Another Hormone Involved in Lipid Mobilization? Atrial Natriuretic Peptide

This article is a bit heady, and I won't go into a detailed analysis but will try instead to present some relevant excerpts to the gist of this post.   That being, adipocyte metabolism, the continual cycling of fats in and out of adipose tissue, the continual cycle of esterification and hydrolysis, is mediated by more than just insulin.

According to the save date on my computer, I found this one a year ago.  Ever heard of atrial natriuretic peptide?  Me neither.  

According to Wikipedia, ANP is:
.... a powerful vasodilator, and a protein (polypeptidehormone secreted by heart muscle cells.[1][2] It is involved in the homeostatic control of body watersodiumpotassium and fat (adipose tissue). It is released by muscle cells in the upper chambers (atria) of the heart (atrial myocytes), in response to high blood pressure. ANP acts to reduce the water, sodium and adipose loads on the circulatory system, thereby reducing blood pressure.[1]
.... ANP binds to a specific set of receptors - ANP receptors. Receptor-agonist binding causes a reduction in blood volume and therefore a reduction in cardiac output and systemic blood pressure. Lipolysis is increased and renal sodium reabsorption is decreased. The overall effect of ANP on the body is to counter increases in blood pressure and volume caused by the renin-angiotensin system. There are other natriuretic peptides (brain - BNP, c-tpe - CNP) that "possess potent natriuretic, diuretic, and vasodilating activities and are implicated in body fluid homeostasis and blood pressure control."
From this paper: (Bullet points are my clarifications of acronyms, etc.)
For a long time, catecholamines released under SNS activation were considered major agents in control of lipid mobilization from adipose tissue during exercise in humans. However, discovery of peptides with lipolytic properties requires various aspects of the regulation of lipid mobilization to be reconsidered. NPs are involved in a cGMP-dependent pathway for control of human fat cell lipolysis in vitro. Present results reveal a contribution of NPs to the enhancement of lipid mobilization during exercise in human SCAT.
  • SNS = sympathetic nervous system  (part of autonomic nervous system responding to stress)
  • SCAT = subcutaneous adipose tissue
  • Catecholamines:  epinephrine (adrenaline), norepinephrine (noradrenaline) and dopamine
Previous investigations have shown that circulating ANP concentrations increased 2- to 3-fold during short-exercise bouts of increasing intensities. Plasma ANP increment was enhanced (at a similar developed power of exercise) when subjects had been pretreated with tertatolol. (a β-AR antagonist that potentiates [increases the effect of or acts synergistically with] plasma ANP increment during exercise. 
    From the intro:  In humans, lipid mobilization is considered to depend mainly on catecholamine action and interplay between fat cell α- and β-adrenergic receptors (AR).
    The most striking argument supporting physiological contribution of ANP in control of lipid mobilization concerns exercise-induced lipid mobilization remaining under oral β -AR-blockade, when highest levels of plasma ANP are attained. In absence of any other relevant factor, NPs represent reasonable candidates to explain exercise-induced lipid mobilization resistant to local propranolol (Fig. 1) and noticeable lipid-mobilizing action observed under oral β -blockade in subjects performing physical exercise (Fig. 2).
    That's all for now.