• Associate Professor
  • Molecular, Cellular, and Developmental Biology
  • Ph.D. Princeton University 1979
  • Department of Biology
  • Temple University

Karen B. Palter


My laboratory has previously shown that Drosophila melanogaster expresses a neuron specific sialyltransferase that is regulated during development. Sialyltransferases add the sugar sialic acid to sugar chains of glycoproteins. Furthermore, we have shown that loss of sialylation in Drosophila, results in behavioral defects, paralysis and neurodegeneration.

Our laboratory has shown that Drosophila melanogaster lacking a functional sialic acid pathway display a range of metabolic defects, that are similar to those observed in patients with Type II diabetes. We have demonstrated that one target of sialylation is a potassium channel in the nervous system. We propose that the metabolic defects are a result of excess insulin secretion from insulin producing cells (IPC), due to the potassium channel dysfunction.

Marban and Roth (1996) have shown that transgenic mice that secrete excess insulin (hyperinsulinemic) become insulin resistant, the hallmark of Type II diabetes. The mechanism of how hyperinsulinemia leads to Type II diabetes is not understood and is being actively studied. We are using our sialic acid mutant Drosophila as a model system to study the onset of insulin resistance, examining the different steps in the insulin signaling pathway in wild type, mutant and rescued fly lines.