Transcriptional regulation of lipid metabolism by fatty acids: A key determinant of pancreatic β-cell function

被引：37

作者：

Fatehi-Hassanabad Z. ^{[1
]}

Chan C.B. ^{[1
]}

机构：

[1] Department of Biomedical Sciences, University of Prince Edward Island, Charlottetown, PEI C1A 4P3

来源：

Nutrition & Metabolism | / 2卷 / 1期

关键词：

Insulin Secretion; Plasma Free Fatty Acid; Sterol Regulatory Element Binding Protein; UCP2 Expression; Plasma Free Fatty Acid Concentration;

D O I：

10.1186/1743-7075-2-1

中图分类号：

学科分类号：

摘要：

Background: Optimal pancreatic β-cell function is essential for the regulation of glucose homeostasis in both humans and animals and its impairment leads to the development of diabetes. Type 2 diabetes is a polygenic disease aggravated by environmental factors such as low physical activity or a hypercaloric high-fat diet. Results: Free fatty acids represent an important factor linking excess fat mass to type 2 diabetes. Several studies have shown that chronically elevated free fatty acids have a negative effect on β-cell function leading to elevated insulin secretion basally but with an impaired response to glucose. The transcription factors PPARα, PPARγ and SREBP-1c respond to changing fat concentrations in tissues, thereby coordinating the genomic response to altered metabolic conditions to promote either fat storage or catabolism. These transcription factors have been identified in β-cells and it appears that each may exert influence on β-cell function in health and disease. Conclusion: The role of the PPARs and SREBP-1c as potential mediators of lipotoxicity is an emerging area of interest. © 2005 Fatehi-Hassanabad and Chan; licensee BioMed Central Ltd.

引用

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