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. 2007 May 1:6:4.
doi: 10.1186/1476-5926-6-4.

"VSports最新版本" CIDE-A is expressed in liver of old mice and in type 2 diabetic mouse liver exhibiting steatosis

Bruce Kelder  1 , Keith Boyce, Andres Kriete, Ryan Clark, Darlene E Berryman, Sheila Nagatomi, Edward O List, Mark Braughler, John J Kopchick
Affiliations

"VSports手机版" CIDE-A is expressed in liver of old mice and in type 2 diabetic mouse liver exhibiting steatosis

Bruce Kelder et al. Comp Hepatol. .

Abstract

Background: Increased levels of circulating fatty acids caused by insulin resistance and increased adipocyte lipolysis can accumulate within the liver resulting in steatosis. This steatosis sensitizes the liver to inflammation and further injury which can lead to liver dysfunction. We performed microarray analysis on normal mouse liver tissue at different ages and type 2 diabetic liver exhibiting steatosis to identify differentially expressed genes involved in lipid accumulation and liver dysfunction. VSports手机版.

Results: Microarray analysis identified CIDE-A as the most differentially expressed gene as a function of age. Mice fed a high fat diet developed hyperinsulinemia, hyperglycemia and liver steatosis, all features of the human metabolic syndrome. Increased CIDE-A expression was observed in type 2 diabetic liver and the elevated CIDE-A expression could be reversed by weight loss and normalization of plasma insulin. Also, CIDE-A expression was found to be correlated with hepatic lipid accumulation V体育安卓版. .

Conclusion: The corresponding increase in CIDE-A expression with hyperinsulinemia and liver steatosis suggests a novel pathway for lipid accumulation in the liver. V体育ios版.

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Figures

Figure 1
Figure 1
CIDE-A is expressed in liver of aging mice. Amersham CodeLink Expression Bioarrays™ were performed on biotinylated cRNA generated from poly(A) mRNA isolated from the liver of mice ranging from 56 to 725 days of age. Expression levels relate to fluorescence detected from processed DNA microarrays. The CIDE-A expression value in each individual liver is shown.
Figure 2
Figure 2
Increased liver steatosis in older mice. H&E stained liver sections isolated from mice fed standard chow at 56 (A), 558 (B) and 725 (C) days of age shows the accumulation of lipid in liver hepatocytes of older mice.
Figure 3
Figure 3
CIDE-A expression is increased in the type 2 diabetic liver. Amersham CodeLink Expression Bioarrays™ were performed on biotinylated cRNA generated from poly(A) mRNA isolated from the liver of mice ranging from 35 to 203 days of age (2, 4, 8, 16 and 26 weeks on diet). The CIDE-A expression value in each individual liver is shown. Black boxes: Type 2 diabetic mice fed the high fat diet. Open triangles: control mice fed standard chow. Expression levels relate to fluorescence detected from processed DNA microarrays.
Figure 4
Figure 4
CIDE-A Northern and Immunoblot analyses. A) Northern analysis of RNA extracted from normal (C) and type 2 diabetic (D) liver and heart tissue. Total RNA (10 μg) from the appropriate tissues was resolved by denaturing agarose gel electrophoresis, transferred to positively charged nylon membrane, hybridized with the [α-32P]dCTP-labeled mouse CIDE-A cDNA and exposed to Bio-Max MR film. Ethidium bromide stain of RNA (10 μg/lane) prior to transfer to nylon membrane. The values represent the level of CIDE-A gene expression for the individual tissue as determined by DNA microarray analysis (ND: not determined). The approximated size (1.3 kb) of the CIDE-A mRNA is noted on the right. B) Immunoblot demonstrating increased CIDE-A protein levels in type 2 diabetic mouse liver. Sixty μg of liver and heart extract was electrophoresed on a 12.5% SDS-polyacrylamide gel and the resolved proteins transferred to a nitrocellulose membrane. The membrane was immunoblotted using a rabbit anti-mouse CIDE-A polyclonal antibody and a goat anti-rabbit IgG polyclonal antibody conjugated to horseradish peroxidase. Arrow indicates mouse CIDE-A. The values represent the level of CIDE-A gene expression for the individual tissue as determined by DNA microarray analysis (ND: not determined).
Figure 5
Figure 5
Steatosis in liver of high-fat diet fed mice. Mice were weaned directly onto either standard chow or a high-fat diet and maintained on the respective diets for up to 26 weeks. The mice were sacrificed and liver tissue isolated. Histology was performed on H&E stained liver tissue as described.
Figure 6
Figure 6
Quantification of percent liver white space. Image analysis was made as described in methods. The CIDE-A expression value in each individual liver is shown. Black boxes: Type 2 diabetic mice fed the high fat diet. Open triangles: control mice fed standard chow. Expression levels relate to fluorescence detected from processed DNA microarrays.
Figure 7
Figure 7
Effect of diet-reversal on CIDE-A expression. Mice were weaned onto the indicated diet for 33 weeks. The mice were then switched to the indicated diets for an additional 14 weeks. RNA was isolated from frozen liver as described. Real Time RT-PCR was performed on the cDNA transcripts using CIDE-A forward and reverse primers. Housekeeping genes, ACTG (actin gamma cytoplasmic) and GADPH (glyceraldehyde-III phosphate dehydrogenase), were utilized for normalization as described. Relative expression levels were calculated using normalization factors derived from geNorm analysis of ACTG and GADPH using the delta-delta CT method. CIDE-A expression levels in control mice fed standard chow for the entire feeding period (SC-SC) were given a value of 1.0. Changes in CIDE-A expression due to diet were expressed relative to the control mice. N = 4 (for each group). SC, standard chow; HF, high-fat diet.
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