#mtor

[bpod-bpod]

Too Small Intestines

The rarity of some genetic disorders can make them difficult to study in patients. An animal model that replicates some of the disease mechanisms can help researchers, and a new study has developed the first zebrafish model for Feingold syndrome type 1, which causes incomplete development of the gastrointestinal tract among other symptoms. The condition is caused by mutations in the gene Mycn (stained green, active throughout the intestines of healthy fish, pictured). The mutant fish developed short intestines with reduced folding, and the deletion of Mycn impacted other genes as well, including those in a central regulator of protein synthesis, the mTOR signalling pathway. Supplementation with leucine, a building block that activates the mTOR pathway, helped restart protein synthesis and led to a partial recovery of intestine size. If the mechanisms translate to human biology, this simple supplement could bring relief to patients with Feingold syndrome type 1.

Written by Anthony Lewis

Image from work by Yun-Fei Li, Tao Cheng and colleagues

Zhejiang University School of Medicine, Hangzhou, China

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in PLOS Biology, November 2022

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[notesonbiology]

mTOR

"Under nutrient-rich conditions mTORC1 promotes cell growth by stimulating biosynthetic pathways, including synthesis of proteins, lipids and nucleotides, and by inhibiting cellular catabolism through repression of the autophagic pathway.

"The convergence point of anabolic and catabolic processes is the mechanistic target of rapamycin (mTOR), which senses fluctuations in extracellular and intracellular nutrients to modulate cellular growth, metabolism and survival.

"Cellular demands for amino acids are cell- and tissue-specific; while glutamine is an important energy source feeding the tricarboxylic acid (TCA) cycle particularly in glycolysis-dependent tumour cells [41], arginine influx and arginase levels are tightly regulated in liver for the urea cycle [42].

"Leucine, glutamine and arginine have been widely shown as the main contributors to mTORC1 activation [43–47]. In particular, glutamine, in addition to serving as a key energy source, cooperates with leucine to activate mTORC1. Glutamine can be deaminated to produce α-ketoglutarate, which is both an intermediate in the TCA cycle and a regulator of mTORC1 activity and autophagy. However, this reaction requires the presence of leucine, which acts as a cofactor of the enzyme that catalyses the last step of glutaminolysis [48].

"It is now clear that cellular homoeostasis of metabolism and growth is exquisitely controlled by the coordination of AMPK and mTORC1. AMPK is crucial to the cellular response to low energy levels and, once active, drives processes which will replenish cellular energy stores, such as autophagy while inhibiting biogenic synthesis [116]. Opposite to AMPK, activated mTORC1 shifts the metabolic programme of the cell from catabolic to anabolic metabolism by up-regulating the synthesis of building blocks for cell proliferation, including proteins, lipids and nucleotides [117].

"Whereas the role of amino acids as key signal factors in the activation of mTORC1 has been accepted, to date, the inhibitory effect of amino acids on AMPK has been a debatable issue. Some studies have observed the inhibition of AMPK by amino acids [124–126], though this has not always been the case [127,128]. A recent work suggests amino acids as novel metabolic activators of AMPK. In this study, AMPK responded acutely and within 1 min to amino acid and its activation was independent of mTORC1 [129]. ...  Furthermore, they demonstrate that AMPK activation occurs via the Ca2+/calmodulin-dependent kinase kinase-β (CaMKKβ) and that activation of the CaMKKβ–AMPK axis by amino acids does not inhibit mTORC1 but sustains autophagy."

[funsimplethings]

[regenexx]

What is Autophagy and Why You Should Care? Autophagy Procedures and Benefits

Welcome to the "Regenexx". Throughout this video, you will learn about Autophagy, why you should care about it, its procedures, and its benefits.

Autophagy is the body's way of cleaning out damaged cells, in order to regenerate newer, healthier cells. Autophagy, the original cellular detox occurs when the body is in a calorically restricted state and starts to consume senescent, old, weak, and dying cells as a source of energy. This benefits us by cleaning house and keeping these old cells from wreaking havoc on other more healthy cells. Autophagy can occur to some extent from exercise or after the body has been in a fasted state for about 48 hours. As one begins to consume food again, the body in its infinite wisdom will release stem cells to begin to rebuild the tissue that the body consumed. Autophagy is triggered when mTOR is suppressed from caloric restriction, and reduced glucose and amino acid ingestion. Eating these macro nutrients will stop the process of autophagy.

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Watching is enough Ver es suficiente

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