Adiponectin and β-Cell Adaptation in Pregnancy

Retnakaran, Ravi

doi:10.2337/dbi17-0001

Cited by 20 publications

(18 citation statements)

References 22 publications

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“…Additionally, the chronic exposure of isolated human islets to leptin, an adipokine also increased during GDM, blunted on one hand the production of the IL-1 receptor antagonist (IL-1Ra), that inhibits IL-1β signaling, and on the other hand induced IL-1β release leading to impaired β-cell function, caspase-3 activation and apoptosis [70]. Moreover, low levels of the antidiabetic adipokine adiponectin have been associated with β-cell dysfunction in women with GDM [71]. Studies in mice have recently shown that this adipokine is involved in β-cell expansion during gestation, without affecting the secretory function of the β-cells [72].…”

Section: Inflammation Underlying Gdm Development and Derived Adverse mentioning

confidence: 99%

Molecular Modelling of Islet β-Cell Adaptation to Inflammation in Pregnancy and Gestational Diabetes Mellitus

Lorenzo

Martín-Montalvo

Vuilleumier

et al. 2019

IJMS

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Gestational diabetes mellitus (GDM), a metabolic disease that develops with the increase in insulin resistance during late pregnancy, is currently one of the most common complications affecting pregnancy. The polygenic nature of GDM, together with the interplay between different genetic variants with nutritional and environmental factors has hindered the full understanding of the etiology of this disease. However, an important genetic overlap has been found with type 2 diabetes mellitus (T2DM) and, as in the case of T2DM, most of the identified loci are associated with β-cell function. Early detection of GDM and adequate interventions to control the maternal glycemia are necessary to avoid the adverse outcomes for both the mother and the offspring. The in utero exposure to the diabetic milieu predispose these children for future diseases, among them T2DM, originating a vicious circle implicated in the increased prevalence of both GDM and T2DM. The involvement of inflammatory processes in the development of GDM highlights the importance of pancreatic β-cell factors able to favor the adaptation processes required during gestation, concomitantly with the protection of the islets from an inflammatory milieu. In this regard, two members of the Pax family of transcription factors, PAX4 and PAX8, together with the chromatin remodeler factor HMG20A, have gained great relevance due to their involvement in β-cell mass adaptation together with their anti-inflammatory properties. Mutations in these factors have been associated with GDM, highlighting these as novel candidates for genetic screening analysis in the identification of women at risk of developing GDM.

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Section: Inflammation Underlying Gdm Development and Derived Adverse mentioning

confidence: 99%

Molecular Modelling of Islet β-Cell Adaptation to Inflammation in Pregnancy and Gestational Diabetes Mellitus

Lorenzo

Martín-Montalvo

Vuilleumier

et al. 2019

IJMS

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“…The authors observed that adiponectin stimulated the β-cell proliferation and impaired the islet mass without differences in insulin sensitivity effects in comparison to the deficient group (4,62,63) . This finding allows suggesting another mechanism on insulin besides the well-established insulinsensitising property of this adipokine (62,63) . In humans, pregnant women present this phenomenon of β-cell proliferation without increase in islet mass, but this particular study was limited because it was conducted in women who died during pregnancy (64) .…”

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confidence: 98%

Longitudinal association of 25-hydroxyvitamin D with adipokines and markers of glucose metabolism among Brazilian pregnant women

Benaim

Cocate

Barros³

et al. 2018

Br J Nutr

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This study aimed to evaluate the longitudinal association of vitamin D status with glycaemia, insulin, homoeostatic model assessment of insulin resistance, adiponectin and leptin. A prospective cohort with 181 healthy, pregnant Brazilian women was followed at the 5th–13th, 20th–26th and 30th–36th gestational weeks. In this cohort, 25-hydroxyvitamin D (25(OH)D) plasma concentrations were analysed using liquid chromatography–tandem MS. Vitamin D status was categorised as sufficient or insufficient using the Endocrine Society Practice Guidelines (≥75/<75 nmol/l) and the Institute of Medicine (≥50/<50 nmol/l) thresholds. Linear mixed-effect regression models were employed to evaluate the association between vitamin D status and each outcome, considering interaction terms between vitamin D status and gestational age (P<0·1). At baseline, 70·7 % of pregnant women had 25(OH)D levels <75 nmol/l and 16 % had levels <50 nmol/l. Women with sufficient vitamin D status at baseline, using both thresholds, presented lower glycaemia than those with insufficient 25(OH)D. Pregnant women with 25(OH)D concentrations <75 nmol/l showed lower insulin (β=−0·12; 95 % CI −0·251, 0·009;P=0·069) and adiponectin (β=−0·070; 95 % CI −0·150, 0·010;P=0·085) concentrations throughout pregnancy than those with 25(OH)D levels ≥75 nmol/l. Pregnant women with 25(OH)D <50 nmol/l at baseline presented significantly higher leptin concentrations than those with 25(OH)D levels ≥50 nmol/l (β=−0·253; 95 % CI −0·044, 0·550;P=0·095). The baseline status of vitamin D influences the biomarkers involved in glucose metabolism. Vitamin D-sufficient women at baseline had higher increases in insulin and adiponectin changes throughout gestation than those who were insufficient.

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“…Second, hypoadiponectinemia in early pregnancy, or even prior to gestation, can predict the subsequent development of GDM in 2nd/3rd trimester [ 23 – 25 ]. Third, it has recently been demonstrated that genetic knock-out of adiponectin results in impaired beta-cell adaptation to pregnancy in mice, thereby yielding a murine model of gestational dysglycemia and potentially linking adiponectin to the pathophysiologic basis of GDM (insufficient beta-cell compensation for the insulin resistance of pregnancy) [ 26 , 27 ]. Taken together with the current demonstration that women with recent GDM have low adiponectin at both 1- and 3-years after delivery, these data collectively suggest that hypoadiponectinemia is a chronic feature of this patient population before, during, and after pregnancy.…”

Section: Discussionmentioning

confidence: 99%

Rising plasminogen activator inhibitor-1 and hypoadiponectinemia characterize the cardiometabolic biomarker profile of women with recent gestational diabetes

Mehmood

Connelly

et al. 2018

Cardiovasc Diabetol

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BackgroundGestational diabetes (GDM) and milder gestational impaired glucose tolerance (GIGT) identify women at risk of developing type 2 diabetes and cardiovascular disease later in life. Accordingly, the postpartum years after gestational dysglycemia can provide insight into early events in the natural history of these disorders. We thus sought to prospectively evaluate the relationship between gestational glucose tolerance and emerging cardiometabolic biomarkers [adiponectin, chemerin, retinol-binding protein-4 (RBP-4), C-reactive protein (CRP), plasminogen activator inhibitor-1 (PAI-1)] at both 1- and 3-years postpartum in a cohort reflecting the full spectrum of gestational dysglycemia (from normal to GIGT to GDM).MethodsThree-hundred-and-thirty-nine women completed a glucose challenge test (GCT) and oral glucose tolerance test (OGTT) in pregnancy, which identified 4 gestational glucose tolerance groups: GDM (n = 105); GIGT (n = 59); abnormal GCT with normal OGTT (n = 99); and normal GCT with normal OGTT (n = 76). At 1- and 3-years postpartum, the women underwent repeat OGTT with measurement of biomarkers (adiponectin/chemerin/RBP-4/CRP/PAI-1).ResultsSerum adiponectin was lower in women with GDM and GIGT at both 1-year and 3-years (both P ≤ 0.002), whereas chemerin, RBP-4, CRP and PAI-1 showed no differences across the 4 groups. Importantly, the change in PAI-1 between 1- and 3-years progressively increased from the normal GCT group to the abnormal GCT group to GIGT to GDM (P = 0.03). Indeed, both GDM (t = 2.98, P = 0.003) and GIGT (t = 2.14, P = 0.03) independently predicted an increase in PAI-1 from 1- to 3-years postpartum.ConclusionsHypoadiponectinemia and rising PAI-1 over time are early features of the cardiometabolic biomarker profile of women with recent gestational dysglycemia.Electronic supplementary materialThe online version of this article (10.1186/s12933-018-0776-y) contains supplementary material, which is available to authorized users.

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Adiponectin and β-Cell Adaptation in Pregnancy

Cited by 20 publications

References 22 publications

Molecular Modelling of Islet β-Cell Adaptation to Inflammation in Pregnancy and Gestational Diabetes Mellitus

Molecular Modelling of Islet β-Cell Adaptation to Inflammation in Pregnancy and Gestational Diabetes Mellitus

Longitudinal association of 25-hydroxyvitamin D with adipokines and markers of glucose metabolism among Brazilian pregnant women

Rising plasminogen activator inhibitor-1 and hypoadiponectinemia characterize the cardiometabolic biomarker profile of women with recent gestational diabetes

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