| Respective contributions of maternal insulin resistance and diet to metabolic and hypothalamic phenotypes of progeny. | |
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MedLine Citation:
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PMID: 20948526 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Maternal obesity can influence susceptibility to obesity and type 2 diabetes in progeny. We examined the relationship of maternal insulin resistance (IR), a metabolically important consequence of increased adiposity, to adverse consequences of obesity for fetal development. We used mice heterozygous for a null allele of the insulin receptor (Insr) to study the contributions of maternal IR to offspring phenotype without the potential confound of obesity per se, and how maternal consumption of high-fat diet (HFD) may, independently and interactively, affect progeny. In progeny fed a 60% HFD, body weight and adiposity were transiently (5-7 weeks) increased in wild-type (+/+) offspring of Insr(+/-) HFD-fed dams compared to offspring of wild-type HFD-fed dams. Offspring of HFD-fed wild-type dams had increased body weight, blood glucose, and plasma insulin concentrations compared to offspring of chow-fed wild-type dams. Quantification of proopiomelanocortin (POMC) and neuropeptide-Y (NPY) populations in the arcuate nucleus of the hypothalamus (ARH) of offspring of wild-type vs. Insr(+/-) dams was performed to determine whether maternal IR affects the formation of central feeding circuits. We found a 20% increase in the number of Pomc-expressing cells at postnatal day 9 in offspring of Insr(+/-) dams. In conclusion, maternal HFD consumption-distinct from overt obesity per se-was a major contributor to increased body weight, adiposity, IR, and liver triglyceride (TG) phenotypes in progeny. Maternal IR played a minor role in predisposing progeny to obesity and IR, though it acted synergistically with maternal HFD to exacerbate early obesity in progeny. |
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Authors:
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Jill S Carmody; Phyllis Wan; Domenico Accili; Lori M Zeltser; Rudolph L Leibel |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-10-14 |
Journal Detail:
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Title: Obesity (Silver Spring, Md.) Volume: 19 ISSN: 1930-7381 ISO Abbreviation: Obesity (Silver Spring) Publication Date: 2011 Mar |
Date Detail:
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Created Date: 2011-02-24 Completed Date: 2011-10-04 Revised Date: 2012-03-22 |
Medline Journal Info:
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Nlm Unique ID: 101264860 Medline TA: Obesity (Silver Spring) Country: United States |
Other Details:
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Languages: eng Pagination: 492-9 Citation Subset: IM |
Affiliation:
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Division of Molecular Genetics, Department of Pediatrics, Columbia University, New York, New York, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adiposity
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drug effects Animals Blood Glucose / metabolism Dietary Fats / adverse effects* Female Hypothalamus / cytology, metabolism* Insulin / blood Insulin Resistance / physiology* Liver / metabolism Male Mice Mice, Inbred C57BL Mice, Knockout Neuropeptide Y / metabolism Obesity / etiology*, physiopathology Phenotype Pregnancy Pregnancy Complications / metabolism* Prenatal Nutritional Physiological Phenomena* Pro-Opiomelanocortin / metabolism Receptor, Insulin / genetics Triglycerides / metabolism Weight Gain / drug effects |
| Grant Support | |
ID/Acronym/Agency:
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P30 DK026687-19/DK/NIDDK NIH HHS; P30 DK063608-01/DK/NIDDK NIH HHS; P30DK26687/DK/NIDDK NIH HHS; P30DK63608/DK/NIDDK NIH HHS; R01 DK052431-09/DK/NIDDK NIH HHS; R01 DK052431-19/DK/NIDDK NIH HHS; R01 DK064819-10/DK/NIDDK NIH HHS; R01DK52431/DK/NIDDK NIH HHS; T32 DK 007647/DK/NIDDK NIH HHS; T32 DK007647-09/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Blood Glucose; 0/Dietary Fats; 0/Insulin; 0/Neuropeptide Y; 0/Triglycerides; 66796-54-1/Pro-Opiomelanocortin; EC 2.7.10.1/Receptor, Insulin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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