Ok so satiety, briefly, is an interaction between the following:
Ghrelin, insulin, leptin, peptide YY, glucagon-like peptide-1, cholecystokinin, apolipoprotein AIV, and stretch receptors in the stomach. These are all anorexigenic signalling hormones/receptors except for ghrelin, which is the main "hunger" hormone.
Protein is the most satiating macronutrient. It produces a lower insulin AUC than CHO, but has higher PYY, GLP-1, CCK, and post-meal ghrelin levels are suppressed longer compared to CHO.
Fat affects CCK and apolipoprotein AIV levels and also changes the absorption kinetics of a meal and thus has effects on the other responses.
CHO and fat in isolation have been shown to have equal effects on satiety despite varying levels of aforementioned satiety hormones.
But keep in mind studies are done with single macronutrient intakes. When you combine them, the story changes drastically, but the individual effects still hold. Also, the male hypothalamus has a stronger response to insulin whereas the female hypothalamus has a stronger response to leptin for energy intake regulation.
If you're obese, your hypothalamus does not respond properly to ANY of these signals.
Here are two good reviews on the endocrine side of it:
Appetite signaling: From gut peptides and enteric nerves to brainhttp://www.ncbi.nlm.nih.gov/pubmed/17582445
The endocrinology of food intakehttp://www.ncbi.nlm.nih.gov/pubmed/23877425
I can post the full texts if someone would like to suggest a decent file hosting site