AI Article Synopsis
- Insulin helps transport glucose into cells by moving GLUT4 proteins to the cell's surface, but CSP1 can interfere with this process.
- Over-expressing CSP1 reduces glucose uptake by preventing the GLUT4 vesicles from docking properly, while lowering CSP1 levels improves glucose uptake.
- In insulin-resistant states, such as those caused by high palmitate levels, CSP1's expression increases, indicating its role in disrupting normal GLUT4 function.
Article Abstract
Insulin stimulates glucose transporter 4 (GLUT4) vesicle recruitment from its intracellular storage site to the plasma membrane. Cysteine string protein 1 (CSP1) is a SNARE-binding protein involved in the vesicular trafficking of neurotransmitters and other exocytic processes. In this study, we investigated the involvement of CSP1 in insulin-dependent GLUT4 recruitment in 3T3-L1 adipocytes. Over-expression of wild-type CSP1 led to attenuated insulin-stimulated glucose uptake without any change in GLUT4 content in the plasma membrane, rather it inhibits docking by blocking the association of VAMP2 with syntaxin 4. In contrast, knockdown of CSP1 enhanced insulin-stimulated glucose uptake. The mRNA and protein expression of CSP1 was elevated in 3T3-L1 adipocytes in insulin resistant states caused by high levels of palmitate and chronic insulin exposure. Taken together, the results of this study suggest that CSP1 is involved in insulin resistance by interrupting GLUT4 vesicle docking with the plasma membrane.
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| http://dx.doi.org/10.2152/jmi.60.197 | DOI Listing |
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