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Joan Stephenson, PhD

JAMA. 2001;285:725.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Serendipitous findings by scientists in Belgium, France, and Canada point to a new potential therapeutic target for type 2 diabetes: a gene called SHIP2 that appears to act as a brake on insulin production. The report appears in the January 4 issue of Nature.

The investigators found that genetically engineered newborn mice that lacked copies of the SHIP2 gene showed signs of hypoglycemia—they were blue or pale, lethargic, showed signs of respiratory distress, and failed to gain weight—and died within 3 days of birth. Further study revealed that the mice were hypoglycemic because of hypersensitivity to insulin rather than overproduction of the hormone.

Mice with one normal copy of SHIP2 also appeared to be more sensitive to insulin than mice with both copies of the gene. Because SHIP2 appears to control sensitivity to insulin, it is possible that mutations in the gene may play a role . . . [Full Text of this Article]