Insulin Resistance, Ceramide Accumulation, and Endoplasmic Reticulum Stress in Human Chronic Alcohol-Related Liver Disease

Table 4

Effects of chronic ethanol consumption on hepatic expression of proceramide genes-biosynthetic pathways.

Protein	Control	Ethanol	𝑃 value
CerS1	0.542 ± 0.162	1.145 ± 0.228	0.025
CerS2	3634 ± 509.2	3982 ± 450
CerS4	160.2 ± 36.36	172.7 ± 22.86
CerS5	1.62 ± 0.22	3.62 ± 0.27	<0.0001
CerS6	15.70 ± 3.59	33.52 ± 5.48	0.0071
SPTLC-1	121.4 ± 9.29	253.3 ± 26.26	0.0001
SPTLC-2	2615 ± 444.8	3187 ± 309.5
SMPD-1	685.7 ± 133.9	1214 ± 244.8	0.036
SMPD-3	765.4 ± 140.5	1353 ± 216.6	0.019
CERD2	6.524 ± 2.439	1.887 ± 0.3439	0.04
CERD3	5.583 ± 1.458	6.896 ± 1.853
UGCG	282.6 ± 68.27	609.9 ± 174.5	0.0006
GM3Syn	56.21 ± 7.80	72.32 ± 6.981	0.006

RNA extracted from normal or chronic alcoholic livers (𝑁=8/group) was reverse transcribed, and the cDNAs were used to measure gene expression by qPCR analysis with gene-specific primer pairs in a duplex qPCR reaction, in which the genes of interest were co-amplified with HPRT for normalization (see Section 2 and Table 1). Table represents relative levels of gene expression for Ceramide synthases (CERS), UDP glucose ceramide glycosyltransferase (UGCG), ceramidases (CERD), GM3-synthase, serine palmitoyl transferase subunits (SPTLC), sphingomyelinases (SMPD). Intergroup comparisons were made using Student’s 𝑡-tests and significant 𝑃 values are shown over the graphs.