Further study showed that the islet cells in the mutant animals created normal amounts of insulin, but the CLOCK mutant cells were defective in releasing the hormone.

Mice with defective CLOCK genes were prone to obesity and other signs of metabolic syndrome and liver dysfunction. Young mice lacking the BMAL1 gene only in their pancreas, however, had normal body weight and composition, and their behavior followed normal circadian patterns, although their blood sugar levels were abnormally high, the researchers found.

"This finding indicates that disruption of clock genes only in the pancreas, and not the rest of the body clock, can produce early signs of diabetes," Dr. Takahashi said "These studies are important because they show a direct link between the clock in pancreatic beta-cells and glucose regulation. This should aid our understanding of the causes of glucose abnormalities."

Source: UT Southwestern Medical Center