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Updated: Apr 25, 2026
Extracellular Glucose Depletion as an Indirect Measure of Glucose Uptake in Cells and Tissues Ex Vivo
Published on: April 6, 2022
Cultured neonatal rat cardiomyocytes display differences in glucose uptake and sensitivity to dexamethasone related
R M Austin1, S C Langley-Evans1
1School of Biosciences, University of Nottingham, Sutton Bonington, Loughborough, UK.
Insights
Prenatal low protein (LP) diet exposure in rats permanently alters cardiomyocyte sensitivity to glucocorticoids, impacting glucose uptake. These programming effects persist in vitro, suggesting lasting endocrine programming from undernutrition.
Area of Science:
- Cardiovascular Physiology
- Developmental Biology
- Endocrinology
Background:
- Maternal low protein (LP) diet during pregnancy is linked to impaired offspring cardiovascular health.
- Tissue remodeling is a potential mechanism for these cardiovascular changes.
- Understanding long-term effects on specific cell types like cardiomyocytes is crucial.
Purpose of the Study:
- To investigate if cardiomyocytes from rats exposed to a prenatal LP diet retain functional differences.
- To assess the impact of prenatal protein restriction on cardiomyocyte response to endocrine signals in vitro.
Main Methods:
- Neonatal rat cardiomyocytes from control and LP-diet exposed mothers were cultured for 10 days.
- Cells were treated with dexamethasone (a glucocorticoid) to assess responses.
- Insulin-stimulated glucose uptake and gene expression of glucocorticoid receptor and glucose transporters (GLUT1, GLUT4) were measured.
Main Results:
- No differences in cardiomyocyte size, proliferation, differentiation, or basal metabolic function were observed between groups.
- Dexamethasone treatment enhanced insulin-stimulated glucose uptake specifically in cardiomyocytes from LP rats.
- This increased glucocorticoid sensitivity was not explained by altered expression of the glucocorticoid receptor, GLUT1, or GLUT4.
Conclusions:
- Prenatal undernutrition via an LP diet can permanently program cardiomyocyte sensitivity to glucocorticoids.
- Enhanced glucocorticoid sensitivity in cardiomyocytes from LP rats affects glucose uptake mechanisms.
- These findings suggest that undernutrition establishes lasting endocrine programming in cardiomyocytes through mechanisms that remain functional in vitro.
Abstract:
Feeding a low protein (LP) diet in rat pregnancy is associated with impaired cardiovascular health and function, possibly as a result of tissue remodelling. To assess whether cardiomyocytes retain differences induced by protein restriction, cells from neonatal rats exposed to control or LP diets in utero were cultured for a period of 10 days. At the end of this period, no differences in cell size, proliferation differentiation or metabolic function were noted. When treated with dexamethasone (0.1-10 μM) for 2 days, it was noted that insulin-stimulated glucose uptake was enhanced, but only in cells from LP rats. Increased glucocorticoid sensitivity of cardiomyocytes from LP rats could not be explained by differential expression of the glucocorticoid receptor or the glucose transporters, GLUT1 and GLUT4. The findings of the study suggest that sensitivity to endocrine signals may be permanently programmed by undernutrition through mechanisms that are preserved in vitro.
