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Samuelsson AM, Matthews PA, Jansen E, et al. Sucrose feeding in mouse pregnancy leads to hypertension, and sex-linked obesity and insulin resistance in female offspring. Front Physiol. 2013;4:14doi: 10.3389/fphys.2013.00014.
Samuelsson, A. M., Matthews, P. A., Jansen, E., Taylor, P. D., & Poston, L. (2013). Sucrose feeding in mouse pregnancy leads to hypertension, and sex-linked obesity and insulin resistance in female offspring. Frontiers in physiology, 414. https://doi.org/10.3389/fphys.2013.00014
Samuelsson, Anne-Maj, et al. "Sucrose feeding in mouse pregnancy leads to hypertension, and sex-linked obesity and insulin resistance in female offspring." Frontiers in physiology vol. 4 (2013): 14. doi: https://doi.org/10.3389/fphys.2013.00014
Samuelsson AM, Matthews PA, Jansen E, Taylor PD, Poston L. Sucrose feeding in mouse pregnancy leads to hypertension, and sex-linked obesity and insulin resistance in female offspring. Front Physiol. 2013 Feb 18;4:14. doi: 10.3389/fphys.2013.00014. eCollection 2013. PMID: 23423541; PMCID: PMC3575022.
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Front Physiol. 2013 Feb 18;4:14. doi: 10.3389/fphys.2013.00014. eCollection 2013.

Sucrose feeding in mouse pregnancy leads to hypertension, and sex-linked obesity and insulin resistance in female offspring.

Frontiers in physiology

Anne-Maj Samuelsson, Phillippa A Matthews, Eugene Jansen, Paul D Taylor, Lucilla Poston

Affiliations

  1. Division of Women's Health, Women's Health Academic Center, King's College London and King's Health Partners London, UK.

PMID: 23423541 PMCID: PMC3575022 DOI: 10.3389/fphys.2013.00014

Abstract

Eating an unbalanced diet during pregnancy may induce long-term health consequences in offspring, in particular obesity, insulin resistance, and hypertension. We tested the hypothesis that a maternal diet rich in simple sugars predispose mouse offspring to obesity, glucose intolerance, and cardiovascular diseases in adulthood. Female C57BL/6J mice were fed either a standard chow or a sucrose-rich diet (26% of total energy) 6 weeks prior to mating, throughout pregnancy and lactation. Offspring of control dams (OC) and high sucrose fed dams (OSF) were weaned onto standard control chow, and metabolic and cardiovascular parameters determined at 3 months of age. Both male and female OSF were hyperphagic by 4 weeks of age and females were heavier than OC at 6 weeks. At 3 months, female OSF showed a significant increase in inguinal fat pad mass, whereas skeletal muscle mass (tibialis anterior) and locomotor activity were decreased relative to OC. A 10-fold increase in fasting serum insulin in female OSF vs. OC at 3 months (Insulin [pmol/L] mean ± SEM, OSF, 200.3 ± 16.1, vs. OC, 20.3 ± 1.8, n = 6 P < 0.001), was associated with impaired glucose tolerance (AUC [mmol/L min] mean ± SEM, OSF 1437.4 ± 124.2 vs. OC, 1076.8 ± 83.9, n = 6, P < 0.05). Both male and female OSF were hypertensive as assessed by radiotelemetry (night-time systolic arterial pressure (SAP) [mmHg] mean ± SEM, male OSF, 128 ± 1 vs. OC, 109 ± 1, n = 6, P < 0.01; female OSF, 130 ± 1 vs. OC, 118 ± 1, n = 6, P < 0.05). Analysis of heart rate variability (HRV) demonstrated an increased low:high frequency ratio in male and female OSF (P < 0.05), indicative of heightened sympathetic efferent tone. Renal tissue noradrenaline (NA) content was markedly raised in the OSF vs. OC (NA [pg/ml/mg tissue] mean ± SEM, male OSF, 2.28 ± 0.19 vs. OC 0.84 ± 0.09, n = 6, P < 0.01). Exposure to a maternal diet rich in sucrose led to obesity and glucose intolerance in female mice offspring, and hypertension in both sexes.

Keywords: hypertension; insulin; leptin; obesity; sucrose feeding

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