scholarly journals Gestational Diabetes Mellitus a Dysfunctional Metabolic State-A Perspective

2019 ◽  
Vol 1 (2) ◽  
pp. 24-28
Author(s):  
Dhastagir Sultan Sheriff ◽  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Beta Cell ◽  
Glucose Intolerance ◽  
Fat Deposition ◽  
Fine Tuning ◽  
Lipid Deposition ◽  
Metabolic State

Pregnancy is considered as a test for beta cell reserve. If there is a good function, insulin resistance will overcome. If not, gestational diabetes will occur. Insulin resistance (IR) present in normal pregnancy is required to provide nutrients to the growing fetus. There is a rapid increase of insulin in such an insulin resistant state. The possibility of lipid deposition in muscle fibers (intramyocellular) could be one of the possible mechanism of IR in gestational diabetes mellitus (GDM). The poor response of insulin release, possible fat deposition in the skeletal muscle or ectopic fat deposition may cause dysfunctional homeostasis in GDM. This will definitely influence the fine tuning of metabolic machinery of a growing fetus. Children born with such subtle metabolic state will probably be more prone to glucose intolerance and ectopic lipid deposition. The finding that children born to GDM mothers are prone to glucose intolerance may be an eye-opener to monitor such children for beta cell function.

Abstract MP70: Pre-pregnancy Beta Cell Compensation for Insulin Resistance Associated With Subsequent Gestational Diabetes Mellitus: The CARDIA Study

Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Erica P Gunderson ◽  
Amy Krefman ◽  
Cora E Lewis ◽  
Janet Catov ◽  
Norrina B Allen
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Family History ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Beta Cell ◽  
Pancreatic Beta Cell ◽  
Family History Of Diabetes ◽  
History Of ◽  
Beta Cell Compensation

Hypothesis: Gestational diabetes mellitus (GDM) is a disorder of glucose metabolism during pregnancy characterized by pancreatic beta cell dysfunction and greater insulin resistance, but it is unclear whether dysfunction exists before pregnancy. The disposition index (DI) is a physiologic measure of beta cell compensation for insulin resistance strongly predictive of future diabetes. This prospective study evaluates whether a clinical approximation of DI before pregnancy is associated with risk of GDM. Methods: This analysis included 696 women (45% black, 55% white) enrolled in the CARDIA Study, a U.S. multi-center prospective cohort of young adults aged 18-30 at baseline (1985-86) who gave birth at least once during 30 years of follow up, reported GDM status and had fasting glucose and insulin measured before one or more post-baseline births. DI was defined as HOMA-B divided by HOMA-IR using standard formulas. Multinomial logistic regression models estimated odds ratios (OR) and 95%CI for GDM among pre-pregnancy DI tertiles (low, moderate, high) and fully adjusted for time to birth, race, age, parity, BMI, lifestyle behaviors and family history of diabetes, and also stratified by pre-pregnancy BMI. Results: 9% of women reported GDM (64/696) for 794 births. 55% of GDM and 30% of non-GDM were categorized as low DI. Low pre-pregnancy DI compared to moderate DI was associated with higher fully adjusted odds of GDM (OR=2.71, 95%CI:1.37-5.35) in the entire sample. In models stratified by pre-pregnancy BMI, low DI was associated with 4-fold higher odds of GDM among Overweight/Obese (OR=4.22, 95%CI: 1.35-13.91) and somewhat attenuated higher odds of GDM among Normal BMI (OR=1.94, 95%CI: 0.78–4.86); Table 1. Only family history of diabetes was strongly associated with GDM independent of DI. Conclusions: Inadequate beta cell compensation is present before pregnancy and discriminates greatest risk of GDM among high BMI, and may identify higher risk among women of normal BMI.

The Infant Born to a Woman with Gestational Diabetes

2017 ◽  
Vol 36 (4) ◽  
pp. 239-244 ◽  
Author(s):  
Theresa Povinelli ◽  
Caitlin Lim ◽  
Deborah A. Raines
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Amino Acids ◽  
Gestational Diabetes ◽  
Glucose Tolerance ◽  
Gestational Diabetes Mellitus ◽  
Glucose Intolerance ◽  
Frequent Episodes ◽  
Altered Glucose

AbstractGestational diabetes mellitus (GDM) is defined as glucose intolerance with onset during pregnancy. During pregnancy, women with GDM develop insulin resistance, which results in altered glucose tolerance. As a result, there are frequent episodes of hyperglycemia and high levels of circulating amino acids, increasing the transfer of nutrients to the fetus. This article discusses the role of the mother–baby nursing in the care of neonates born to women with gestational diabetes.

scholarly journals Arsenic exposure during pregnancy and postpartum maternal glucose tolerance: evidence from Bangladesh

2022 ◽  
Vol 21 (1) ◽  
Author(s):  
Abby F. Fleisch ◽  
Sudipta Kumer Mukherjee ◽  
Subrata K. Biswas ◽  
John F. Obrycki ◽  
Sheikh Muhammad Ekramullah ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Arsenic Exposure ◽  
Pregnancy And Postpartum ◽  
Exposure During Pregnancy

Abstract Background Arsenic exposure has been associated with gestational diabetes mellitus. However, the extent to which arsenic exposure during pregnancy is associated with postpartum glucose intolerance is unknown. Methods We studied 323 women in Bangladesh. We assessed arsenic exposure in early pregnancy via toenail and water samples. We measured fasting glucose and insulin in serum at a mean (SD) of 4.0 (3.5) weeks post-delivery. We ran covariate-adjusted, linear regression models to examine associations of arsenic concentrations with HOMA-IR, a marker of insulin resistance, and HOMA-β, a marker of beta cell function. Results Median (IQR) arsenic concentration was 0.45 (0.67) μg/g in toenails and 2.0 (6.5) μg/L in drinking water. Arsenic concentrations during pregnancy were not associated with insulin resistance or beta cell function postpartum. HOMA-IR was 0.07% (− 3.13, 3.37) higher and HOMA-β was 0.96% (− 3.83, 1.99) lower per IQR increment in toenail arsenic, but effect estimates were small and confidence intervals crossed the null. Conclusions Although arsenic exposure during pregnancy has been consistently associated with gestational diabetes mellitus, we found no clear evidence for an adverse effect on postpartum insulin resistance or beta cell function.

scholarly journals Plasma retinol-binding protein 4 in the first and second trimester and risk of gestational diabetes mellitus in Chinese women: a nested case-control study

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Chuyao Jin ◽  
Lizi Lin ◽  
Na Han ◽  
Zhiling Zhao ◽  
Zheng Liu ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Binding Protein ◽  
First Trimester ◽  
Retinol Binding Protein ◽  
Second Trimester ◽  
Retinol Binding Protein 4 ◽  
Plasma Retinol

Abstract Background To assess the association between plasma retinol-binding protein 4 (RBP4) levels both in the first trimester and second trimester and risk of gestational diabetes mellitus (GDM). Methods Plasma RBP4 levels and insulin were measured among 135 GDM cases and 135 controls nested within the Peking University Birth Cohort in Tongzhou. Multivariable linear regression analysis was conducted to assess the influence of RBP4 levels on insulin resistance. Conditional logistic regression models were used to compute the odds ratio (OR) and 95% confidence interval (CI) between RBP4 levels and risk of GDM. Results The GDM cases had significantly higher levels of RBP4 in the first trimester than controls (medians: 18.0 μg/L vs 14.4 μg/L; P < 0.05). Plasma RBP4 concentrations in the first and second trimester were associated with fasting insulin, homeostasis model assessment for insulin resistance (HOMA-IR), and the quantitative insulin sensitivity check index (QUICKI) in the second trimester (all P < 0.001). With adjustment for diet, physical activity, and other risk factors for GDM, the risk of GDM increased with every 1-log μg/L increment of RBP4 levels, and the OR (95% CI) was 3.12 (1.08–9.04) for RBP4 in the first trimester and 3.38 (1.03–11.08) for RBP4 in the second trimester. Conclusions Plasma RBP4 levels both in the first trimester and second trimester were dose-dependently associated with increased risk of GDM.

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