Insulin and nitric oxide stimulates glucose transport in human placenta

Acevedo, C.G.; Márquez, José Luis; Rojas, Susana; Bravo, Iván

doi:10.1016/j.lfs.2004.09.039

Cited by 26 publications

(13 citation statements)

References 40 publications

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“…The upregulation of INSR expression in the placenta from the saturated fat-rich diet can contribute to the increase in placental mass, although further studies exploring protein expression are needed to clarify this point. Also, this increased placental INSR expression and hyperinsulinemia may enhance glucose and amino acid transport and modulate placental flow, thus improving placental efficiency, discussed above, for the saturated fat-rich diet-fed group (Acevedo et al 2005, Jones et al 2007, 2010, Hiden et al 2009). …”

Section: Discussionmentioning

confidence: 97%

Saturated fat-rich diet increases fetal lipids and modulates LPL and leptin receptor expression in rat placentas

Mazzucco

Higa

Capobianco

et al. 2013

Journal of Endocrinology

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Metabolic alterations in obese and overweight mothers impact the placenta and the fetus, leading to anomalies in fetal growth and lipid accretion. The primary aim of the study was to examine the effect of a saturated fat-rich diet (FD) on growth, lipid accretion, and lipases, leptin and leptin receptor (ObR) expression in the placenta and fetal liver. We also aimed to find a role for fetal leptin in the modulation of placental and fetal liver lipase and ObR expression. Six-week-old rats were fed with a standard rat chow (control) or a 25% FD for 7 weeks until mating and during pregnancy. Also, in a group of control rats, fetuses were injected with leptin on days 19, 20, and 21 of pregnancy. On day 21, we assessed lipidemia, insulinemia, and leptinemia in mothers and fetuses. In the placenta and fetal liver, lipid concentration was assessed by thin layer chromatography (TLC) and the gene expression of lipoprotein lipase (LPL), endothelial lipase, insulin receptor (Insr), leptin, and ObR by RT-PCR. The FD induced hypertriglyceridemia and hyperleptinemia (P!0.01) in mothers and fetuses, an increase in maternal (P!0.05) and fetal weight (P!0.01), overaccumulation of lipids in fetal liver (P!0.01), and enhanced leptin expression in the placenta and fetal liver (P!0.05). Placental expression of IR and LPL was increased (P!0.05), and ObR decreased (P!0.05) in the FD group. Fetal administration of leptin induced the placental and fetal liver downregulation of ObR (P!0.05) and upregulation of LPL expression (P!0.05). The FD led to increased fetal lipid levels, which may result from high maternal lipid availability and fetal leptin effects. Key Words" Saturated fat-rich diet

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Section: Discussionmentioning

confidence: 97%

Saturated fat-rich diet increases fetal lipids and modulates LPL and leptin receptor expression in rat placentas

Mazzucco

Higa

Capobianco

et al. 2013

Journal of Endocrinology

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“…Insulin does not affect glucose uptake in perfused term placenta [148] or in term villous fragments [39, 136]. However, other investigators have reported stimulation of placental glucose uptake by insulin at term [83, 84]. Ericsson and coworkers found that insulin stimulates glucose uptake in villous fragments from first trimester placenta but not from term placenta [136].…”

Section: Glucosementioning

confidence: 99%

Regulation of Nutrient Transport across the Placenta

Lager

Powell

2012

Journal of Pregnancy

353

278

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Abnormal fetal growth, both growth restriction and overgrowth, is associated with perinatal complications and an increased risk of metabolic and cardiovascular disease later in life. Fetal growth is dependent on nutrient availability, which in turn is related to the capacity of the placenta to transport these nutrients. The activity of a range of nutrient transporters has been reported to be decreased in placentas of growth restricted fetuses, whereas at least some studies indicate that placental nutrient transport is upregulated in fetal overgrowth. These findings suggest that changes in placental nutrient transport may directly contribute to the development of abnormal fetal growth. Detailed information on the mechanisms by which placental nutrient transporters are regulated will therefore help us to better understand how important pregnancy complications develop and may provide a foundation for designing novel intervention strategies. In this paper we will focus on recent studies of regulatory mechanisms that modulate placental transport of amino acids, fatty acids, and glucose.

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“…The uptake of materials such as glucose, amino acids, potassium, magnesium, and phosphate ions is vastly enhanced in its presence. [9][10][11] Hence, insulin is known to be a modifier of the metabolism of cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Insulin-induced enhancement of MCF-7 breast cancer cell response to 5-fluorouracil and cyclophosphamide

et al. 2017

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The study was designed to evaluate the potential use of insulin for cancer-specific treatment. Insulin-induced sensitivity of MCF-7 breast cancer cells to chemotherapeutic agents 5-fluorouracil and cyclophosphamide was evaluated. To investigate and establish the possible mechanisms of this phenomenon, we assessed cell proliferation, induction of apoptosis, activation of apoptotic and autophagic pathways, expression of glucose transporters 1 and 3, formation of reactive oxygen species, and wound-healing assay. Additionally, we reviewed the literature regarding theuse of insulin in cancer-specific treatment. We found that insulin increases the cytotoxic effect of 5-fluorouracil and cyclophosphamide in vitro up to two-fold. The effect was linked to enhancement of apoptosis, activation of apoptotic and autophagic pathways, and overexpression of glucose transporters 1 and 3 as well as inhibition of cell proliferation and motility. We propose a model for insulin-induced sensitization process. Insulin acts as a sensitizer of cancer cells to cytotoxic therapy through various mechanisms opening a possibility for metronomic insulin-based treatments.

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Insulin and nitric oxide stimulates glucose transport in human placenta

Cited by 26 publications

References 40 publications

Saturated fat-rich diet increases fetal lipids and modulates LPL and leptin receptor expression in rat placentas

Saturated fat-rich diet increases fetal lipids and modulates LPL and leptin receptor expression in rat placentas

Regulation of Nutrient Transport across the Placenta

Insulin-induced enhancement of MCF-7 breast cancer cell response to 5-fluorouracil and cyclophosphamide

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