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Updated: Aug 18, 2026

The 4-vessel Sampling Approach to Integrative Studies of Human Placental Physiology In Vivo
Published on: August 2, 2017
Insulin and nitric oxide stimulates glucose transport in human placenta
C Gloria Acevedo1, J Luis Márquez, Susana Rojas
1Departamento de Fisiología, Facultad de Ciencias Biológicas, Universidad de Concepción, Casilla 160-C, Concepción, Chile. cacevedo@udec.cl
Abstract:
The present work examines whether insulin and NO can act as regulators of glucose transport in placenta. Glucose uptake (2-deoxy D-[(3)H]glucose) was measured in the absence (control or basal values) and in the presence of insulin (1200 microU/ml) or SNP (20 microM) in isolated perfused cotyledons and tissue slices preparations of human placenta. Both insulin and NO significantly increased glucose uptake by 20 and 27 per cent, respectively. Insulin decreased the Km of glucose transport from 42.5 +/- 2.69 to 35.1 +/- 2.58 mM. The stimulatory effect of SNP was mimicked by 8-CPT-cGMP and was completely blocked by the guanylate cyclase inhibitor, ODQ (10 microM). ODQ and the NOS inhibitor, L-NAME (100 microM), decreased basal glucose uptake but did not affect insulin-stimulated glucose transport. Taken together, these findings indicate that insulin and NO stimulate glucose uptake in human placenta and suggest that both potential regulators of glucose transport use different signaling pathways.
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