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There is a between the the hormone neuropeptide Y, and LPL levels which play a role in appetite.
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this usually occurs in the morning (from what i learned in school).
Neuropeptide Y certainly plays an important role in appetite regulation. My original querry related to your assertion regarding high LPL levels in fasted states.
obviously insulin plays a role in this NPY and LPL levels, anf after fasting and ingesting a high carbohydrate meal (like a breakfast cereal or something with a lot of sugar) your body over secretes insulin to deal with this amount of sugar (again something i learned while in school) this in turn is why id rather not have my carbs in the morning.
Insulin response to carbohydrate consumption is a metabolic activity that is certainly not restricted to morning (carbohydrate) meals alone. It is the body's default response to carbohydrate intake, irrespective of time of day, assuming no dysfunction in pancreatic beta-cell activity.
It is, in fact, reasonable to expect a more effective macronutrient absorption in the mornings, as the body is in an optimal state for nutrient uptake, a state termed by some as an "Anabolic Window of Opportunity".
...then again theres a lot of interaction between LPL NPY and Leptin, When NPY is low HSL is higher which helps with FFA metabolism
It might help to examine some concepts and relationships more closely, in order to promote targeted understanding of certain assertions.
Now, abundantly available in the fat-cell membrane, hormone-sensitive lipase (HSL) is actually a crucial enzyme in the hydrolysis of triacylglycerol (TAG) [to diacyglycerol (DAG) and free fatty acids (FFA)] and degradation of cholesteryl ester (into free cholesterol for the production of steroid hormones), in different tissues, including adipocytes. HSL is regulated via reversible phosphorylation on four residues. When the body’s energy needs rise, the secretion of hormone-sensitive lipase is stimulated. The activation of HSL leads to the breakdown of triglycerides (made up of fatty acids and glycerol), and the release of fatty acids for the production of adenosine triphosphate (ATP). HSL shows a synergistic relationship with glucagon, cathecholamines, and adrenocorticotropic hormone (ACTH), but responds negatively to insulin. In fact, down-regulation of hormone-sensitive lipase inhibits adipogenesis and obesity.
Now to leptin. The adipocytokine leptin is an adipocyte protein. Leptin is involved in the inhibition of appetite and regulates the enzymes involved in the synthesis of fatty acids. Now, let’s introduce neuropeptide Y (NPY). Appetite regulation is broadly governed by two hypothalamic neuronal groups.
The first is the so-called neuropeptide Y/Agouti-related protein or Agouti-related peptide (NPY/AgRP) group. When these neurons are activated, NPY and AgRP are released, leading to the stimulation of appetite. Leptin suppresses the expression of these neurons. In effect, low levels of leptin leads to a high hypothalamic concentration of NPY/AgRB, leading to appetite stimulation and potential fat accumulation. Something else: Hypothalamic insulin receptors inhibit NPY secretion; furthermore, PYY3-36 (a gastro-intestinal-tract appetite-stimulating hormone) down-regulates appetite by inhibiting the secretion of NPY/AgRP; while Ghrelin (an appetite-stimulating peptide secreted in fasting states) stimulates NPY activity.
The other group of hypothalamic neuronal hormones is the so-called pro-opiomelanocortin/cocaine and amphetamine-regulated transcript (POMC/CART) group. The stimulation of these neurons eventually leads to the inhibition of appetite. Leptin stimulates the expression of these neurons.
Malonyl-CoA is the first committed step in the synthesis of fatty acids, and does not inhibit lipolysis.however i do understand that malonyl CoA inhibits lipolysis, but i have not learned much about that in my short semester in bio chem.
this was a decent read tho.
EDIT: should have worded my words better in the original post with carb craving...
Agree. Tight terminology helps a lot!