infusion in normal human pregnancy

Fisher, Peter; Sutherland, H. W.; Bewsher, P. D.

doi:10.1007/bf00258304

Cited by 36 publications

(17 citation statements)

References 33 publications

(33 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…17;21–23;26–28;42;58;64;103;104;106;109;149;157;164;177 This important metabolic alteration is thought to be induced by placental hormones. Several lines of evidence support this view: 1) in vitro, exposure of adipocytes to progesterone, cortisol, prolactin, or human placental lactogen, induced post binding defect in insulin action; 163 2) insulin resistance can be induced by administration of human placental lactogen (HPL), 92;165 progesterone, 14;41;91 estrogen 41;150 and glucocorticosteroids 92 to non-pregnant subjects and mice; 13 and 3) insulin resistance during pregnancy rises in the third trimester 17;21;29;164;176;193 with the increase in the placental hormone secretion.…”

Section: Discussionmentioning

confidence: 99%

Maternal visfatin concentration in normal pregnancy

Mazaki‐Tovi¹,

Romero²,

Kusanovic³

et al. 2008

Journal of Perinatal Medicine

View full text Add to dashboard Cite

Objective Adipose tissue has now emerged as a powerful endocrine organ via the production of adipokines. Visfatin, a novel adipokine with diabetogenic and immunomodulatory properties has been implicated in the pathophysiology of insulin resistance in patients with obesity and Type-2 diabetes mellitus. The aim of this study was to determine whether there are changes in the maternal plasma concentration of visfatin with advancing gestation and as a function of maternal weight. Study design In this cross-sectional study, maternal plasma concentrations of visfatin were determined in normal weight and overweight/obese pregnant women in the following gestational age groups: 1) 11–14 weeks (n= 52); 2) 19–26 weeks (n=68); 3) 27–34 weeks (n=93); and 4) >37 weeks (n=60). Visfatin concentrations were determined by ELISA. Non parametric statistics were used for analysis. Results 1) The median maternal plasma visfatin concentration was higher in pregnant women between 19–26 weeks of gestation than that of those between 11–14 weeks of gestation (p<0.01) and those between 27–34 weeks of gestation (p <0.01); 2) among normal weight pregnant women, the median plasma visfatin concentrations of women between 19–26 weeks of gestation was higher than that of those between 11–14 weeks (p<0.01) and those between 27–34 weeks (p < 0.01); and 3) among overweight/obese patients, the median maternal visfatin concentration was similar between the different gestational age groups Conclusion The median maternal plasma concentration of visfatin peaks between 19–26 and has a nadir between 27–34 weeks of gestation. Normal and overweight/obese pregnant women differed in the pattern of changes in circulating visfatin concentrations as a function of gestational age.

show abstract

Section: Discussionmentioning

confidence: 99%

Maternal visfatin concentration in normal pregnancy

Mazaki‐Tovi¹,

Romero²,

Kusanovic³

et al. 2008

Journal of Perinatal Medicine

View full text Add to dashboard Cite

show abstract

“…As gestation progresses, insulin secretion increases, reaching a maximum in the third trimester [50][51][52][53] whereas insulin sensitivity decreases progressively by about 70% [51][52][53][54][55][56][57][58]. In normal pregnancy, pancreatic beta cells compensate for the increased insulin resistance to control blood glucose [55,56].…”

Section: Pathophysiology Of Gdmmentioning

confidence: 99%

Genetics of Gestational Diabetes Mellitus

Shaat¹,

Groop

2007

CMC

View full text Add to dashboard Cite

About 2-5% of all pregnant women develop gestational diabetes mellitus (GDM) during their pregnancies and the prevalence has increased considerably during the last decade. GDM is a heterogeneous disorder that is defined as carbohydrate intolerance with onset or first recognition during pregnancy. It is manifested when pancreatic beta cells are no longer able to compensate for the increased insulin resistance during pregnancy, but the pathogenesis of the disease is still largely unknown. GDM is considered to result from interaction between genetic and environmental risk factors. Genetic predisposition to GDM has been suggested since GDM clusters in families. Also, women with mutations in MODY (Maturity onset diabetes of the young) genes often present with GDM. In addition, common variants in several candidate genes (e.g. potassium inwardly rectifying channel subfamily J, member 11 [KCNJ11], Glucokinase [GCK], Hepatocyte nuclear factor-1alpha [HNF1A] etc.) have been demonstrated to increase the risk of GDM. Old age, obesity and high fat diet represent some important non-genetic factors. There are several approaches to search for genes predisposing to a polygenic disease like GDM including linkage and association studies, expression profiling and animal models. A combination of several methods is usually necessary. Identification of the underlying genetic causes of GDM will eventually give a better view of the mechanisms that contribute to the pathophysiology of the disease. Furthermore, it may improve options to possibly prevent GDM and complications for the mother and her child. This review focuses on the genetics of GDM and possible implications in clinical practice.

show abstract

“…Pregnancy is a unique condition characterized by transient physiologic insulin resistance 21;24;25;30–32;58;65;105;109;114;158;167;177 which progresses with advancing gestation and approaches that of non-pregnant patients with type-2 diabetes mellitus (DM). 18 Teleologically, this physiological adaptation is aimed to facilitate delivery of nutrients to the fetus.…”

Section: Introductionmentioning

confidence: 99%

Visfatin in human pregnancy: maternal gestational diabetesvis-à-visneonatal birthweight

Mazaki‐Tovi¹,

Romero²,

Kusanovic³

et al. 2008

Journal of Perinatal Medicine

View full text Add to dashboard Cite

Objective Adipose tissue dysfunction, characterized by dysregulation of adipokines production and/or secretion, has been implicated in the pathophysiology of type-2 diabetes mellitus, a metabolic complication closely related to gestational diabetes mellitus (GDM). Recently, an association between circulating maternal visfatin, a novel adipokine with metabolic and immunoregulatory properties, and impaired glucose metabolism as well as with altered fetal growth, has been proposed. The aims of this study were to determine whether there is an association between maternal plasma visfatin concentration, GDM, and a large-for-gestational-age (LGA) newborn. Study design This cross-sectional study, included pregnant women at term in the following groups: 1) normal pregnancy and an appropriate-for-gestational-age (AGA) neonate (n=54); 2) normal pregnancy and an LGA newborn (n=47); 3) GDM and an AGA newborn (n=56); 4) GDM and an LGA newborn (n=45). The study population was further stratified by first trimester BMI (<25 vs. ≥25 kg/m2). Maternal plasma visfatin concentration was determined by ELISA. Parametric and non-parametric statistics were used for analysis. Results 1) Among women who delivered an AGA neonate, the median maternal plasma concentration of visfatin was higher in patients with GDM than in those with a normal pregnancy; 2) Among women with a normal pregnancy, those who delivered an LGA neonate had a higher median maternal plasma visfatin concentration than those who delivered an AGA neonate; 3) among patients with normal BMI, there were no significant differences in the median maternal plasma visfatin concentration between the four study groups; and 4) maternal GDM, as well as delivery of an LGA neonate were independently associated with a higher maternal plasma visfatin concentrations. Conclusion The linkage between increased maternal circulating visfatin and the presence of GDM or delivery of an LGA neonate supports the hypothesis that perturbation of adipokines homeostasis may play a role in the pathophysiology of GDM or excess fetal growth.

show abstract

The insulin response to glucose infusion in normal human pregnancy

Cited by 36 publications

References 33 publications

Maternal visfatin concentration in normal pregnancy

Maternal visfatin concentration in normal pregnancy

Genetics of Gestational Diabetes Mellitus

Visfatin in human pregnancy: maternal gestational diabetesvis-à-visneonatal birthweight

Contact Info

Product

Resources

About