Increased Plasma Levels of FABP4 and PTEN Is Associated with More Severe Insulin Resistance in Women with Gestational Diabetes Mellitus

Li, Yuanyuan; Xiao, Rui; Li, Caiping; Huangfu, Jian; Mao, Jiangfeng

doi:10.12659/msm.892431

Cited by 50 publications

(34 citation statements)

References 27 publications

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“…the GDM group had a higher AFABP level than did the control group. A second cross‐sectional study12 showed that AFABP levels in the GDM group were significantly higher than those of controls, and that AFABP was an independent risk factor for increased insulin resistance. Another cross‐sectional study showed inconsistent results.…”

Section: Discussionmentioning

confidence: 98%

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Changes in serum adipocyte fatty acid‐binding protein in women with gestational diabetes mellitus and normal pregnant women during mid‐ and late pregnancy

Zhang

Lü

et al. 2016

J of Diabetes Invest

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Aims/IntroductionTo observe the longitudinal changes in serum adipocyte fatty acid‐binding protein (AFABP), carbohydrate, and lipid metabolism parameters in women with and without gestational diabetes mellitus (GDM) during mid‐ and late pregnancy periods, as well as to identify whether there is any association between AFABP and development of GDM.Materials and MethodsA total of 40 GDM and 240 normal glucose tolerance participants were enrolled at 24–28 weeks and completed the study. The clinical features, serum AFABP, other adipocytokines (leptin, adiponectin, retinol‐binding protein 4), homeostasis model assessment of insulin resistance, and lipid profiles were measured in the second and third trimesters of pregnancy.ResultsCompared with the normal glucose tolerance group, the GDM group showed greater levels of AFABP, leptin and retinol‐binding protein 4; and a decreased level of adiponectin (P < 0.05 or P < 0.01) during mid‐ and late pregnancy periods. Prepregnancy body mass index was the independent factor impacting serum AFABP levels in the second (β = 0.567, P = 0.004) and third trimesters (β = 0.619, P = 0.001). Furthermore, GDM was independently associated with AFABP concentrations in multiple regression analysis in the second and third trimester (all P < 0.01). Serum AFABP, leptin and retinol‐binding protein 4 are risk factors for GDM; adiponectin is a protective factor for GDM (P < 0.05 or P < 0.01).ConclusionsThe GDM group had a higher level of AFABP during mid‐ and late stages of pregnancy; prepregnancy body mass index and GDM were the independent factors with respect to serum AFABP. AFABP might be closely related to obesity, insulin resistance and leptin resistance in pregnancy, and is a major risk factor for GDM.

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Section: Discussionmentioning

confidence: 98%

“…We know of few studies where the level of AFABP in GDM women has been determined11, 12, 13, and results have been contradictory. For example, it has not been well documented whether AFABP is associated with the pathogenesis of GDM.…”

Section: Introductionmentioning

confidence: 99%

Changes in serum adipocyte fatty acid‐binding protein in women with gestational diabetes mellitus and normal pregnant women during mid‐ and late pregnancy

Zhang

Lü

et al. 2016

J of Diabetes Invest

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“…For the liver, aberrant PI3K/AKT signaling has increasingly emerged as one of the major reasons for liver dysfunction and the metabolic syndrome10. A number of external stimuli and substantial regulators were indicated to regulate the activity of PI3K/ AKT signaling11. Among them, phosphatase and tensin homolog deleted on chromosome 10 (PTEN) antagonizes PI3K actions to negatively regulate the phosphorylation of AKT.…”

mentioning

confidence: 99%

Hepatic MiR-291b-3p Mediated Glucose Metabolism by Directly Targeting p65 to Upregulate PTEN Expression

Guo

Dou

Meng

et al. 2017

Sci Rep

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Several studies have suggested an important role of miR-291b-3p in the development of embryonic stem cells. In previous study, we found that the expression of miR-291b-3p was significantly upregulated in the liver of db/db mice. However, the role of miR-291b-3p in glucose metabolism and its underlying mechanisms remain unknown. In the present study, we demonstrated that miR-291b-3p was abundantly expressed in the liver. Of note, hepatic miR-291b-3p expression was upregulated in HFD-fed mice and induced by fasting in C57BL/6 J normal mice. Importantly, hepatic inhibition miR-291b-3p expression ameliorated hyperglycemia and insulin resistance in HFD-fed mice, whereas hepatic overexpression of miR-291b-3p led to hyperglycemia and insulin resistance in C57BL/6 J normal mice. Further study revealed that miR-291b-3p suppressed insulin-stimulated AKT/GSK signaling and increased the expression of gluconeogenic genes in hepatocytes. Moreover, we identified that p65, a subunit of nuclear factor-κB (NF-κB), is a target of miR-291b-3p by bioinformatics analysis and luciferase reporter assay. Silencing of p65 significantly augmented the expression of PTEN and impaired AKT activation. In conclusion, we found novel evidence suggesting that hepatic miR-291b-3p mediated glycogen synthesis and gluconeogenesis through targeting p65 to regulate PTEN expression. Our findings indicate the therapeutic potential of miR-291b-3p inhibitor in hyperglycemia and insulin resistance.

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“…Fatty acid-binding protein 4 (FABP4) is an important carrier of intracellular fatty acids [48]. Its role in the development of metabolic disorders, type 2 diabetes and insulin resistance during pregnancy and GDM is of interest to many scientists.…”

Section: Factors Affecting Insulin Resistance In Pregnancymentioning

confidence: 99%

“…One study showed that higher FABP4 concentrations are associated with higher insulin resistance in patients with GDM, which may be one of the pathomechanisms responsible for GDM development [48]. Subsequent studies of larger patient groups confirmed that FABP4 is associated with insulin resistance during pregnancy and its higher concentrations in the first trimester are associated with an increased risk of developing GDM and may be early clinical markers of GDM [49][50][51].…”

Section: Factors Affecting Insulin Resistance In Pregnancymentioning

confidence: 99%

Insulin resistance and adaptation of pancreatic beta cells during pregnancy

Zielinska–Maciulewska

Krętowski

Szelachowska

2018

Clinical Diabetology

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Insulin resistance is described as reduced sensitivity of the body tissues to insulin. In pregnant women insulin resistance increases during each trimester of pregnancy due to the hormones produced by the placenta and many other factors which are not yet fully recognised. Growing insulin resistance leads to an increase in beta cell mass and number and insulin secretion, which helps to maintain glucose homeostasis and normal foetal development. However, in cases of severe insulin resistance, insufficient compensation of pancreatic beta cells or reduced pancreatic beta-cell function, glycaemic levels are increased and gestational diabetes mellitus develops. The aim of the present review is to analyse the factors affecting insulin resistance and the adaptation of pancreatic beta cells during pregnancy and methods of insulin resistance assessment.

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Increased Plasma Levels of FABP4 and PTEN Is Associated with More Severe Insulin Resistance in Women with Gestational Diabetes Mellitus

Cited by 50 publications

References 27 publications

Changes in serum adipocyte fatty acid‐binding protein in women with gestational diabetes mellitus and normal pregnant women during mid‐ and late pregnancy

Changes in serum adipocyte fatty acid‐binding protein in women with gestational diabetes mellitus and normal pregnant women during mid‐ and late pregnancy

Hepatic MiR-291b-3p Mediated Glucose Metabolism by Directly Targeting p65 to Upregulate PTEN Expression

Insulin resistance and adaptation of pancreatic beta cells during pregnancy

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