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CREG1 heterozygous mice are susceptible to high fat diet-induced obesity and insulin resistance

PloS one, 2017-05, Vol.12 (5), p.e0176873-e0176873 [Peer Reviewed Journal]

COPYRIGHT 2017 Public Library of Science ;COPYRIGHT 2017 Public Library of Science ;2017 Tian et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2017 Tian et al 2017 Tian et al ;ISSN: 1932-6203 ;EISSN: 1932-6203 ;DOI: 10.1371/journal.pone.0176873 ;PMID: 28459882

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Title:
CREG1 heterozygous mice are susceptible to high fat diet-induced obesity and insulin resistance
Author: Tian, Xiaoxiang ; Yan, Chenghui ; Liu, Meili ; Zhang, Quanyu ; Liu, Dan ; Liu, Yanxia ; Li, Shaohua ; Han, Yaling
Ma, Xin-Liang
Subjects: 1-Phosphatidylinositol 3-kinase ; 3T3-L1 Cells ; Activation ; Activation analysis ; Adipocytes - immunology ; Adipocytes - pathology ; Adipogenesis ; Adiponectin ; Adipose tissue ; Adipose Tissue - immunology ; Adipose Tissue - pathology ; Aging ; Aging (artificial) ; AKT protein ; Ambient temperature ; Amino acids ; Anesthesia ; Animals ; Apoptosis ; Arteriosclerosis ; Atherosclerosis ; Attenuation ; Biochemical analysis ; Biochemistry ; Biology and Life Sciences ; Cachexia ; Calories ; Carbohydrates ; Cardiology ; Cardiomyocytes ; Carotid artery ; Cell differentiation ; Centrifugation ; Compartments ; Coronary artery disease ; Cytokines - metabolism ; Diabetes mellitus ; Diet ; Diet, High-Fat - adverse effects ; Differentiation (biology) ; Disease Models, Animal ; Food ; Food consumption ; Gene expression ; Genes ; Genetic aspects ; Glycoproteins ; Haploinsufficiency ; Health aspects ; Health risks ; Heart diseases ; Heterozygote ; High fat diet ; Homeostasis ; Hypertension ; Inflammation ; Inhibition ; Insulin ; Insulin resistance ; Insulin Resistance - physiology ; Ketogenic diet ; Laboratory tests ; Leukemia ; Liver ; Liver - metabolism ; Liver - pathology ; Liver diseases ; Medical research ; Medicine ; Medicine and Health Sciences ; Metabolic disorders ; Metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Military ; Monocytic leukemia ; Muscles ; NF-kappa B - metabolism ; Obesity ; Obesity - etiology ; Obesity - metabolism ; Obesity - pathology ; Pathogenesis ; Permeability ; Phenotype ; Physical Sciences ; Quality ; Repressor Proteins - deficiency ; Repressor Proteins - genetics ; Residues ; Risk factors ; RNA, Small Interfering ; Rodents ; Salicylates ; Surgery ; Temperature effects ; Transfection ; Vascular endothelial growth factor ; Ventricle
Is Part Of: PloS one, 2017-05, Vol.12 (5), p.e0176873-e0176873
Description: Cellular repressor of E1A-stimulated genes 1 (CREG1) is a small glycoprotein whose physiological function is unknown. In cell culture studies, CREG1 promotes cellular differentiation and maturation. To elucidate its physiological functions, we deleted the Creg1 gene in mice and found that loss of CREG1 leads to early embryonic death, suggesting that it is essential for early development. In the analysis of Creg1 heterozygous mice, we unexpectedly observed that they developed obesity as they get older. In this study, we further studied this phenotype by feeding wild type (WT) and Creg1 heterozygote (Creg1+/-) mice a high fat diet (HFD) for 16 weeks. Our data showed that Creg1+/- mice exhibited a more prominent obesity phenotype with no change in food intake compared with WT controls when challenged with HFD. Creg1 haploinsufficiency also exacerbated HFD-induced liver steatosis, dyslipidemia and insulin resistance. In addition, HFD markedly increased pro-inflammatory cytokines in plasma and epididymal adipose tissue in Creg1+/- mice as compared with WT controls. The activation level of NF-κB, a major regulator of inflammatory response, in epididymal adipose tissue was also elevated in parallel with the cytokines in Creg1+/- mice. These pro-inflammatory responses elicited by CREG1 reduction were confirmed in 3T3-L1-derived adipocytes with CREG1 depletion by siRNA transfection. Given that adipose tissue inflammation has been shown to play a key role in obesity-induced insulin resistance and metabolic syndrome, our results suggest that Creg1 haploinsufficiency confers increased susceptibility of adipose tissue to inflammation, leading to aggravated obesity and insulin resistance when challenged with HFD. This study uncovered a novel function of CREG1 in metabolic disorders.
Publisher: United States: Public Library of Science
Language: English
Identifier: ISSN: 1932-6203
EISSN: 1932-6203
DOI: 10.1371/journal.pone.0176873
PMID: 28459882
Source: PLoS (Open access)
PubMed Central (Open access)
Geneva Foundation Free Medical Journals at publisher websites
AUTh Library subscriptions: ProQuest Central
MEDLINE
DOAJ (Directory of Open Access Journals)

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CREG1 heterozygous mice are susceptible to high fat diet-induced obesity and insulin resistance

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