Maternal obesity impairs brain glucose metabolism and neural response to hyperglycemia in male rat offspring

Chen, H; Simar, D; Morris, MJ

Maternal obesity impairs brain glucose metabolism and neural response to hyperglycemia in male rat offspring

Chen, H

Simar, D Morris, MJ

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Publication Type:: Journal Article
Citation:: Journal of Neurochemistry, 2014, 129 (2), pp. 297 - 303
Issue Date:: 2014-01-01

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Field	Value	Language
dc.contributor.author	Chen, H https://orcid.org/0000-0001-6883-3752	en_US
dc.contributor.author	Simar, D	en_US
dc.contributor.author	Morris, MJ	en_US
dc.date.available	2013-11-21	en_US
dc.date.issued	2014-01-01	en_US
dc.identifier.citation	Journal of Neurochemistry, 2014, 129 (2), pp. 297 - 303	en_US
dc.identifier.issn	0022-3042	en_US
dc.identifier.uri	http://hdl.handle.net/10453/27469
dc.identifier.uri	http://hdl.handle.net/10453/30355
dc.description.abstract	Hypothalamic appetite regulators neuropeptide Y (NPY) and pro-opiomelanocortin (POMC) are modulated by glucose. This study investigated how maternal obesity disturbs glucose regulation of NPY and POMC, and whether this deregulation is linked to abnormal hypothalamic glucose uptake-lactate conversion. As post-natal high-fat diet (HFD) can exaggerate the effects of maternal obesity, its additional impact was also investigated. Female Sprague Dawley rats were fed a HFD (20 kJ/g) to model maternal obesity. At weaning, male pups were fed chow or HFD. At 9 weeks, in vivo hypothalamic NPY and POMC mRNA responses to acute hyperglycemia were measured; while hypothalami were glucose challenged in vitro to assess glucose uptake-lactate release and related gene expression. Maternal obesity dampened in vivo hypothalamic NPY response to acute hyperglycemia, and lowered in vitro hypothalamic glucose uptake and lactate release. When challenged with 20 mM glucose, hypothalamic glucose transporter 1, monocarboxylate transporters, lactate dehydrogenase-b, NPY and POMC mRNA expression were down-regulated in offspring exposed to maternal obesity. Post-natal HFD consumption reduced in vitro lactate release and monocarboxylate transporter 2 mRNA, but increased POMC mRNA levels when challenged with 20 mM glucose. Overall, maternal obesity produced stronger effects than post-natal HFD consumption to impair hypothalamic glucose metabolism. However, they both disturbed NPY response to hyperglycemia, potentially leading to hyperphagia. © 2013 International Society for Neurochemistry.	en_US
dc.relation.ispartof	Journal of Neurochemistry	en_US
dc.relation.isbasedon	10.1111/jnc.12623	en_US
dc.subject.classification	Neurology & Neurosurgery	en_US
dc.subject.mesh	Hypothalamus	en_US
dc.subject.mesh	Animals	en_US
dc.subject.mesh	Rats	en_US
dc.subject.mesh	Rats, Sprague-Dawley	en_US
dc.subject.mesh	Prenatal Exposure Delayed Effects	en_US
dc.subject.mesh	Hyperglycemia	en_US
dc.subject.mesh	Obesity	en_US
dc.subject.mesh	Pro-Opiomelanocortin	en_US
dc.subject.mesh	Glucose	en_US
dc.subject.mesh	Triglycerides	en_US
dc.subject.mesh	Neuropeptide Y	en_US
dc.subject.mesh	RNA, Messenger	en_US
dc.subject.mesh	Cohort Studies	en_US
dc.subject.mesh	Brain Chemistry	en_US
dc.subject.mesh	Growth	en_US
dc.subject.mesh	Pregnancy	en_US
dc.subject.mesh	Female	en_US
dc.subject.mesh	Male	en_US
dc.subject.mesh	Adiposity	en_US
dc.subject.mesh	Glucose Transporter Type 1	en_US
dc.subject.mesh	TOR Serine-Threonine Kinases	en_US
dc.title	Maternal obesity impairs brain glucose metabolism and neural response to hyperglycemia in male rat offspring	en_US
dc.type	Journal Article
utslib.citation.volume	2	en_US
utslib.citation.volume	129	en_US
utslib.for	060105 Cell Neurochemistry	en_US
utslib.for	0601 Biochemistry and Cell Biology	en_US
utslib.for	1109 Neurosciences	en_US
pubs.embargo.period	Not known	en_US
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
pubs.organisational-group	/University of Technology Sydney/Strength - CHT - Health Technologies
utslib.copyright.status	closed_access
pubs.issue	2	en_US
pubs.publication-status	Published	en_US
pubs.volume	129	en_US

Abstract:

Hypothalamic appetite regulators neuropeptide Y (NPY) and pro-opiomelanocortin (POMC) are modulated by glucose. This study investigated how maternal obesity disturbs glucose regulation of NPY and POMC, and whether this deregulation is linked to abnormal hypothalamic glucose uptake-lactate conversion. As post-natal high-fat diet (HFD) can exaggerate the effects of maternal obesity, its additional impact was also investigated. Female Sprague Dawley rats were fed a HFD (20 kJ/g) to model maternal obesity. At weaning, male pups were fed chow or HFD. At 9 weeks, in vivo hypothalamic NPY and POMC mRNA responses to acute hyperglycemia were measured; while hypothalami were glucose challenged in vitro to assess glucose uptake-lactate release and related gene expression. Maternal obesity dampened in vivo hypothalamic NPY response to acute hyperglycemia, and lowered in vitro hypothalamic glucose uptake and lactate release. When challenged with 20 mM glucose, hypothalamic glucose transporter 1, monocarboxylate transporters, lactate dehydrogenase-b, NPY and POMC mRNA expression were down-regulated in offspring exposed to maternal obesity. Post-natal HFD consumption reduced in vitro lactate release and monocarboxylate transporter 2 mRNA, but increased POMC mRNA levels when challenged with 20 mM glucose. Overall, maternal obesity produced stronger effects than post-natal HFD consumption to impair hypothalamic glucose metabolism. However, they both disturbed NPY response to hyperglycemia, potentially leading to hyperphagia. © 2013 International Society for Neurochemistry.

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http://hdl.handle.net/10453/27469