Lately there's been a lot of buzz around the internet about leptin and leptin resistance. I've come across a few things over the past several months I wish to share, basically focusing on whether levels of this hormone can be manipulated by varying the macronutrient composition of one's diet.
My general feeling on this is a cautiously stated: no. While some studies show differences in postprandrial leptin, fasting leptin, leptin AUC, there doesn't seem to be an overarching trend in this regard one way or the other. It would appear that leptin has more of a chronic role in energy homeostasis rather than an acute one. Insulin, OTOH, appears to have a somewhat dual role -- levels respond acutely to nutrient intake, while a basal insulin level generally correlates with one's degree of adiposity. Indeed in many diet comparison studies, fasting insulin levels go down modestly (usually with weight loss) but to the surprise of low carbers everywhere, I've not seen consistent findings of significant reductions in fasting insulin for LC vs HC diets.
Leptin, however, seems to be less subject to acute responses and is highly correlated with fat mass. The screenshot I'm posting below has been posted here before. One of these days I hope to find the study I snagged this from, but I can tell you that it was the differing responses to isocaloric "meals" of each isolated macronutrient.
Do LC diets somehow re-set or re-establish normal leptin signaling? I'm not sure we can conclude this based on this study in T2's I've blogged on previously: Effect of a Low-Carbohydrate Diet on Appetite, Blood Glucose Levels, and Insulin Resistance in Obese Patients with Type 2 Diabetes. In this 2 week study, the low carbers spontaneously reduced caloric consumption by ~1000 cal/day and lost an average of 3.6 lbs and "Mean 24-hour serum insulin and leptin levels profiles were statistically significantly lower at the end of the low-carbohydrate diet than before this diet, while ghrelin profiles increased marginally."
Most acknowledge the appetite suppressive quality of LC diets, and this apparently happened here to the tune of a substantial spontaneous intake reduction. Clearly this is not due to leptin which is lower (rather than higher) after the LC diet. It is possible (but a stretch IMO) that along with caloric deficit-induced leptin reduction, leptin resistance was reduced even more.