Enterostatin up-regulates the expression of the beta-subunit of F(1)F(o)-ATPase in the plasma membrane of INS-1 cells.

Exposure to high-fat diet easily promotes overeating while at the same time disrupting insulin secretion and islet function. Enterostatin is a peptide which is secreted from the pancreas in response to high-fat feeding and has been shown to inhibit fat intake as well as insulin secretion in experimental animal models. Until recently, there was no known receptor for enterostatin. In 2002, Berger and co-workers found enterostatin to target the beta-subunit of the F(1)-ATPase in rat brain membranes as well as in a clonal beta-cell line (INS-1). In this study, we found the beta-subunit of F(1)-ATPase to be ectopically expressed in the plasma membrane of INS-1 cells using both immunohistochemistry and Western blotting. Incubation with enterostatin for 60 min resulted in a 3.5-fold increase of the protein expression of the beta-subunit of F(1)-ATPase in the plasma membrane. Furthermore, we found ATP to be able to displace the binding of enterostatin to purified bovine F(1)-ATPase. This reported targeting of enterostatin to the beta-subunit of F(1)-ATPase in insulin cells may provide a link between high-fat intake and islet function.

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