NDLI: CGI-58 knockdown in mice causes hepatic steatosis but prevents diet-induced obesity and glucose intolerance.

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CGI-58 knockdown in mice causes hepatic steatosis but prevents diet-induced obesity and glucose intolerance.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Brown, J. Mark Betters, Jenna L. Lord, Caleb Ma, Yinyan Han, Xianlin Yang, Kui Alger, Heather M. Melchior, John Sawyer, Janet Shah, Ramesh Wilson, Martha D. Liu, Xiuli Graham, Mark J. Lee, Richard Crooke, Rosanne Shulman, Gerald I. Xue, Bingzhong Shi, Hang Yu, Liqing
Description	Country affiliation: United States Author Affiliation: Brown JM ( Departments of Pathology Section on Lipid Sciences, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.)
Abstract	Mutations of Comparative Gene Identification-58 (CGI-58) in humans cause triglyceride (TG) accumulation in multiple tissues. Mice genetically lacking CGI-58 die shortly after birth due to a skin barrier defect. To study the role of CGI-58 in integrated lipid and energy metabolism, we utilized antisense oligonucleotides (ASOs) to inhibit CGI-58 expression in adult mice. Treatment with two distinct CGI-58-targeting ASOs resulted in â¼80-95% knockdown of CGI-58 protein expression in both liver and white adipose tissue. In chow-fed mice, ASO-mediated depletion of CGI-58 did not alter weight gain, plasma TG, or plasma glucose, yet raised hepatic TG levels â¼4-fold. When challenged with a high-fat diet (HFD), CGI-58 ASO-treated mice were protected against diet-induced obesity, but their hepatic contents of TG, diacylglycerols, and ceramides were all elevated, and intriguingly, their hepatic phosphatidylglycerol content was increased by 10-fold. These hepatic lipid alterations were associated with significant decreases in hepatic TG hydrolase activity, hepatic lipoprotein-TG secretion, and plasma concentrations of ketones, nonesterified fatty acids, and insulin. Additionally, HFD-fed CGI-58 ASO-treated mice were more glucose tolerant and insulin sensitive. Collectively, this work demonstrates that CGI-58 plays a critical role in limiting hepatic steatosis and maintaining hepatic glycerophospholipid homeostasis and has unmasked an unexpected role for CGI-58 in promoting HFD-induced obesity and insulin resistance.
File Format	HTM / HTML
ISSN	00222275
e-ISSN	15397262
DOI	10.1194/jlr.M010256
Journal	The Journal of Lipid Research
Issue Number	11
Volume Number	51
Language	English
Publisher	American Society for Biochemistry and Molecular Biology
Publisher Date	2010-11-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Biochemistry 1-acylglycerol-3-phosphate O-acyltransferase Deficiency Genetics Diet Adverse Effects Fatty Liver Gene Knockdown Techniques Glucose Intolerance Prevention & Control Obesity Adipocytes, White Metabolism Animals Dietary Fats Gene Expression Regulation Etiology Insulin Resistance Liver Secretion Mice Mice, Inbred C57bl Oligonucleotides, Antisense Phospholipids Triglycerides Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Endocrinology

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CGI-58 knockdown in mice causes hepatic steatosis but prevents diet-induced obesity and glucose intolerance[S]

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CGI-58 knockdown in mice causes hepatic steatosis but prevents diet-induced obesity and glucose intolerance.

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CGI-58 knockdown in mice causes hepatic steatosis but prevents diet-induced obesity and glucose intolerance[S]

CGI-58 knockdown sequesters diacylglycerols in lipid droplets/ER-preventing diacylglycerol-mediated hepatic insulin resistance.

Deletion of CGI-58 or adipose triglyceride lipase differently affects macrophage function and atherosclerosis.

Intestine-specific expression of acyl CoA:diacylglycerol acyltransferase 1 reverses resistance to diet-induced hepatic steatosis and obesity in Dgat1-/- mice.

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CGI-58 knockdown in mice causes hepatic steatosis but prevents diet-induced obesity and glucose intolerance.