Glysiinistä: Suoliston mikrobit konsumoivat glysiiniä

Näyttää siltä että suolistomikrobit eivät ole mitään glysiinin tekijöitä, vaan glysiinin kuluttajia.  Ne käyttävät glysiiniä kasvuunsa ehkä myös ihmisellä tämän 2016  hiirikokeen perusteella. Sikäli ei olisi suositeltavaa mikään varinainen  "vahvaglysiininen ravinto", vaan aivan normaalia aminohappotasapainoa omaava  sekaravinnon proteiini kuten  yleensä tavallisessa ruoassa ja sellainen  ravinto, jonka kuitupitoisuus on hyvä, jotta mikrobit pysyvät kurissa ja hyvänlaatuisina  ja suoliston  toiminta  normaalina.  
Tuollinen näkymätön glysiinin menetys suolistossa voi kostautua oman suolistokudoksen ja muidenkin kudosten  heikkouteen krooniselle sairaudelle tyypillisenä ilmiöntä.  ihminen tarvitsee muun muassa glysiiniä antioksdanttiseen puolustukseensa - tripeptidin osana (GSH) . (cysteiini, glysiini ja glutamiinihappo muodostavat , joka on tärkeä  antioksidanttijärjestelmässä ja puolustuksen  aktiivisuudessa, detoksikaatiossa).
Hiirikoetuloksien perusteella tutkija  viittaa mahdolliseen hyötyyn glysiinisupplementista eräissä tapauksissa: lihavuudessa ja rasvamaksassa, joka ei ole alkoholista johtuvaa, sillä näissä tapauksisa on havaittu plasman glysiinissä matalia arvoja.

• http://www.asmscience.org/content/journal/microbe/10.1128/microbe.11.54.1

 

The gut microbiota in mice consumes glycine, one of three amino acids needed by host animals to make the powerful antioxidant peptide glutathione, according to Adil Mardinoglu at the Royal Institute of Technology in Stockholm and Chalmers University of Technology, Gothenburg, both in Sweden, and his collaborators in Sweden and Denmark. He calls this example of the gut microbiota exerting partial control over this host metabolic pathway “surprising,” and suggests that “imbalances in the composition of bacteria [within the microbiota] may lead to the progression of chronic diseases.” Details appeared 16 October 2015 in Molecular Systems Biology (doi:10.15252/msb.20156487). 

 Mardinoglu and his collaborators compared metabolic differences between conventional mice—that is, host animals with a full complement of microorganisms in the gastrointestinal tract and other anatomic sites—and germ-free animals. Those comparisons drew on direct experiments with mice, analyses of gene expression data, some 28 tissue-specific genome-scale metabolic models, and a generic mouse metabolic reaction that the researchers developed, they note. Their approach combined proteomics, metabolomics, and transcriptomics, with computer modeling of organs such as the small intestine and liver.
By measuring levels in the hepatic portal vein of the three amino acids needed for making glutathione, the researchers determined that amounts of glycine shunted to the liver and glutathione production are lower in conventional mice than in germ-free mice. In other words, the microbiota within the gastrointestinal tract of the host mice consumed glycine, supporting their own growth while depriving their hosts of what they need to produce glutathione.
Moreover, expression of the gene encoding nicotinamide nucleotide transhydrogenase (NNT), an enzyme that is needed for making glutathione, is higher in mice with a full-fledged microbiota than it is in germ-free mice, Mardinoglu continues. Although the limited availability of glycine in such mice prevents them from making glutathione, they try to compensate by making more NNT, he says.
Lipid metabolism in such mice also is altered compared to germ-free animals. The small intestine of conventional mice produces lower levels of high-density lipoproteins and chylomicrons. Overall, the gut microbiota regulates amino acids, glutathione, and lipid metabolism in mice. 

These metabolic shifts could be clinically relevant for particular groups of human patients, according to Mardinoglu. For example, individuals who are obese and patients with non-alcoholic fatty liver disease have low levels of glycine in plasma, he says. “The effect of glycine supplements should be investigated in these metabolic disorders.”
 More generally, deficiencies of glutathione contribute to oxidative stress, obesity, type 2 diabetes, and non-alcoholic fatty liver disease, he adds.
 “The link between gut bacteria and glutathione metabolism could lead to the development of probiotics that deliver beneficial bacteria to the gut.”

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  The gut microbiota in mice exert partial control over the mouse glutathione metabolic pathway, an indication that the composition of the microbiota play a role in chronic diseases. (Image © iStockphoto/filo.)

 

This research “introduces a novel methodological approach for inferring the impact of microbiome composition on metabolism in different tissues in mice,” says Costas Maranas at Pennsylvania State University in State College, who was not involved in the work. “Their efforts open the door for more investigations that will link detailed descriptions of the gut microbiome with a mouse tissue model.”