Premium
Early activation of the fatty acid metabolism pathway by chronic high glucose exposure in rat insulin secretory β‐cells
Author(s) -
Couté Yohann,
Brunner Yannick,
Schvartz Domitille,
Hernandez Céline,
Masselot Alexandre,
Lisacek Frédérique,
Wollheim Claes B.,
Sanchez JeanCharles
Publication year - 2009
Publication title -
proteomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.26
H-Index - 167
eISSN - 1615-9861
pISSN - 1615-9853
DOI - 10.1002/pmic.200900080
Subject(s) - lipogenesis , medicine , glucose homeostasis , insulin , endocrinology , homeostasis , carbohydrate metabolism , metabolism , biology , secretion , cell culture , fatty acid metabolism , lipid metabolism , insulin resistance , biochemistry , chemistry , genetics
Pancreatic β‐cells are responsible for insulin secretion that regulates blood glucose homeostasis. In the development of type II diabetes, a progressive impairment of insulin secretion by the pancreatic β‐cells occurs called β‐cell dysfunction or β‐cell failure. Chronic hyperglycemia has been shown being involved in β‐cell dysfunction, a phenomenon known as glucotoxicity. The molecular mechanisms underlying the impairment of insulin secretion by β‐cells induced by glucotoxicity are still not fully understood. In this work, quantitative proteomics was employed to identify early key players involved in β‐cell dysfunction induced by glucotoxicity. For this, the stable isotope labeling by amino acids in cell culture strategy was used on the slowly‐growing rat β‐cell line INS‐1E. We showed that the stable isotope labeling by amino acids in cell culture approach did not induce any detectable biological effects on these β‐cells, as measured at both the transcriptomic and proteomic levels. Proteins differentially expressed between control cells and cells submitted to chronic high glucose concentrations were identified and verified. The results obtained reinforce the link between glucotoxicity and lipogenesis and suggest that the fatty acid metabolism pathway may rapidly be stimulated in β‐cells submitted to chronic high glucose concentrations.