Difference between revisions of "Carballal 2021 J Biol Chem"

Revision as of 10:49, 15 July 2021

Carballal S, Vitvitsky V, Kumar R, Hanna DA, Libiad M, Gupta A, Jones JW, Banerjee R (2021) Hydrogen sulfide stimulates lipid biogenesis from glutamine that is dependent on the mitochondrial NAD(P)H pool. J Biol Chem 100950.

» PMID: 34252456 Open Access

Carballal Sebastian, Vitvitsky Victor, Kumar Roshan, Hanna David A, Libiad Marouane, Gupta Aditi, Jones Jace W, Banerjee Ruma (2021) J Biol Chem

Abstract: Mammalian cells synthesize H₂S from sulfur containing amino acids and are also exposed to exogenous sources of this signaling molecule, notably from gut microbes. As an inhibitor of complex IV in the electron transport chain, H₂S can have a profound impact on metabolism, suggesting the hypothesis that metabolic reprogramming is a primary mechanism by which H₂S signals. In this study, we report that H₂S increases lipogenesis in many cell types, using carbon derived from glutamine rather than from glucose. H₂S-stimulated lipid synthesis is sensitive to the mitochondrial NAD(P)H pools and is enabled by reductive carboxylation of α-ketoglutarate. Lipidomics analysis revealed that H₂S elicits time-dependent changes across several lipid classes, e.g., upregulating triglycerides while down regulating phosphatidylcholine. Direct analysis of triglyceride concentration revealed that H₂S induces a net increase in the size of this lipid pool. These results provide a mechanistic framework for understanding the effects of H₂S on increasing lipid droplets in adipocytes and population studies that have pointed to a positive correlation between cysteine (a substrate for H₂S synthesis) and fat mass.

• Bioblast editor: Reiswig R

Labels: MiParea: Respiration, Pharmacology;toxicology

Organism: Human Tissue;cell: Other cell lines Preparation: Intact cells

Regulation: Substrate

HRR: Oxygraph-2k

2021-07

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 |year=2021
 |journal=J Biol Chem
-|abstract=Mammalian cells synthesize H<sub>2<\sub>S from sulfur containing amino acids and are also exposed to exogenous sources of this signaling molecule, notably from gut microbes. As an inhibitor of complex IV in the electron transport chain, H<sub>2<\sub>S can have a profound impact on metabolism, suggesting the hypothesis that metabolic reprogramming is a primary mechanism by which H<sub>2<\sub>S signals. In this study, we report that H<sub>2<\sub>S increases lipogenesis in many cell types, using carbon derived from glutamine rather than from glucose. H<sub>2<\sub>S-stimulated lipid synthesis is sensitive to the mitochondrial NAD(P)H pools and is enabled by reductive carboxylation of α-ketoglutarate. Lipidomics analysis revealed that H<sub>2<\sub>S elicits time-dependent changes across several lipid classes, e.g., upregulating triglycerides while down regulating phosphatidylcholine. Direct analysis of triglyceride concentration revealed that H<sub>2<\sub>S induces a net increase in the size of this lipid pool. These results provide a mechanistic framework for understanding the effects of H<sub>2<\sub>S on increasing lipid droplets in adipocytes and population studies that have pointed to a positive correlation between cysteine (a substrate for H<sub>2<\sub>S synthesis) and fat mass.
+|abstract=Mammalian cells synthesize H<sub>2</sub>S from sulfur containing amino acids and are also exposed to exogenous sources of this signaling molecule, notably from gut microbes. As an inhibitor of complex IV in the electron transport chain, H<sub>2</sub>S can have a profound impact on metabolism, suggesting the hypothesis that metabolic reprogramming is a primary mechanism by which H<sub>2</sub>S signals. In this study, we report that H<sub>2</sub>S increases lipogenesis in many cell types, using carbon derived from glutamine rather than from glucose. H<sub>2</sub>S-stimulated lipid synthesis is sensitive to the mitochondrial NAD(P)H pools and is enabled by reductive carboxylation of α-ketoglutarate. Lipidomics analysis revealed that H<sub>2</sub>S elicits time-dependent changes across several lipid classes, e.g., upregulating triglycerides while down regulating phosphatidylcholine. Direct analysis of triglyceride concentration revealed that H<sub>2</sub>S induces a net increase in the size of this lipid pool. These results provide a mechanistic framework for understanding the effects of H<sub>2</sub>S on increasing lipid droplets in adipocytes and population studies that have pointed to a positive correlation between cysteine (a substrate for H<sub>2</sub>S synthesis) and fat mass.
 |editor=[[Reiswig R]]
 }}