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Nutr Diabetes. 2017 Feb 20;7(2):e244. doi: 10.1038/nutd.2016.56.

Effects of fetal exposure to high-fat diet or maternal hyperglycemia on L-arginine and nitric oxide metabolism in lung.

Author information

1
Pediatric Endocrinology and Diabetology, Kinderklinik II, Universitätsklinikum Essen and University of Duisburg-Essen, Essen, Germany.
2
Division of Neonatology, Kinderklinik I, Universitätsklinikum Essen and University of Duisburg-Essen, Essen, Germany.
3
Division of Pediatric Endocrinology, Department of Pediatrics, The Hospital For Sick Children, Toronto, ON, Canada.
4
Department of Physiology, The University of Toronto, Toronto, ON, Canada.
5
Division of Respiratory Medicine, Department of Pediatrics, The Hospital For Sick Children, Toronto, ON, Canada.
6
Program in Physiology and Experimental Medicine, Research Institute, The Hospital for Sick Children, Toronto, ON, Canada.

Abstract

BACKGROUND/OBJECTIVES:

Alterations in the L-arginine/nitric oxide (NO) metabolism contribute to diseases such as obesity, metabolic syndrome and airway dysfunction. The impact of early-life exposures on the L-arginine/NO metabolism in lung later in life is not well understood. The objective of this work was to study the effects of intrauterine exposures to maternal hyperglycemia and high-fat diet (HFD) on pulmonary L-arginine/NO metabolism in mice.

METHODS:

We used two murine models of intrauterine exposures to maternal (a) hyperglycemia and (b) HFD to study the effects of these exposures on the L-arginine/NO metabolism in lung in normal chow-fed offspring.

RESULTS:

Both intrauterine exposures resulted in NO deficiency in the lung of the offspring at 6 weeks of age. However, each of the exposures leading to different metabolic phenotypes caused a distinct alteration in the L-arginine/NO metabolism. Maternal hyperglycemia leading to impaired glucose tolerance but no obesity in the offspring resulted in increased levels of asymmetric dimethylarginine and impairment of NO synthases. Although maternal HFD led to obesity without impairment in glucose tolerance in the offspring, it resulted in increased expression and activity of arginase in the lung of the normal chow-fed offspring.

CONCLUSIONS:

These data suggest that maternal hyperglycemia and HFD can cause alterations in the pulmonary L-arginine/NO metabolism in offspring.

PMID:
28218737
PMCID:
PMC5360860
DOI:
10.1038/nutd.2016.56
[Indexed for MEDLINE]
Free PMC Article

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