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Aortic cholesterol accumulation correlates with systemic inflammation but not hepatic and gonadal adipose tissue inflammation in low-density lipoprotein receptor null mice.
Nutr Res. 2013 Dec; 33(12):1072-82.NR

Abstract

Inflammation is a major contributor to the development of atherosclerotic plaque, yet the involvement of liver and visceral adipose tissue inflammatory status in atherosclerotic lesion development has yet to be fully elucidated. We hypothesized that an atherogenic diet would increase inflammatory response and lipid accumulation in the liver and gonadal adipose tissue (GAT) and would correlate with systemic inflammation and aortic lesion formation in low-density lipoprotein (LDL) receptor null (LDLr-/-) mice. For 32 weeks, LDLr-/- mice (n = 10/group) were fed either an atherogenic (high saturated fat and cholesterol) or control (low fat and cholesterol) diet. Hepatic and GAT lipid content and expression of inflammatory factors were measured using standard procedures. Compared with the control diet, the atherogenic diet significantly increased hepatic triglyceride and total cholesterol (TC), primarily esterified cholesterol, and GAT triglyceride content. These changes were accompanied by increased expression of acyl-CoA synthetase long-chain family member 5, CD36, ATP-binding cassette, subfamily A, member 1 and scavenger receptor B class 1, and they decreased the expression of cytochrome P450, family 7 and subfamily a, polypeptide 1 in GAT. Aortic TC content was positively associated with hepatic TC, triglyceride, and GAT triglyceride contents as well as plasma interleukin 6 and monocyte chemoattractant protein-1 concentrations. Although when compared with the control diet, the atherogenic diet increased hepatic tumor necrosis factor α production, they were not associated with aortic TC content. These data suggest that the LDLr-/- mice responded to the atherogenic diet by increasing lipid accumulation in the liver and GAT, which may have increased inflammatory response. Aortic TC content was positively associated with systemic inflammation but not hepatic and GAT inflammatory status.

Authors+Show Affiliations

Nutritional Sciences Program, Texas Tech University, Lubbock, TX, USA. Electronic address: shu.wang@ttu.edu.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

24267047

Citation

Wang, Shu, et al. "Aortic Cholesterol Accumulation Correlates With Systemic Inflammation but Not Hepatic and Gonadal Adipose Tissue Inflammation in Low-density Lipoprotein Receptor Null Mice." Nutrition Research (New York, N.Y.), vol. 33, no. 12, 2013, pp. 1072-82.
Wang S, Miller B, Matthan NR, et al. Aortic cholesterol accumulation correlates with systemic inflammation but not hepatic and gonadal adipose tissue inflammation in low-density lipoprotein receptor null mice. Nutr Res. 2013;33(12):1072-82.
Wang, S., Miller, B., Matthan, N. R., Goktas, Z., Wu, D., Reed, D. B., Yin, X., Grammas, P., Moustaid-Moussa, N., Shen, C. L., & Lichtenstein, A. H. (2013). Aortic cholesterol accumulation correlates with systemic inflammation but not hepatic and gonadal adipose tissue inflammation in low-density lipoprotein receptor null mice. Nutrition Research (New York, N.Y.), 33(12), 1072-82. https://doi.org/10.1016/j.nutres.2013.09.002
Wang S, et al. Aortic Cholesterol Accumulation Correlates With Systemic Inflammation but Not Hepatic and Gonadal Adipose Tissue Inflammation in Low-density Lipoprotein Receptor Null Mice. Nutr Res. 2013;33(12):1072-82. PubMed PMID: 24267047.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Aortic cholesterol accumulation correlates with systemic inflammation but not hepatic and gonadal adipose tissue inflammation in low-density lipoprotein receptor null mice. AU - Wang,Shu, AU - Miller,Bradley, AU - Matthan,Nirupa R, AU - Goktas,Zeynep, AU - Wu,Dayong, AU - Reed,Debra B, AU - Yin,Xiangling, AU - Grammas,Paula, AU - Moustaid-Moussa,Naima, AU - Shen,Chwan-Li, AU - Lichtenstein,Alice H, PY - 2013/06/13/received PY - 2013/08/31/revised PY - 2013/09/11/accepted PY - 2013/11/26/entrez PY - 2013/11/26/pubmed PY - 2014/7/8/medline KW - 3-hydroxy-3-methylglutaryl-coenzyme A reductase KW - ABCA1 KW - ACACA KW - ACSL5 KW - ATP-binding cassette, subfamily A, member 1 KW - Atherogenic diet KW - Atherosclerosis KW - CYP7α1 KW - EC KW - FABP5 KW - FASN KW - FC KW - GAT KW - Gonadal adipose tissue KW - HDL-C KW - HMGCR KW - IL-6 KW - Inflammation KW - LDL-C KW - LDLr−/− KW - Liver steatosis KW - MCP-1 KW - MUFA KW - Mice KW - PUFA KW - SFA KW - SR-B1 KW - TC KW - TG KW - TNF-α KW - Total cholesterol KW - acetyl-coenzyme A carboxylase α KW - acyl-CoA synthetase long-chain family member 5 KW - cytochrome P450, family 7, subfamily a, polypeptide 1 KW - esterified cholesterol KW - fatty acid synthase KW - fatty acid–binding protein 5 KW - free cholesterol KW - gonadal adipose tissue KW - high-density lipoprotein cholesterol KW - interleukin 6 KW - low-density lipoprotein cholesterol KW - low-density lipoprotein receptor null KW - monocyte chemoattractant protein 1 KW - monounsaturated fatty acids KW - polyunsaturated fatty acids KW - saturated fatty acids KW - scavenger receptor class B, member 1 KW - triglyceride KW - tumor necrosis factor α SP - 1072 EP - 82 JF - Nutrition research (New York, N.Y.) JO - Nutr Res VL - 33 IS - 12 N2 - Inflammation is a major contributor to the development of atherosclerotic plaque, yet the involvement of liver and visceral adipose tissue inflammatory status in atherosclerotic lesion development has yet to be fully elucidated. We hypothesized that an atherogenic diet would increase inflammatory response and lipid accumulation in the liver and gonadal adipose tissue (GAT) and would correlate with systemic inflammation and aortic lesion formation in low-density lipoprotein (LDL) receptor null (LDLr-/-) mice. For 32 weeks, LDLr-/- mice (n = 10/group) were fed either an atherogenic (high saturated fat and cholesterol) or control (low fat and cholesterol) diet. Hepatic and GAT lipid content and expression of inflammatory factors were measured using standard procedures. Compared with the control diet, the atherogenic diet significantly increased hepatic triglyceride and total cholesterol (TC), primarily esterified cholesterol, and GAT triglyceride content. These changes were accompanied by increased expression of acyl-CoA synthetase long-chain family member 5, CD36, ATP-binding cassette, subfamily A, member 1 and scavenger receptor B class 1, and they decreased the expression of cytochrome P450, family 7 and subfamily a, polypeptide 1 in GAT. Aortic TC content was positively associated with hepatic TC, triglyceride, and GAT triglyceride contents as well as plasma interleukin 6 and monocyte chemoattractant protein-1 concentrations. Although when compared with the control diet, the atherogenic diet increased hepatic tumor necrosis factor α production, they were not associated with aortic TC content. These data suggest that the LDLr-/- mice responded to the atherogenic diet by increasing lipid accumulation in the liver and GAT, which may have increased inflammatory response. Aortic TC content was positively associated with systemic inflammation but not hepatic and GAT inflammatory status. SN - 1879-0739 UR - https://www.unboundmedicine.com/medline/citation/24267047/Aortic_cholesterol_accumulation_correlates_with_systemic_inflammation_but_not_hepatic_and_gonadal_adipose_tissue_inflammation_in_low_density_lipoprotein_receptor_null_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0271-5317(13)00214-5 DB - PRIME DP - Unbound Medicine ER -