When you get some time I'd like to talk about Lipoenesis-
De Novo Synthesis in Humans
In humans, fatty acids are formed predominantly in the liver and lactating mammary glands, and, to a lesser extent, the adipose tissue. Most acetyl-CoA is formed from pyruvate by pyruvate dehydrogenase in the mitochondria. Acetyl-CoAproduced in the mitochondria is condensed with oxaloacetate by citrate synthase to form citrate, which is then transported into the cytosol and broken down to yield acetyl-CoA and oxaloacetate by ATP citrate lyase. Oxaloacetate in the cytosol is reduced to malate by cytoplasmic malate dehydrogenase, and malate is transported back into the mitochondria to participate in the Citric acid cycle.
Thus, stimulation of this lactogenic function by prolactin is not the result of its contamination with vasopressin. And vasopressin increases lipogenesis availability of lipogenic substrate (lactate+ pyruvate) and by activating acetyl-CoA carboxylase. Vasopressin (pituitary hormone, up regulates BP and water retention) stimulates fatty acid synthesis by 30-110%, but also up regulates BP and water rentention. Progesterone stimulates alveolar growth, estrogen stimulates ducal growth. Fatty acid synthesis stimulates mammary epithelial growth factor.
Oxytocin and Vasopressin: Genetics and Behavioral Implications
The pathway for fatty acid synthesis occurs in the cytoplasm, whereas, oxidation occurs in the mitochondria. (Preventing oxidation is the key, it's that ratio again lol, more omega 3's). IMO, a dose of 2000-3000mg of omega 3 to 1000mg of omega 6, 1:3
Metabolism uses various ways to ensure that 2 opposing pathways do not occur at the same time. For the following pair of pathways list 2 ways (different cell location, allosteric effector, covalent modification, different intermediate, different enzyme, or different means of transport).
Fatty acid oxidation and fatty acid synthesis are different from one another in following respects: The pathway for fatty acid synthesis occurs in the cytoplasm, adipose and liver whereas, oxidation occurs in the mitochondrial matrix and muscle.
The other major difference is the use of nucleotide co-factors. Oxidation of fats involves the reduction of FADH+ and NAD+. Synthesis of fats involves the oxidation of NADPH.
Lipoenesis stimulates breast growth, Lipogenesis is the process by which acetyl-CoA is converted to fatty acids. Lipogenesis encompasses both the process of fatty acid synthesis and triglyceride synthesis (where fatty acids are esterifiedwith glycerol to form fats). The products are secreted from the liver in the form of very-low-density lipoproteins (VLDL). VLDL are secreted directly into blood, where they mature and function to deliver the endogenously derived lipids to peripheral tissues.
Glycerol-3-phosphate dehydrogenase (GAPDH) enzyme which increases Adipocyte volume in the fatty breast tissues.
Activation of AMP-activated protein kinase stimulates the nuclear localization of glyceraldehyde 3-phosphate dehydrogenase in human diploid fibroblasts.
In addition to its well-known glycolytic activity, GAPDH displays multiple functions, such as nuclear RNA export, DNA replication and repair, and apoptotic cell death. This functional diversity depends on its intracellular localization. In this study, we explored the signal transduction pathways involved in the nuclear translocation of GAPDH using confocal laser scanning microscopy of immunostained human diploid fibroblasts (HDFs). GAPDH was present mainly in the cytoplasm when cultured with 10% FBS. Serum depletion by culturing cells in a serum-free medium (SFM) led to a gradual accumulation of GAPDH in the nucleus, and this nuclear accumulation was reversed by the re-addition of serum or growth factors, such as PDGF and lysophosphatidic acid. The nuclear export induced by the re-addition of serum or growth factors was prevented by LY 294002 and SH-5, inhibitors of phosphoinositide 3-kinase (PI3K) and Akt/protein kinase B, respectively, suggesting an involvement of the PI3K signaling pathway in the nuclear export of GAPDH. In addition, 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR), an activator of AMP-activated protein kinase (AMPK), stimulated the nuclear translocation of GAPDH and prevented serum- and growth factor-induced GAPDH export. AMPK inhibition by compound C or AMPK depletion by siRNA treatment partially prevented SFM- and AICAR-induced nuclear translocation of GAPDH. Our data suggest that the nuclear translocation of GAPDH might be regulated by the PI3K signaling pathway acting mainly as a nuclear export signal and the AMPK signaling pathway acting as a nuclear import signal.
Biotin breaks down carbs and fats, the speed of which I don't know yet, ALA, B5, eggs whites cause interactions. What do you think?. Potentiator?
(Biotin is a coenzyme for carboxylase enzymes, involved in the synthesis of fatty acids, isoleucine, and valine, and in gluconeogenesis.)