alpha-MSH (melanocyte stimulating hormone) inhibits fat deposition

norepinephrine and epinephrine from the sympathetic nerves and blood stream inhibit fat deposition.(this effect is enhanced by estrogen ) These sympathetic agents also stimulate fatty acid release from adipocytes via stimulation of hormone sensitive lipase.

cortisol stimulates fat deposition in visceral and intrabdominal areas but has been reported to inhibit lipogenesis in subcutaneous distributions. Children with increased cortisol production due to increased 17 keto steroid dehydrogenase activity are obese.

progesterone stimulates fat deposition in subcutaneous adipocytes.

insulin stimulates fat deposition in adipocytes via hormone sensitive lipase inhibition and acetyl CoA Carboxylase stimulation. Therefore, reducing insulin release is a goal in most fat weight loss plans.

estrogen and testosterone regulate the deposition and distribution of fat in intrabdominal adipocytes, subcutaneous adipocytes, and visceral organs in a complex and integrated way.

TNF-alpha stimulates lipolysis in adipoctyes and their reversion to the preadipocyte phenotype

The human albumin protein helps carry released fatty acids away from adipocytes and towards their place of disposition. Therefore, increased levels of this important blood protein (which is produced by the liver) should help in removal of fat from adipocyte storage.

FOX-A2 protein -blocks preadipocyte differentiation and prevents mature adipocytes from continuing to build fat.

C3a-desArg/Acylation Stimulation Protein binds to the C5L2 Receptor on Fat cells (ie. adipocytes) and stimulates fat storage. Potential inhibition of this system could prevent fat accumulation.