Abstract
Recent epidemiological studies suggest that alcohol consumption is one of the risk factors leading to type 2 diabetes, but the direct effect of ethanol on beta-cell gene expression is not known. Here, using cDNA RDA method, we isolated 43 ethanol-induced genes in pancreatic beta-cells, and confirmed their differential expression by Northern blot or semi-quantitative RT-PCR. These genes were further categorized by the functional criteria based on the published data; Translation, Transcription, Metabolism, Signal transduction, Transport, Structure, Cytoskeleton, Regulation, or Putative/Unknown genes. The effects of each gene on beta-cell function need to be further investigated, however, the present data strongly suggest that these genes might be related to the metabolic alterations caused by ethanol as indicated in earlier study. In particular, RPS3 gene expression was increased by ethanol, glucosamine, and cytokines, implying that ethanol might decrease the metabolic activity by oxidative stress in beta-cells. Therefore, cloning of these genes in full-length and the detailed studies of each gene on beta-cell functions might provide clues on the pathophysiology of type 2 diabetes caused by alcohol.
Highlights
Recent epidemiological studies suggest that alcohol consumption is one of the risk factors leading to type 2 diabetes, but the direct effect of ethanol on β-cell gene expression is not know n
H ere, using cDNA representational difference analysis (RDA) method, we isolated 43 ethanolinduced genes in pancreatic β-cells, and con firmed their differential expression by Northern blot or semi-quantitative RT-PCR
Various epidemiological studies suggest that alcohol intake is one of the risk factors leading to type 2 diabetes (Wei et al, 2000; Linda Kao et al, 2001), the effects of alcohol on insulin secretion and glucose tolerance are not fully understood
Summary
Various epidemiological studies suggest that alcohol intake is one of the risk factors leading to type 2 diabetes (Wei et al, 2000; Linda Kao et al, 2001), the effects of alcohol on insulin secretion and glucose tolerance are not fully understood. Our results suggest that the ethanol priming effect on insulin secretion in pancreatic β-cells might be caused by overwork in order to compensate for the inhibited basal insulin secretion by ethanol (Shin et al, 2002). As the pleiotropic effect of ethanol was mediated by the alterations in gene expression (Diamond and Gordon, 1997), a comprehensive and non-biased assessment of the effects of ethanol on gene expression should be considered. To this end, others have used a variety of methods to isolate the differentially expressed ethanol-responsive genes in cell culture (Miles et al, 1994; Rahman and Miles, 2001) and animal model systems (Tunici et al, 1999), including subtractive hybridization, DNA microarray, and differential display PCR (DD-PCR). We used the cDNA RDA method to clone ethanol-induced genes, and to seek for the causal relationship of these genes to ethanol-mediated metabolic alterations in pancreatic β-cells (HIT cells)
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