DNA Fragments for Rapidly Decreasing Triglyceride

Triacylglycerols are highly concentrated energy stores, fatty acids are physiologically important as (1) fuel molecules, (2) components of phospholipids and glycolipids, (3) hydrophobic modifiers of proteins, and (4) hormones and intracellular messengers. They are stored in adipose tissue as triacylglycerols (neutral fat). Triacylglycerols can be mobilized by the hydrolytic action of lipases that are under hormonal control. Glucagon and epinephrine stimulate triacylglycerol breakdown by activating the lipase. Insulin, in contrast, inhibits lipolysis. Fatty acids were activated to acyl CoAs, transported across the inner mitochondrial membrane by carnitine, and degraded in the mitochondrial matrix by a recurring sequence of four reactions: oxidation by FAD, hydration, oxidation by NAD+, and thiolysis by coenzyme A. The FADH2 and NADH formed in the oxidation steps transfer their electrons to O2 by means of the respiratory chain, whereas the acetyl CoA formed in the thiolysis step normally enters the citric acid cycle by condensing with oxaloacetate. Mammals are unable to convert fatty acids into glucose, because they lack a pathway for the net production of oxaloacetate, pyruvate, or other gluconeogenic intermediates from acetyl CoA.

Unsaturated and odd-chain fatty acids require additional steps for degradation.Fatty acids that contain double bonds or odd numbers of carbon atoms require ancillary steps to be degraded. An isomerase and a reductase are required for the oxidation of unsaturated fatty acids, whereas propionyl CoA derived from chains with odd numbers of carbon atoms requires a vitamin B12-dependent enzyme to be converted into succinyl CoA.

Fatty acids are synthesized in the cytoplasm by a different pathway from that of β oxidation. Synthesis starts with the carboxylation of acetyl CoA to malonyl CoA, the committed step. This ATP-driven reaction is catalyzed by acetyl CoA carboxylase, a biotin enzyme. The intermediates in fatty acid synthesis are linked to an acyl carrier protein. Acetyl ACP is formed from acetyl CoA, and malonyl AGP is formed from malonyl CoA. Acetyl ACP and malonyl AGP condense to form acetoacetyl ACP, a reaction driven by the release of CO2 from the activated malonyl unit. A reduction, a dehydration, and a second reduction follow. NADPH is the reductant in these steps. The butyryl ACP formed in this way is ready for a second round of elongation, starting with the addition of a two-carbon unit from malonyl ACP. Seven rounds of elongation yield palmitoyl ACP, which is hydrolyzed to palmitate. In higher organisms, the enzymes catalyzing fatty acid synthesis are covalently linked in a multifunctional enzyme complex. A reaction cycle based on the formation and cleavage of citrate carries acetyl groups from mitochondria to the cytoplasm. NADPH needed for synthesis is generated in the transfer of reducing equivalents from mitochondria by the malate-pyruvate shuttle and by the pentose phosphate pathway.

Fatty acid synthesis and degradation are reciprocally regulated so that both are not simultaneously active. Acetyl CoA carboxylase, the essential control site, is phosphorylated and inactivated by AMP- dependent kinase. The phosphorylation is reversed by a protein, phosphatase. Citrate, which signals an abundance of building blocks and energy, partly reverses the inhibition by phosphorylation. Carboxylase activity is stimulated by insulin and inhibited by glucagon and epinephrine. In times of plenty, fatty acyl CoAs do not enter the mitochondrial matrix, because malonyl CoA inhibits carnitine acyltransferaseΙ.

The elongation and unsaturation of fatty acids are accomplished by accessory enzyme systems.Fatty acids are elongated and desaturated by enzyme systems in the endoplasmic reticulum membrane. Desaturation requires NADH and O2 and is carried out by a complex consisting of a flavoprotein, a cytochrome, and a nonheme iron protein. Mammals lack the enzymes to introduce double bonds distal to C-9, and so they require linoleate and linolenate in their diets. Arachidonate, an essential precursor of prostaglandins and other signal molecules, is derived from linoleate. This 20:4 polyunsaturated fatty acid is the precursor of several classes of signal molecules— prostaglandins, prostacyclins, thromboxanes, and leukotrienes—that act as messengers and local hormones because of their transience. They are called eicosanoids because they contain 20 carbon atoms. Aspirin (acetylsalicylate), an anti-inflammatory and antithrombotic drug, irreversibly blocks the synthesis of these eicosanoids. It is only basic theory of triglyceride metabolism.

The high level of triglyceride relates to atherosclerosis, if combines with high blood pressure, it has large chance to cause coronary arteriosclerosis and stroke, it also causes pancreatitis because high level of triglyceride makes too sticky blood which affects the blood function to carry oxygen, special in brain area. Best methods in lowering triglyceride are control diet and medication. On control diet, one has to control intake of sugar, fat, and alcohol, and keep healthy weight and lifestyle. On medication, takes fibric acid derivatives, bile acid sequestrates, and nicotinic acid for 3 to 6 months and periodic examination of concentration of blood fat. Some diseases cannot cure at all.

The American Heart Association publishes that a triglyceride level index:

The Sensory Humans is a free organism system in the domain of Eukarya Homeostasis, he utilizes the Absolute Homeostasis Energy Source to activate the biochemical processes in the body and regulates the free energy to activate the chemical reactions of carbohydrate, lipids, proteins, amino acids, enzymes, nucleic acids, vitamins, hormones, and trace elements. It can convert spontaneous irreversible processes to spontaneous reversible processes. The special strong promoter function is to strong activate of gene transcription promoter and ribosome and controls process of peptides of special amino acids sequence and protein and induces cellular division, reproduction, and new organelle formation and let body rapidly recover to normal condition.

For controlling high level of triglyceride, it is different between the Sensory Humans and modern people, the Sensory Humans can strong activate DNA fragment (LYF of triglyceride) to rapidly decrease the level of triglyceride, this fragment locates in the control pathway cells of pancreas, liver, and bile. After activation of normal procedures, the two rapid metabolism reactions will happen: 1. Rapid activation: it can rapidly excrete the intake foods containing carbohydrate and lipid which can convert to triglyceride after 30 minutes. 2. Adaptable activation: it can adapt metabolism of excess triglyceride and excretes foods which will form triglyceride.

The following is the clinical data for Mr. Yuan Lin. When his level of triglyceride was 700 mg/dL, he passed through strong promoter function to activate DNA fragment (LYF of triglyceride) to rapidly decrease of triglyceride and took one pill of 40mg Lipitor as precursor every day. After 33 days, his level of triglyceride almost reached normal level.

After 49 days, the medical test report from Chang Gung hospital showed that triglyceride and cholesterol of Mr. Yuan Lin are normal level.

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