Parental SIRT1 Overexpression Attenuate Metabolic Disorders Due to Maternal High-Fat Feeding.

Nguyen, LT; Saad, S; Chen, H; Pollock, CA

Parental SIRT1 Overexpression Attenuate Metabolic Disorders Due to Maternal High-Fat Feeding.

Nguyen, LT Saad, S Chen, H

Pollock, CA

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Publisher:: MDPI
Publication Type:: Journal Article
Citation:: International journal of molecular sciences, 2020, 21, (19)
Issue Date:: 2020-10-05

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Field	Value	Language
dc.contributor.author	Nguyen, LT
dc.contributor.author	Saad, S
dc.contributor.author	Chen, H https://orcid.org/0000-0001-6883-3752
dc.contributor.author	Pollock, CA
dc.date.accessioned	2021-01-12T02:24:29Z
dc.date.available	2020-10-02
dc.date.available	2021-01-12T02:24:29Z
dc.date.issued	2020-10-05
dc.identifier.citation	International journal of molecular sciences, 2020, 21, (19)
dc.identifier.issn	1422-0067
dc.identifier.issn	1422-0067
dc.identifier.uri	http://hdl.handle.net/10453/145322
dc.description.abstract	Maternal obesity can contribute to the development of obesity and related metabolic disorders in progeny. Sirtuin (SIRT)1, an essential regulator of metabolism and stress responses, has recently emerged as an important modifying factor of developmental programming. In this study, to elucidate the effects of parental SIRT1 overexpression on offspring mechanism, four experimental groups were included: (1) Chow-fed wild-type (WT)-dam × Chow-fed WT-sire; (2) High-fat diet (HFD)-fed WT-dam × Chow-fed WT-sire; (3) HFD-fed hemizygous SIRT1-transgenic (Tg)-dam × Chow-fed WT-sire; and (4) HFD-fed WT dam × Chow-fed Tg-sire. Our results indicate that Tg breeders had lower body weight and fat mass compared to WT counterparts and gave birth to WT offspring with reductions in body weight, adiposity and hyperlipidaemia compared to those born of WT parents. Maternal SIRT1 overexpression also reversed glucose intolerance, and normalised abnormal fat morphology and the expression of dysregulated lipid metabolism markers, including SIRT1. Despite having persistent hepatic steatosis, offspring born to Tg parents showed an improved balance of hepatic glucose/lipid metabolic markers, as well as reduced levels of inflammatory markers and TGF-β/Smad3 fibrotic signalling. Collectively, the data suggest that parental SIRT1 overexpression can ameliorate adverse metabolic programming effects by maternal obesity.
dc.format	Electronic
dc.language	eng
dc.publisher	MDPI
dc.relation.ispartof	International journal of molecular sciences
dc.relation.isbasedon	10.3390/ijms21197342
dc.rights	info:eu-repo/semantics/restrictedAccess
dc.subject	0399 Other Chemical Sciences, 0604 Genetics, 0699 Other Biological Sciences
dc.subject.classification	Chemical Physics
dc.title	Parental SIRT1 Overexpression Attenuate Metabolic Disorders Due to Maternal High-Fat Feeding.
dc.type	Journal Article
utslib.citation.volume	21
utslib.location.activity	Switzerland
utslib.for	1114 Paediatrics and Reproductive Medicine
utslib.for	0304 Medicinal and Biomolecular Chemistry
utslib.for	1117 Public Health and Health Services
utslib.for	0399 Other Chemical Sciences
utslib.for	0604 Genetics
utslib.for	0699 Other Biological Sciences
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Strength - CHT - Health Technologies
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
pubs.organisational-group	/University of Technology Sydney
utslib.copyright.status	closed_access	*
pubs.consider-herdc	false
dc.date.updated	2021-01-12T02:24:17Z
pubs.issue	19
pubs.publication-status	Published
pubs.volume	21
utslib.citation.issue	19

Abstract:

Maternal obesity can contribute to the development of obesity and related metabolic disorders in progeny. Sirtuin (SIRT)1, an essential regulator of metabolism and stress responses, has recently emerged as an important modifying factor of developmental programming. In this study, to elucidate the effects of parental SIRT1 overexpression on offspring mechanism, four experimental groups were included: (1) Chow-fed wild-type (WT)-dam × Chow-fed WT-sire; (2) High-fat diet (HFD)-fed WT-dam × Chow-fed WT-sire; (3) HFD-fed hemizygous SIRT1-transgenic (Tg)-dam × Chow-fed WT-sire; and (4) HFD-fed WT dam × Chow-fed Tg-sire. Our results indicate that Tg breeders had lower body weight and fat mass compared to WT counterparts and gave birth to WT offspring with reductions in body weight, adiposity and hyperlipidaemia compared to those born of WT parents. Maternal SIRT1 overexpression also reversed glucose intolerance, and normalised abnormal fat morphology and the expression of dysregulated lipid metabolism markers, including SIRT1. Despite having persistent hepatic steatosis, offspring born to Tg parents showed an improved balance of hepatic glucose/lipid metabolic markers, as well as reduced levels of inflammatory markers and TGF-β/Smad3 fibrotic signalling. Collectively, the data suggest that parental SIRT1 overexpression can ameliorate adverse metabolic programming effects by maternal obesity.

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http://hdl.handle.net/10453/145322