http://www.ncbi.nlm.nih.gov/pmc/article ... figure/F1/ shows how wwhite adipose tissue ( WAT ) generates leptin that acts on the brain as does insulin. RThe brain can then affect storage of fat in the WAT via the sympathetic nervous system (SNS).
Insulin increase can act on the brain via the SNS to increase fat storage (lipogenesis) and reduce fat release from storage (lipolysis). This is in addition to insulin acting directly on the fat cells.
Leptin works the other way, extra leptin acting on the brain decreases fat storage and increases fat release.
Leptin decificient mice / humans or those with the leptin receptor knocked out genetically get very obese, as the leptin being released from their growing fat cells doesn't influence them to eat less or reduce fat storage. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC150795/ also see ob/ob mouse.
The bit I'm struggling with is that obese people tend to have high leptin, because they have a lot of fat cells releasing it. However the leptin doesn't do what it should - it looks like "leptin resistance". On the TV show Embarrassing Fat Bodies the slender Dr Dawn had low levels of leptin but her obese friend had high levels.
Other reading material
http://ajpendo.physiology.org/content/277/5/E855.long - "Leptin response to carbohydrate or fat meal and association with subsequent satiety and energy intake"
http://www.ncbi.nlm.nih.gov/pubmed/9084 ... t=Abstract talks of leptin being proportional to carbohydrate intake and falling during diet as less CHO intake.