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An insulin-stimulated proteolytic mechanism links energy expenditure with glucose uptake

ABSTRACT: An insulin-stimulated proteolytic mechanism links energy expenditure with glucose uptake

PROVIDER: PRJNA556648 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9833210.fastq.gz	Fastqsanger.gz
	SRR9833211.fastq.gz	Fastqsanger.gz
	SRR9833212.fastq.gz	Fastqsanger.gz
	SRR9833213.fastq.gz	Fastqsanger.gz
	SRR9833208.fastq.gz	Fastqsanger.gz

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An insulin-stimulated proteolytic mechanism links energy expenditure with glucose uptake

Project description:Mechanisms to coordinately regulate oxidative metabolism and glucose transport into cells are not well described. In muscle and fat, insulin mobilizes GLUT4 glucose transporters to the cell surface in part by stimulating the site-specific endoproteolytic cleavage of TUG proteins. Here, we show that the TUG C-terminal cleavage product enters the nucleus, binds the transcriptional 30 regulators PGC-1a and PPARg, and increases oxidative metabolism, thermogenic protein expression, and energy expenditure. The PPARg2 Pro12Gly polymorphism, which confers reduced diabetes risk, enhances TUG binding. The TUG cleavage product stabilizes PGC-1a, so that both proteins are susceptible to an Ate1 arginyltransferase -dependent degradation mechanism. We conclude that TUG cleavage coordinates energy expenditure with glucose 35 uptake, and that alterations in this pathway may contribute to metabolic disease.

2020-07-23 | GSE134846 | GEO

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Insulin-stimulated endoproteolytic TUG cleavage links energy expenditure with glucose uptake.

Project description:TUG tethering proteins bind and sequester GLUT4 glucose transporters intracellularly, and insulin stimulates TUG cleavage to translocate GLUT4 to the cell surface and increase glucose uptake. This effect of insulin is independent of phosphatidylinositol 3-kinase, and its physiological relevance remains uncertain. Here we show that this TUG cleavage pathway regulates both insulin-stimulated glucose uptake in muscle and organism-level energy expenditure. Using mice with muscle-specific Tug (Aspscr1)-knockout and muscle-specific constitutive TUG cleavage, we show that, after GLUT4 release, the TUG C-terminal cleavage product enters the nucleus, binds peroxisome proliferator-activated receptor (PPAR)γ and its coactivator PGC-1α and regulates gene expression to promote lipid oxidation and thermogenesis. This pathway acts in muscle and adipose cells to upregulate sarcolipin and uncoupling protein 1 (UCP1), respectively. The PPARγ2 Pro12Ala polymorphism, which reduces diabetes risk, enhances TUG binding. The ATE1 arginyltransferase, which mediates a specific protein degradation pathway and controls thermogenesis, regulates the stability of the TUG product. We conclude that insulin-stimulated TUG cleavage coordinates whole-body energy expenditure with glucose uptake, that this mechanism might contribute to the thermic effect of food and that its attenuation could promote obesity.

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Project description:The combination of decreasing food intake and increasing energy expenditure represents a powerful strategy for counteracting cardiometabolic diseases, such as obesity and type 2 diabetes1. Yet current approaches require conjugating multiple receptor agonists to achieve both effects2–4 and, thus far, no safe energy-expending option has reached the clinic. Here we show that activation of Neurokinin 2 Receptor (NK2R) is sufficient to suppress appetite centrally and increase energy expenditure peripherally. We focused on NK2R after discovering its genetic links to obesity and glucose control. However, therapeutically exploiting NK2R signalling has previously been unattainable because its endogenous ligand, Neurokinin A (NKA), is short-lived and lacks receptor specificity5,6. Therefore, we developed selective, long-acting NK2R agonists, with potential for once-weekly administration in humans. In mice, these agonists elicit weight loss by inducing energy expenditure and non-aversive appetite suppression that circumvents canonical leptin signalling. Additionally, a hyperinsulinemic-euglycemic clamp reveals that NK2R agonism acutely enhances insulin sensitization. In diabetic, obese nonhuman primates, NK2R activation significantly decreases body weight, blood glucose, triglycerides, and cholesterol, and ameliorates insulin resistance. These findings identify a single receptor target that leverages both energy-expending and appetite-suppressing programs to improve energy homeostasis and reverse cardiometabolic dysfunction across species.

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