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Reprograming of Proteasomal Degradation by Branched Chain Amino Acid Metabolism

ABSTRACT: Reprograming of Proteasomal Degradation by Branched Chain Amino Acid Metabolism

PROVIDER: PRJNA769111 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16219876_1.fastq.gz	Fastqsanger.gz
	SRR16219876_2.fastq.gz	Fastqsanger.gz
	SRR16219877_1.fastq.gz	Fastqsanger.gz
	SRR16219877_2.fastq.gz	Fastqsanger.gz
	SRR16219878_1.fastq.gz	Fastqsanger.gz

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Reprograming of Proteasomal Degradation by Branched Chain Amino Acid Metabolism

Project description:Branched‐chain amino acid (BCAA) metabolism is a central hub for energy production and regulation of numerous physiological processes. Controversially, both increased and decreased levels of BCAAs are associated with longevity. Using genetics and multi‐omics analyses in Caenorhabditis elegans, we identified adaptive regulation of the ubiquitin‐proteasome system (UPS) in response to defective BCAA catabolic reactions after the initial transamination step. Worms with impaired BCAA metabolism show a slower turnover of a GFP‐based proteasome substrate, which is suppressed by loss‐of‐function of the first BCAA catabolic enzyme, the branched‐chain aminotransferase BCAT‐1. The exogenous supply of BCAA‐derived carboxylic acids, which are known to accumulate in the body fluid of patients with BCAA metabolic disorders, is sufficient to regulate the UPS. The link between BCAA intermediates and UPS function presented here sheds light on the unexplained role of BCAAs in the aging process and opens future possibilities for therapeutic interventions.

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Reprograming of Proteasomal Degradation by Branched Chain Amino Acid Metabolism

Project description:Branched chain amino acids (BCAAs) play an important role in energy and protein regulation. Defects in BCAA metabolism are linked to numerous pathologies, including diabetes, neurodegeneration, and premature aging. Isovaleric acidemia is a metabolic disease caused by defective leucine breakdown and an abnormal accumulation of isovaleric acid in the body fluids; however, the cytotoxic effects caused by excess isovaleric acid remained unclear. Here, we provide a regulatory connection between BCAA metabolism and the ubiquitin/proteasome-system (UPS) in Caenorhabditis elegans. Multi-omic analysis identified that worms lacking the isovaleryl-CoA dehydrogenase IVD-1 exhibit reduced expression of regulatory proteasome subunits and defects in ubiquitin-dependent proteolysis. Conversely, proteasomal protein degradation was supported by the branched chain amino transferase BCAT-1. Adding extra isovaleric acid to the growth medium triggered UPS defects, implying a causative role of perturbed proteostasis in isovaleric academia.

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Project description:Postoperative insulin resistance refers to the phenomenon that the body’s glucose uptake stimulated by insulin is reduced due to stress effects such as trauma or the inhibitory effect of insulin on liver glucose output is weakened after surgery. There is a clear link between postoperative insulin resistance and poor perioperative prognosis. Therefore, exploring interventions to reduce postoperative stress insulin resistance, stabilize postoperative blood glucose, and reduce postoperative complications are clinical problems that need to be solved urgently. In recent years, research on branched-chain amino acids and metabolic diseases has become a hot spot. Studies have found that in the rat model, preoperatively given a high branched-chain amino acid diet can inhibit postoperative insulin resistance and stabilize blood glucose levels. This research plan is to try to add branched-chain amino acids before surgery to observe the occurrence of postoperative insulin resistance in patients.

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Reprograming of proteasomal degradation by branched chain amino acid metabolism.

Project description:Branched-chain amino acid (BCAA) metabolism is a central hub for energy production and regulation of numerous physiological processes. Controversially, both increased and decreased levels of BCAAs are associated with longevity. Using genetics and multi-omics analyses in Caenorhabditis elegans, we identified adaptive regulation of the ubiquitin-proteasome system (UPS) in response to defective BCAA catabolic reactions after the initial transamination step. Worms with impaired BCAA metabolism show a slower turnover of a GFP-based proteasome substrate, which is suppressed by loss-of-function of the first BCAA catabolic enzyme, the branched-chain aminotransferase BCAT-1. The exogenous supply of BCAA-derived carboxylic acids, which are known to accumulate in the body fluid of patients with BCAA metabolic disorders, is sufficient to regulate the UPS. The link between BCAA intermediates and UPS function presented here sheds light on the unexplained role of BCAAs in the aging process and opens future possibilities for therapeutic interventions.

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Branched chain amino acids impact health and lifespan indirectly via amino acid balance and appetite control

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