Great Bro-Science, but I would suggest going to Google Scholar, type in some keywords like, Leptin, Obesity, Leptin-resistance, etc... Then sort the hits to 2011 and newer, uncheck the 'patents' button and see what you get, then read some of the studies. You will see things related to Leptin resistance as the real problem. Leptin doesn't matter, it's the leptin receptors that matter. Just like in diabetes, insulin isn't the problem--just the result, it's the insulin receptors that are out of whack. I just pulled this from Google Scholar for instance.
The hormone leptin, secreted predominantly from adipose tissue, plays a crucial role in the regulation of numerous neuroendocrine functions, from energy homeostasis to reproduction. Genetic deficiency as a consequence of leptin or leptin receptor mutations, although rare in humans, leads to early onset of chronic hyperphagia and massive obesity. In most human obesity, however, leptin levels are chronically elevated. Under these conditions of persistent hyperleptinaemia, leptin resistance develops, and signalling through the leptin receptor is curtailed, fuelling further weight gain. Here, we review the role of leptin receptors in the regulation of feeding and obesity development. Leptin receptors are found in each of the major components of the CNS “feeding” circuitry—the brainstem, hypothalamus and distributed reward centres. Through these receptors, leptin exerts influences on signalling and integration within these circuits to alter feeding behaviours. Although some progress is now being made with peptide analogues, the leptin receptor has not proved to be amenable to small molecule pharmacological intervention to date. Where clinical benefit from recombinant leptin administration has been achieved, this has been under circumstances of complete endogenous leptin deficiency or relative hypoleptinaemia such as in lipodystrophy.
Keywords Leptin – Leptin receptors – Obesity