Hydrolyzed Keratin CAS 69430-36-0

When the body is in a state of stress due to trauma, surgery, severe infection, etc., it can show a negative ammonia balance, which is mainly caused by the increase of skeletal muscle protein decomposition, and the degree of decomposition depends on the severity and duration of the stress. A metabolic feature of stress is that muscle and plasma glutamine concentrations decrease, but glutamine release from skeletal muscle increases.} In addition, the activity of glutamine synthase can be increased by 50% in stressed animals. Accordingly, it has been suggested that the increased rate of muscle protein degradation provides BCAAs, which in turn provide the ammonia required for muscle synthesis of glutamine. In vivo studies have also found that the use of BCAA can reduce the negative nitrogen balance associated with trauma, surgery and other stress.

Under normal circumstances, the composition of various amino acids in plasma remains basically constant. The liver is the main organ in the body to decompose and convert amino acids other than BCAA, so it plays a major role in the balance of amino acid metabolism in the body. Most reports still show that BCAA treatment of hepatic encephalopathy has a certain effect, at least not worse than the traditional treatment.

mechanism:

1) After the infusion of BCAA increases the plasma concentration, it can reduce the accumulation of AAA and other neutral amino acids in brain cells through the competitive transport with AAA and other neutral amino acids, which can reduce the generation of pseudo-neurotransmitters and the harm to neural activity.

2) BCAA, especially leucine, can increase protein synthesis and reduce protein degradation such as muscle, thereby reducing plasma AAA concentration and preventing severe negative nitrogen balance.

3) BCAA can help improve the nutritional status of the body when liver insufficiency occurs, that is, provide energy through the special metabolic type of BCAA. Therefore, it shows that long-term oral BCAA can effectively improve the survival rate and quality of life of patients.

Similar to portal venous encephalopathy, the plasma BCAA and its ketoacid concentrations are below normal values ​​in patients with chronic renal failure. Some people supplemented patients with chronic renal failure with essential amino acids or supplemented with solutions containing a high proportion of BCAA and found that although the clinical symptoms improved, However, plasma BCAA levels were not significantly elevated.

The innate immune response was recovered to some extent after BCAA supplementation. Naka-mura et al [6] reported. Neutrophil phagocytosis and NK cell activity and Fischer’s ratio were significantly improved in patients with decompensated cirrhosis after taking 12 g BCAA daily for 3 months. The mechanism may be that BCAA supplementation promotes albumin synthesis by activating the mTOR signal transduction system, and also enhances the synthesis of hepatocyte growth factor [7]. Therefore, BCAA not only improves the poor nutritional status of patients with liver cirrhosis, but also restores the inherent immunity of patients.

BCAA inhibits the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) pathway, not only by promoting the mammalian target of rapamycin complex 1. mTORC 1/ Negative feedback from S6 kinase 1 to the PI3K/Akt pathway and also inhibits mTORC2 kinase activity. It is suggested that supplementation of BCAA may be effective in inhibiting the progression of liver cancer by inhibiting insulin-mediated PI3K/Akt and subsequent anti-apoptotic pathways. It also suggests that BCAA supplementation is important in diabetic patients with advanced liver disease.