Apolipoprotein
Apolipoprotein E
Lipoprotein A

https://en.m.wikipedia.org/wiki/Apolipoprotein

https://en.m.wikipedia.org/wiki/Lipoprotein(a)

https://en.m.wikipedia.org/wiki/Apolipoprotein_E

The current simplest treatment for elevated Lp(a) is to take 1–3 grams of niacin daily, typically in an extended-release form. Niacin therapy may reduce Lp(a) levels by 20–30%. However more recent research suggests that the inflammatory effects of the breakdown products of excess niacin lead to an increase in risk of major adverse cardiovascular event.

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Ketoglutarate
Oxaloacetate
Succinyl-CoA
Pyruvate
Pyruvate Oxidation
Oxidative Decarboxylation
Tricarboxylic

Tricarboxylate Transport Protein Mitochondrial

Mitochondrial Carrier

https://en.m.wikipedia.org/wiki/Mitochondrial_carrier

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The citric acid cycle (TCA cycle) is a central metabolic pathway where glucose, fatty acids, and amino acids are oxidized, and its intermediates serve as precursors for various biosynthetic processes, including amino acid synthesis.

The Citric Acid Cycle (TCA Cycle):

Also known as the Krebs cycle or tricarboxylic acid cycle, it's a series of chemical reactions that occur in the mitochondria of cells.

The cycle is the final common pathway for the oxidation of carbohydrates, fatty acids, and amino acids.
It plays a crucial role in energy production (ATP) and provides building blocks for other metabolic processes.

Precursors for Amino Acid Synthesis:

Amino acids: can be synthesized from intermediates of the citric acid cycle, such as α-ketoglutarate, oxaloacetate, and succinyl-CoA.
For example, α-ketoglutarate is a precursor for glutamate, and oxaloacetate is a precursor for aspartate.

Some amino acids are glucogenic (can be converted to glucose) and some are ketogenic (can be converted to ketone bodies).

Gluconeogenesis: The process of synthesizing glucose from non-carbohydrate sources (like amino acids, glycerol, and lactate) also relies on the citric acid cycle.

Metabolism of Other Nutrients:

Glucose: Glucose is metabolized to pyruvate, which then enters the citric acid cycle as acetyl-CoA.

Fatty acids: Fatty acids are broken down into acetyl-CoA, which also enters the citric acid cycle.

Amino acids: Amino acids are converted to various intermediates of the citric acid cycle, depending on the specific amino acid.

Interconnections:

The citric acid cycle is interconnected with other metabolic pathways, including glycolysis, fatty acid synthesis, and gluconeogenesis.

It serves as a central hub for the metabolism of carbohydrates, fats, and proteins.

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Hydroxycarboxylic Acid
Receptor 2
Neprilysin

https://en.m.wikipedia.org/wiki/Hydroxycarboxylic_acid_receptor_2

https://en.m.wikipedia.org/wiki/Neprilysin

https://en.m.wikipedia.org/wiki/%CE%92-Hydroxybutyric_acid

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Myalgic Encephalomyelitis
Nitrosative Stress
Peroxynitrite
Nitrotyrosine

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Niacin, a B vitamin, interacts with the HCAR2 receptor (also known as GPR109A), which is expressed by microglia in the brain, and its activation by niacin can lead to reduced amyloid plaque burden and improved cognition in Alzheimer's disease (AD) mouse models.

Neprilysin, an enzyme that degrades amyloid-beta (Aβ), is also implicated in AD pathology, and increased neprilysin levels have been associated with reduced Aβ levels and plaque formation.

Niacin, a form of vitamin B3, acts as a high-affinity ligand for HCAR2, a G-protein-coupled receptor (GPCR).

In the brain, HCAR2 is selectively expressed by microglia, which are immune cells that play a role in the brain's response to amyloid pathology.

Neprilysin (NEP) is an enzyme that degrades Aβ, the main component of amyloid plaques in AD.

Increased NEP levels in the brain have been associated with reduced Aβ levels and prevention of amyloid plaque formation.

Conversely, decreased NEP levels have been linked to increased Aβ levels, impaired synaptic plasticity, and cognitive abnormalities.

Studies have shown that activation of HCAR2 by niacin can lead to increased expression and activity of neprilysin, further supporting the potential therapeutic benefits of targeting this pathway in AD.

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Butyrate

Fermentable Fiber Sources

Highly-fermentable fiber residues, such as those from resistant starch, oat bran, pectin, and guar are transformed by colonic bacteria into short-chain fatty acids (SCFA) including butyrate, producing more SCFA than less fermentable fibers such as celluloses. Resistant starch consistently produces more butyrate than other types of dietary fiber.

Sulfur Fructans Butyrate

Fructans are another source of prebiotic soluble dietary fibers which can be digested to produce butyrate. They are often found in the soluble fibers of foods which are high in sulfur, such as the allium and cruciferous vegetables.

Butyrate is a short-chain fatty acid (SCFA) produced by gut bacteria through the fermentation of dietary fiber.

Butyrate is primarily produced by gut bacteria in the colon as a byproduct of fermenting dietary fiber, especially resistant starch and other non-digestible carbohydrates.

Butyrate is a primary energy source for colonocytes (cells lining the colon), providing approximately 70% of their energy needs.

Histone Deacetylase (HDAC) Inhibition:

Butyrate acts as an HDAC inhibitor, which can influence gene expression and potentially have anti-inflammatory and anti-cancer effects.

G Protein-Coupled Receptors (GPCRs):

Butyrate interacts with certain GPCRs, which are involved in signaling pathways that regulate various cellular functions.