XXXX -induced gene expression profiling in clonal b-cell line INS-1E cells.

@entity6 @entity1255 @entity535 @entity368 @entity5784 @entity164 @entity1521 @entity165
BACKGROUND: There is abundant evidence that glucotoxicity and lipotoxicity contribute to impaired b-cell function in @entity164 2 @entity6 . Interestingly, @entity535 (AA) derangement is also a characteristic part of the @entity6 state. The acute effects of AA on pancreatic b-cell function have been widely explored; however, to our knowledge, the chronic effects of AA, e.g. @entity1521 (Pro), @entity1255 ( @entity5784 ), and @entity368 (Leu), on pancreatic b-cell function and integrity have not yet been studied. We aimed to investigate global alterations in b-cell gene expression after long-term exposure of clonal INS-1E cells to elevated level of specific AA in vitro. METHODS: Global gene expression profiling was performed to characterize genes differently modified by Pro, @entity5784 , and Leu, respectively, in INS-1E cells. RESULTS: Gene expression profiling revealed significant changes in INS-1E cell mRNAs involved in the control of several aspects of b-cell function, e.g. epigenetic regulation of gene expression, metabolism, innate and adaptive immune responses, cellular signalling, protein synthesis, apoptosis, and cellular stress response. After 72 h, INS-1E cells were differentially regulated (>= 1.5- or  <= -1.5-fold) by Pro (295 transcripts), @entity5784 (301 transcripts), and Leu (701 transcripts). It appears that @entity5784 effects changes opposite to those induced by Leu and/or Pro. CONCLUSIONS: AA appears to participate in and to influence many physiological processes including those involved in @entity165 metabolism, immune responses, and oxidative phosphorylation. Whether such events promote the b-cell dysfunction and the b-cell failure in @entity6 remains to be elucidated. Our data strongly indicate that AA elevation may take part in the progressive development of @entity164 2 @entity6 .
