Is weight loss and diabetes control only a neuron away?
Without the hormone leptin, mice (and people) become morbidly obese, diabetic and lethargic. First discovered as an unknown “satiety factor” by Douglas Coleman at The Jackson Laboratory in the 1970s, it has since been identified, characterized and intensively researched for its pivotal role in energy balance and its potential for weight loss applications.
A recent study using JAX® Mice further refined our understanding of how leptin functions. Researchers led by Christian Bjorbaek of Harvard Medical School found that restoring leptin sensitivity only to one particular type of neuron in the brain-pro-opiomelanocortin or POMC neurons-restores blood sugar control and spontaneously increases activity level (Cell Metabolism, June 3, 2009).
Isolating the POMC neurons provides researchers with better clues into how to affect leptin function. In cases of morbid obesity and diabetes, enhancing leptin sensitivity and activity holds the potential for significant benefit through weight loss, more activity and lower blood sugar.
