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Mlycd deficiency in Dahl salt-sensitive rats

ABSTRACT: Mlycd (malonyl-CoA decarboxylase) is a regulator of fatty acid metabolism. Lysine supplementation depletes kidney malonyl-CoA in hypertensive Dahl SS rats. As a key regulatory mechanism, lysine malonylation influences mitochondrial enzymes and fatty acid metabolism, with implications for CKD, hypertension, and other disorders. Yet how the balance between malonylation and acetylation is altered, and how this affects salt-sensitive hypertension, remains unclear. In this study, we examined the proteomic and metabolomic alterations resulting from Mlycd deficiency in Dahl salt-sensitive rats. This dataset contains proteomic profiles of heart, kidney, liver tissues as well as plasma and urine samples obtained from both Mlycd+/+ and Mlycd+/- animals.

INSTRUMENT(S):

ORGANISM(S): Rattus Norvegicus (rat)

TISSUE(S): Urine, Heart, Blood Plasma, Liver, Kidney

SUBMITTER: Yifan Tan

LAB HEAD: Alexander Staruschenko

PROVIDER: PXD062350 | Pride | 2025-12-14

REPOSITORIES: Pride

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			Action	DRS
	221126_Rat_G_Kidney_DIA_13.raw	Raw
	221126_Rat_G_Kidney_DIA_14.raw	Raw
	221126_Rat_G_Kidney_DIA_15.raw	Raw
	221126_Rat_G_Kidney_DIA_16.raw	Raw
	221126_Rat_G_Kidney_DIA_17.raw	Raw

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Project description:Hypertension and kidney disease, two related, common, and severe disease entities have been repeatedly associated with genomic variants and metabolic alterations of lysine metabolism. Here, we developed a stable isotope labeling strategy compatible with untargeted metabolomics acquisition to investigate the physiology and molecular spectrum of lysine’s metabolic fate in vivo. Mice received 13C6 labeled lysine through the diet over two months to track more than 100 lysine metabolites across various organs and body fluids. Globally, lysine reacts rapidly with molecules of the central carbon metabolism, as opposed to slow or incorporation into proteins and metabolization into acylcarnitines. Lysine metabolism is accelerated in the rat model of the Dahl salt-sensitive hypertension and kidney damage, chiefly through N-alpha-mediated degradation. Here, lysine administration completely diminished the development of salt-sensitive hypertension and kidney injury. Administration of lysine leads to diuresis, even further acceleration of 13C6 lysine conjugate formation, and inhibition of albumin uptake, thereby protecting from nephron injury and metabolic stress. Lysine conjugates with malonyl-CoA to form a novel metabolite N-malonyl-lysine, to deplete malonyl-CoA from fatty acid synthesis. This process occurs at the expense of protein malonylation. In hypertensive rats with kidney damage, lysine molecules were excreted as fructoselysine, saccharopine and Nε-acetyllysine, via the urine, leading to an overall depletion of central carbon metabolites from the organism and kidney. Consistent with findings in the salt-sensitive rat, lysine challenge of patients with mild kidney damage inhibited tubular albumin uptake, increased lysine conjugate formation in the urine, and reduced TCA cycle metabolites, in contrast to kidney-healthy volunteers. In conclusion, comprehensive lysine isotope tracing mapped an accelerated lysine metabolism in hypertension, and further, lysine administration induced kidney protection in kidney disease.

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Mlycd deficiency in Dahl salt-sensitive rats

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