BCAAs

2022-08-17: reference:

BCAA (branched-chain Amino Acids) #

Includes Leucine, Isoleucine, Valine, as well as 2-aminoisobutyric acid.

• Dietary branched chain amino acids and metabolic health: when less is more
  • Repletion of branched chain amino acids reverses mTORC1 signaling but not improved metabolism during dietary protein dilution (Maida et al. 2017)
    • BCAA depletion -> lower mTORC1 & liver releases FGF21, the expression and secretion of which is induced as part of a liver integrated stress response (like ISRIB)
      • dietary BCAA repletion did not curb the induction of the hepatic ISR
    • Serum BCAAs are elevated in obesity.
  • Restoration of metabolic health by decreased consumption of branched‐chain amino acids (Cummings et al. 2018)
  • Decreased consumption of branched‐chain amino acids improves metabolic health
  • Brain Responses to High-Protein Diets
    • After protein consumption, peptide hormones released from the gastrointestinal tract (mainly anorexigenic gut peptides such as cholecystokinin, glucagon peptide 1, and peptide YY) communicate information about the energy status to the brain.
    • Proteins inhibit anabolic neuronal signaling (decreased NPY and agouti-related protein mRNA levels) and activate the catabolic signaling (POMC neurons producing α-melanocyte-stimulating hormone) in the hypothalamus. High-protein intake releases Peptide YY.
      • Orexigenic agents such as Agouti-related protein activate hypothalamic AMPK and inhibit mTOR; anorexigenic agents such as leptin have the opposite effects. Thus, AMPK overexpression in the Hypothalamus increases food intake and body weight.
        • Don’t get caught up in the word games, I guess. Leucine’s increasing of ‘catabolic’ Arc signals is the body’s way of negative feedback for the anabolic signal.
  • A central role for neuronal AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) in high-protein diet-induced weight loss
    • mTOR and AMPK colocalize with NPY and POMC neurons.
• Branched-chain amino acid restriction in Zucker-fatty rats improves muscle insulin sensitivity by enhancing efficiency of fatty acid oxidation and acyl-glycine export
  • Obesity inhibits BCKDH (branched-chain α-ketoacid dehydrogenase complex) which decarboxylates α-Keto Acids.
  • This “BCAA overload” in skeletal muscle interferes with the complete oxidation of fatty acids, leading to accumulation of even chain fatty acyl CoAs in skeletal muscle. This effect is compounded by BCAA-driven depletion of skeletal muscle Glycine levels, which limits acyl CoA excretion as acyl-glycines in the urine.
    • And basically, Glycine conjugates all these free acetly groups, whereby it can be excreted in the urine.
  • They also talk about the α-Keto Acids.
• Chronic dietary exposure to branched chain amino acids impairs glucose disposal in vegans but not in omnivores
  • In omnivores the BCAA intervention led to an increased expresion of lipogenic genes (DGAT2, Fatty Acid Synthase, PPAR-γ, Δ9 Desaturase)
• Restriction is thermogenic? According to fireinabottle. Obese people have a difficult time breaking them down, unlike in his idea of a healthy metabolism.