Czupryn et al. "Transplanted Hypothalamic Neurons Restore Leptin Signaling and Ameliorate Obesity in db/db Mice" Science, 2011.

We'll start with the db/db mouse [...]. This mouse is genetically designed to develop severe morbid obesity and diabetes soon after birth. This is because it lacks a receptor for a hormone called leptin. Leptin is a hormone that plays a major role in appetite and metabolism. Decreasing your sensitivity to leptin, by decreasing leptin receptors, say (as in the the db/db mouse), produces striking obesity and type 2 diabetes in humans and mice. Increasing your sensitivity to leptin, by, say, increasing your leptin receptors, can rescue this, resulting in lower body weight and more sensitivity to insulin.

But these are global changes, throughout the body. The question is, where in the body do these leptin receptor changes really make a difference? Recent papers have suggested that the hypothalamus could play a major role. The hypothalamus, an area of your brain right above your pituitary gland, is a big connection between the brain and the endocrine system, an area where sensitivity to hormones could have a major impact on behavior and body regulation. And the hypothalamus regulates things like sleep, thirst, body temperature, and hunger.

The authors of this study wanted to see HOW increasing leptin-receptor containing neurons in the hypothalamus could work to help db/db mice. They took newborn db/db mice and controls, and gave them an implant of neurons containing, not just the leptin receptor, but a fluorescent protein to they could track their growth and position.

After the mice grew up, the authors looked to see where the neurons went, and what they did when they got there. They found that the neurons were able to integrate into the circuitry of the hypothalamus, expressing the leptin receptor, and forming synapses with local cells. The new neurons responded not only to leptin signals, but also to signals from glucose and insulin, an important step in how leptin sensitive cells can regulate insulin sensitivity.

But new neurons that glow are no good unless they have function. As it happens, these did.

[...]

The full article on ScientificAmerican can be found here, an news feature about the paper in The Harvard Gazette can be found here, and the full paper can be accessed here.