The role of the small intestine in the development of dietary fat-induced obesity and insulin resistance in C57BL/6J mice-8

Ance test was performed after 7 weeks of diet intervention. After an oral gavage of 100 mg glucose, blood glucose levels were monitored for 150 minutes. The changes in blood glucose levels (upper figure) and the area under he curve were calculated (lower figure). In (A) and (B), data are means ± SE. * p < 0.05. LF = low-fat diet, HF = high-fat diet.<p><b>Copyright information:</b></p><p>Taken from "The role of the small intestine in the development of dietary fat-induced obesity and insulin resistance in C57BL/6J mice"</p><p>http://www.biomedcentral.com/1755-8794/1/14</p><p>BMC Medical Genomics 2008;1():14-14.</p><p>Published online 6 May 2008</p><p>PMCID:PMC2396659.</p><p></p

The role of the small intestine in the development of dietary fat-induced obesity and insulin resistance in C57BL/6J mice-5

Ined after 2 weeks of low-fat diet intervention. qPCR data of the nuclear receptors are visualized as the mean expression of individual mice ± SE. Expression in the middle and distal part of the small intestine is relative to the expression in the proximal part, which was set to 1. , , and indicate significant (p < 0.05, two-tailed Student's test) differential gene expression between the distinct parts of the small intestine (between the proximal and middle part, between the middle and distal part and between the proximal and distal part).<p><b>Copyright information:</b></p><p>Taken from "The role of the small intestine in the development of dietary fat-induced obesity and insulin resistance in C57BL/6J mice"</p><p>http://www.biomedcentral.com/1755-8794/1/14</p><p>BMC Medical Genomics 2008;1():14-14.</p><p>Published online 6 May 2008</p><p>PMCID:PMC2396659.</p><p></p

The role of the small intestine in the development of dietary fat-induced obesity and insulin resistance in C57BL/6J mice-7

Ly expressed genes with fold changes < -1.5 and > +1.5 in at least one week of diet intervention. Red and green boxes indicate a significant up- and down-regulation, respectively. NC = no change, A = absent.<p><b>Copyright information:</b></p><p>Taken from "The role of the small intestine in the development of dietary fat-induced obesity and insulin resistance in C57BL/6J mice"</p><p>http://www.biomedcentral.com/1755-8794/1/14</p><p>BMC Medical Genomics 2008;1():14-14.</p><p>Published online 6 May 2008</p><p>PMCID:PMC2396659.</p><p></p

The role of the small intestine in the development of dietary fat-induced obesity and insulin resistance in C57BL/6J mice-1

N at least one week of diet intervention are plotted (grey bars). Among those are genes that were consistently up- (I) or down-regulated (D) on a high-fat diet (white and black bars, respectively).<p><b>Copyright information:</b></p><p>Taken from "The role of the small intestine in the development of dietary fat-induced obesity and insulin resistance in C57BL/6J mice"</p><p>http://www.biomedcentral.com/1755-8794/1/14</p><p>BMC Medical Genomics 2008;1():14-14.</p><p>Published online 6 May 2008</p><p>PMCID:PMC2396659.</p><p></p

The role of the small intestine in the development of dietary fat-induced obesity and insulin resistance in C57BL/6J mice-6

Of nuclear (hormone) receptors and their target genes was determined by microarray analysis, after 2, 4, and 8 weeks of high-fat diet intervention. Red and green boxes indicate a significant up- and down-regulation, respectively. NC = no change, A = absent.<p><b>Copyright information:</b></p><p>Taken from "The role of the small intestine in the development of dietary fat-induced obesity and insulin resistance in C57BL/6J mice"</p><p>http://www.biomedcentral.com/1755-8794/1/14</p><p>BMC Medical Genomics 2008;1():14-14.</p><p>Published online 6 May 2008</p><p>PMCID:PMC2396659.</p><p></p

The role of the small intestine in the development of dietary fat-induced obesity and insulin resistance in C57BL/6J mice-4

Ng Ki67-specific antibodies. Besides the villus length (A) and total number of villus cells (B), also the number of Ki67-positive cells per villus (C) were determined. Per mouse, 15 villi were counted and the mean values were calculated. * p < 0.05, # p = 0.07. LF = low-fat diet, HF = high-fat diet.<p><b>Copyright information:</b></p><p>Taken from "The role of the small intestine in the development of dietary fat-induced obesity and insulin resistance in C57BL/6J mice"</p><p>http://www.biomedcentral.com/1755-8794/1/14</p><p>BMC Medical Genomics 2008;1():14-14.</p><p>Published online 6 May 2008</p><p>PMCID:PMC2396659.</p><p></p

The role of the small intestine in the development of dietary fat-induced obesity and insulin resistance in C57BL/6J mice-2

the proximal, middle and distal part of the small intestine, GO Biological Process subsets with a FDR < 0.01 and a RawScore = 10 in at least one week of diet intervention are considered significantly overrepresented. Black boxes indicate 1.0E-31 < FDR < 1.0E-08; dark grey boxes indicate 1.0E-08 < FDR < 0.01; white boxes indicate FDR > 0.01, so not significant. An empty row indicates that this part of small intestine did meet the above mentioned selection criteria (i.e. FDR > 0.01 at all time points).<p><b>Copyright information:</b></p><p>Taken from "The role of the small intestine in the development of dietary fat-induced obesity and insulin resistance in C57BL/6J mice"</p><p>http://www.biomedcentral.com/1755-8794/1/14</p><p>BMC Medical Genomics 2008;1():14-14.</p><p>Published online 6 May 2008</p><p>PMCID:PMC2396659.</p><p></p

The role of the small intestine in the development of dietary fat-induced obesity and insulin resistance in C57BL/6J mice-0

Ance test was performed after 7 weeks of diet intervention. After an oral gavage of 100 mg glucose, blood glucose levels were monitored for 150 minutes. The changes in blood glucose levels (upper figure) and the area under he curve were calculated (lower figure). In (A) and (B), data are means ± SE. * p < 0.05. LF = low-fat diet, HF = high-fat diet.<p><b>Copyright information:</b></p><p>Taken from "The role of the small intestine in the development of dietary fat-induced obesity and insulin resistance in C57BL/6J mice"</p><p>http://www.biomedcentral.com/1755-8794/1/14</p><p>BMC Medical Genomics 2008;1():14-14.</p><p>Published online 6 May 2008</p><p>PMCID:PMC2396659.</p><p></p

The role of the small intestine in the development of dietary fat-induced obesity and insulin resistance in C57BL/6J mice-3

are clustered in a heat map diagram for the proximal, middle and distal part of the small intestine. Green and red indicate down- and up-regulation of gene expression, respectively. In general, three expression patterns can be distinguished; consistently up-regulated, consistently down-regulated or alternate up- and down-regulation during diet intervention. Amongst other genes that display similar expression patterns on a high-fat diet, the boxes include differentially expressed genes that share association with particular biological processes (numbered). Differentially expressed genes with a -0.3 > SLR > 0.3 in at least one week of diet intervention were included and the color scheme ranges from SLR -1.5 to 1.5.<p><b>Copyright information:</b></p><p>Taken from "The role of the small intestine in the development of dietary fat-induced obesity and insulin resistance in C57BL/6J mice"</p><p>http://www.biomedcentral.com/1755-8794/1/14</p><p>BMC Medical Genomics 2008;1():14-14.</p><p>Published online 6 May 2008</p><p>PMCID:PMC2396659.</p><p></p

Prophylactic administration of JQ-1 suppresses the expression of <i>IFIT1</i> and <i>MX2</i> mRNA levels.

(A-B) Quantification of the dose-dependent effect of DMSO and JQ-1 on the mRNA expression levels of (A) IFIT1 and (B) MX2 in Calu-3 cells. Calu-3 cells were pretreated for 48 hours with corresponding concentrations of DMSO or JQ-1 (0.04–5.12 μM) prior to infection with SARS-CoV-2 (MOI = 0.1) for 24 hours under continuous treatment. At post infection, infected cells were RNA-extracted and analysed by qRT-PCR for mRNA expression from the indicated genes. Unpaired parametric t-test with the Holm-Šídák correction for multiple testing was used to compare the means from three independent experiments. (PDF)</p