Tue, Apr-18-17, 04:29
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Senior Member
Posts: 15,075
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Plan: mostly milkfat
Stats: 190/152.4/154
BF:
Progress: 104%
Location: Ontario
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https://www.ncbi.nlm.nih.gov/pubmed/27843095
Quote:
Branched Chain Amino Acids Cause Liver Injury in Obese/Diabetic Mice by Promoting Adipocyte Lipolysis and Inhibiting Hepatic Autophagy.
Zhang F1, Zhao S1, Yan W1, Xia Y1, Chen X2, Wang W1, Zhang J1, Gao C1, Peng C1, Yan F1, Zhao H1, Lian K1, Lee Y1, Zhang L1, Lau WB3, Ma X3, Tao L4.
Author information
Abstract
The Western meat-rich diet is both high in protein and fat. Although the hazardous effect of a high fat diet (HFD) upon liver structure and function is well recognized, whether the co-presence of high protein intake contributes to, or protects against, HF-induced hepatic injury remains unclear. Increased intake of branched chain amino acids (BCAA, essential amino acids compromising 20% of total protein intake) reduces body weight. However, elevated circulating BCAA is associated with non-alcoholic fatty liver disease and injury. The mechanisms responsible for this quandary remain unknown; the role of BCAA in HF-induced liver injury is unclear. Utilizing HFD or HFD+BCAA models, we demonstrated BCAA supplementation attenuated HFD-induced weight gain, decreased fat mass, activated mammalian target of rapamycin (mTOR), inhibited hepatic lipogenic enzymes, and reduced hepatic triglyceride content. However, BCAA caused significant hepatic damage in HFD mice, evidenced by exacerbated hepatic oxidative stress, increased hepatic apoptosis, and elevated circulation hepatic enzymes. Compared to solely HFD-fed animals, plasma levels of free fatty acids (FFA) in the HFD+BCAA group are significantly further increased, due largely to AMPKα2-mediated adipocyte lipolysis. Lipolysis inhibition normalized plasma FFA levels, and improved insulin sensitivity. Surprisingly, blocking lipolysis failed to abolish BCAA-induced liver injury. Mechanistically, hepatic mTOR activation by BCAA inhibited lipid-induced hepatic autophagy, increased hepatic apoptosis, blocked hepatic FFA/triglyceride conversion, and increased hepatocyte susceptibility to FFA-mediated lipotoxicity. These data demonstrated that BCAA reduces HFD-induced body weight, at the expense of abnormal lipolysis and hyperlipidemia, causing hepatic lipotoxicity. Furthermore, BCAA directly exacerbate hepatic lipotoxicity by reducing lipogenesis and inhibiting autophagy in the hepatocyte.
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Okay, so in mice at least, maybe branched chain amino acids "supercharge" the metabolism. Increased lipolysis, they're surprised when blocking lipolysis fails to completely reverse this, the explanation given is that inhibiting autophagy is damaging. Paranoid bodybuilders taking leucine to avoid catabolism during fasting or exercise come to mind. Maybe it increases lean mass, is it good for you?
The increased lipolysis--one way that might work, there's a fatty liver model in rodents where deficiency of methionine results in increased lipolysis. In some models, this leads to fatty liver, in others methionine restriction leads to increased lifespan. In the increased lifespan studies, energy fraction from mitochondrial respiration does increase, that fits with increased fatty acid oxidation. Maybe it comes down to other components in the diet, like choline. Or age of diet initiation, methionine restriction in young animals makes them fatter instead of leaner.
Restricting methionine would increase the ratio of branch chained amino acids to methionine in the diet, obviously supplementing BCAA's to a balanced protein diet would have the same effect on that ratio. You could see leucine at least transiently reducing methionine availability in fat tissue due to the increase in protein synthesis in lean tissue.
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Dr. Fred Pescatore Claims Amino Acids Key to Faster LC Weight Loss
Just Eat Real Food
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