Measurement of glucose metabolism and insulin secretion during normal pregnancy and pregnancy complicated by gestational diabetes

Bowes, S. B.; Hennessy, T. R.; Umpleby, AM; Benn, Jonathan; Jackson, Nicola; Boroujerdi, M; Sönksen, P. H.; Lowy, C.

doi:10.1007/bf00403918

Cited by 57 publications

(23 citation statements)

References 28 publications

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“…Although the pathophysiological mechanisms of GDM have not been fully elucidated, it was well known that the insufficient adaptability of pancreatic β cell to insulin resistance, which is characterized by mid‐late pregnancy, maybe the primary cause of GDM . During normal pregnancy, the stability of glucose in pregnant women depends on the physiological accumulation of insulin secretion; furthermore, this compensatory accumulation is closely related to the biological functions of pancreatic β cells: it is speculated that several regulatory molecules, such as cell growth regulator, which can regulate the biological function of the pancreatic β cell, play a crucial effect in these adaptive changes to meet these compensatory requirements . Therefore, studies about β cells upstream and downstream regulatory factors could make a lot of sense to develop a new treatment target for GDM …”

Section: Introductionmentioning

confidence: 99%

MiR‐330‐3p contributes to INS‐1 cell dysfunction by targeting glucokinase in gestational diabetes mellitus

Xiao

Ding

Shi³

et al. 2020

J of Obstet and Gynaecol

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Aims: High-expressed miR-330-3p in gestational diabetes mellitus (GDM) patients was reported. However, the role and mechanism of miR-330-3p in GDM are rarely reported. In this research, we aim to investigate the effects of miR-330-3p on GDM. Methods: MiR-330-3p expression in the GDM patients' blood was determined by q-PCR. Blood glucose of blood samples was detected using blood glucose detection kits. Glucokinase (GCK) was confirmed to be a target gene of miR-330-3p by bioinformatics and luciferase analysis. Correlations between miR-330-3p with GCK and blood glucose were analyzed by Pearson correlation analysis. After INS-1 cells were treated with glucose and transfected with mimic, inhibitor or siGCK, GCK expression was detected by western blot, and q-PCR, enzyme-linked immunosorbent assays, cell counting kit-8 and Annexin-V/propidium iodide were conducted to examine the expression of insulin, cell viability and apoptosis. Results: MiR-330-3p was high-expressed in GDM patients' blood, while GCK was low-expressed. The miR-330-3p expression level positively correlated with blood glucoseand and it was highly expressed in glucosetreated INS-1 cells (11 and 22 mmol/L), while miR-330-3p expression negatively correlated with GCK expression. GCK expression was inhibited by miR-330-3p mimic and enhanced by the miR-330-3p inhibitor. MiR-330-3p mimic inhibited INS-1 cells' insulin expression, cell viability and induced apoptosis. Yet miR-330-3p inhibitor and siGCK exhibited opposite effects which miR-330-3p mimic and GCK played on INS-1 cells. In addition, siGCK reversed the effect of miR-330-3p inhibitor on INS-1 cells. Conclusion: Our findings proved that miR-330-3p targeting GCK lead to the dysfunction of INS-1 cells in GDM, and could become a therapeutic target for GDM treatment.

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Section: Introductionmentioning

confidence: 99%

MiR‐330‐3p contributes to INS‐1 cell dysfunction by targeting glucokinase in gestational diabetes mellitus

Xiao

Ding

Shi³

et al. 2020

J of Obstet and Gynaecol

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“…2) A physiologic increase in insulin resistance that occurs in all women during the second half of pregnancy and disappears postpartum. Supporting this concept, several studies have shown insulin resistance in women with GDM to be equal or greater than that in nondiabetic pregnant women [20][21][22]. This applies equally to insulin resistance in skeletal muscle and liver and to insulin resistance in the adipose tissue, the latter resulting in increased lipolysis [17,23].…”

Section: Ffas and Insulin Resistance During Gdmmentioning

confidence: 85%

Free fatty acids, insulin resistance, and pregnancy

Sivan¹,

Boden

2003

Curr Diab Rep

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Acute elevation of plasma free fatty acid (FFA) levels causes insulin resistance to rise dose dependently in pregnant and nonpregnant women. Plasma FFA levels are commonly elevated during late pregnancy, partly due to rising blood levels of lipolytic placental hormones, and are a likely cause for much of the increase in insulin resistance occurring at that time in all pregnant women. Plasma FFA levels are similar or higher and the insulin resistance is comparable or more severe in women with gestational diabetes mellitus (GDM) than in nondiabetic pregnant women. In contrast to healthy pregnant women, insulin secretion in women with GDM is defective and, therefore, is unable to rise adequately to compensate for the insulin resistance; the result is hyperglycemia. The mechanism by which elevated plasma FFA levels cause insulin resistance in skeletal muscle includes intramyocellular accumulation of diacylglycerol, which activates protein kinase C (the b II and d isoforms). This results in reduction of tyrosine phosphorylation of the insulin receptor substrate-1 and inhibits activation of phosphoinositol-3 kinase, an enzyme that is essential for normal insulin-stimulated glucose uptake.

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“…A cross-sectional study performed by Buchanan et al [47] in 1990 demonstrated lower insulin sensitivity in women with GDM. However, later studies by Bowes et al [48] and Persson et al [49] contradicted those results and showed that insulin sensitivity was signifi cantly lower during pregnancy than after delivery in patients with GDM. Also, insulin secretion was increased during pregnancy in normal individuals compared with the immediate postpartum period.…”

Section: Gdm and Insulin Resistancementioning

confidence: 93%

Insulin resistance: The possible link between gestational diabetes mellitus and hypertensive disorders of pregnancy

Mastrogiannis

Spiliopoulos²,

Mulla³

et al. 2009

Curr Diab Rep

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Gestational hypertension, preeclampsia, and diabetes are all associated with increased risks of poor maternal and perinatal outcomes. Pregnant women with gestational diabetes have been shown in population studies to have increased risk of pregnancy-associated hypertension compared with nondiabetic women. Moreover, pregnant patients with hypertension are at increased risk for developing gestational diabetes mellitus. It has been hypothesized that this association could be due, at least in part, to insulin resistance. Although insulin resistance is a physiologic phenomenon in normal pregnancy, in predisposed individuals this could lead to hyperinsulinemia with the development of gestational hypertension, gestational diabetes mellitus, or both.

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Measurement of glucose metabolism and insulin secretion during normal pregnancy and pregnancy complicated by gestational diabetes

Cited by 57 publications

References 28 publications

MiR‐330‐3p contributes to INS‐1 cell dysfunction by targeting glucokinase in gestational diabetes mellitus

MiR‐330‐3p contributes to INS‐1 cell dysfunction by targeting glucokinase in gestational diabetes mellitus

Free fatty acids, insulin resistance, and pregnancy

Insulin resistance: The possible link between gestational diabetes mellitus and hypertensive disorders of pregnancy

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