(A) Satiety effect by
Vagas Nerve Stimulation :

Achyranthes seeds have protein, fatty acids like Oleic acid and Lenoleic acid and Saponin Glycosides.

Dietary Oleic acid can convert into a fat messenger called Oleoylethanolamide (OEA). Oleoylethanolamide (OEA), a lipid synthesized in the intestine, reduces food intake and stimulates lipolysis through peroxisome proliferator-activated receptor. OEA also activates transient receptor potential vanilloid type 1 (TRPV1) in vitro.

Oleic acid, a major digestive product of dietary fat, is transported into small-intestinal enterocytes by the fatty acid translocase CD36. There, a fraction of Oleic acid is converted to OEA.

OEA suppresses feeding without causing visceral illness and that neither ghrelin, peptide YY, glucagon-like peptide 1, apolipoprotein A-IV, nor CCK plays a critical role in this effect 1. Giving the body time to handle the metabolic challenge presented by a fatty meal, OEA affects sensory vagus nerve activity through PPAR-α to induce satiety and decrease meal frequency.

It does not impact upon the size of a meal: satiation prompts meal termination and is mediated by gut peptides, whereas satiety is a separate response.

This acts as a sensor for ingestion of fat, activating PPAR-α to enhance lipid absorption (including by increased expression of CD36). OEA is disrupted in mutant mice lacking the membrane fatty-acid transporter CD36. Targeted disruption of CD36 or PPAR-α abrogates the satiety response induced by fat².

OEA decreases meal frequency by engaging peroxisome proliferator-activated receptors-α (PPAR-α). The activation of small-intestinal OEA mobilization, enabled by CD36-mediated uptake of dietary oleic acid, serves as a molecular sensor linking fat ingestion to satiety².

(B) Fat Reduction Action by
stimulation of Lypilysis :

OEA acts independently of the cannabinoid pathway and regulates PPAR-α activity to stimulate lipolysis (the breakdown of fat stored in fat cells)^[3]

In adipocytes and hepatocytes, OEA inhibits mitogenic and metabolic signaling by the insulin receptor and produces glucose intolerance⁴.

Activation of the TRPV1 channel leads to an increase in cytosolic calcium and that lead to prevention of adipogenesis⁵.

Activation of TRPV1 channel is necessary to prevent preadipocyte-to-adipocyte differentiation. TRPV1 activation may ultimately reduce the number and size of fat cells, and therefore reduce the tendency for fat to develop⁶.

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