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Estimated stearoyl-CoA desaturase activity mediates the associations of total cysteine with adiposity: The Maastricht Study

EC. Tore, BC. Adriaans, T. Olsen, KJ. Vinknes, ME. Kooi, AK. Elshorbagy, NE. Bastani, PC. Dagnelie, SJPM. Eussen, TE. Gundersen, V. Kožich, H. Refsum, K. Retterstøl, ETK. Stolt, MMJ. van Greevenbroek

. 2025 ; 19 (2) : 348-357. [pub] 20241117

Language English

Document type Journal Article

Persistent link   https://www.medvik.cz/link/bmc25016372

BACKGROUND: Plasma sulfur amino acids (SAAs), particularly cysteine, are associated with obesity. One proposed mechanism is the altered regulation of the stearoyl-CoA desaturase (SCD) enzyme. Changes in the SCD enzyme activity have been linked to obesity, as well as to plasma SAA concentrations. OBJECTIVE: This study aimed to investigate whether estimated SCD activity mediates the associations between plasma SAAs and measures of overall adiposity and specific fat depots. METHODS: We examined cross-sectional data from a subset of the Maastricht Study (n = 1129, 50.7% men, 56.7% with (pre)diabetes). Concentrations of methionine, total homocysteine, cystathionine, total cysteine (tCys), total glutathione (tGSH), and taurine were measured in fasting plasma. Outcomes included measures of overall, peripheral and central adiposity, and liver fat. SCD activity was estimated by ratios of serum fatty acids as SCD16 and SCD18 indices. The associations between plasma SAAs and measures of adiposity or liver fat were examined with multiple linear regression analysis. Multiple mediation analysis was used to investigate whether the significant associations were mediated by SCD16 and SCD18 indices. RESULTS: Plasma tCys was positively associated with all adiposity measures (β ranged from 0.15 to 0.30). SCD16 significantly mediated all associations (proportion mediated ranged from 5.1% to 9.7%). Inconsistent mediation effects were found for SCD18. Despite a significant inverse association of plasma tGSH with all adiposity measures (β ranged from -0.08 to -0.16), no significant mediation effect was found. CONCLUSIONS: Plasma tCys may promote excessive body fat accumulation via upregulation of SCD activity.

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$a Tore, Elena C $u Department of Internal Medicine, Maastricht University, Maastricht, The Netherlands (Drs Tore, Adriaans, Dagnelie, van Greevenbroek); CARIM, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands (Drs Tore, Adriaans, Kooi, Dagnelie, Eussen, van Greevenbroek). Electronic address: e.tore@maastrichtuniversity.nl
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$a BACKGROUND: Plasma sulfur amino acids (SAAs), particularly cysteine, are associated with obesity. One proposed mechanism is the altered regulation of the stearoyl-CoA desaturase (SCD) enzyme. Changes in the SCD enzyme activity have been linked to obesity, as well as to plasma SAA concentrations. OBJECTIVE: This study aimed to investigate whether estimated SCD activity mediates the associations between plasma SAAs and measures of overall adiposity and specific fat depots. METHODS: We examined cross-sectional data from a subset of the Maastricht Study (n = 1129, 50.7% men, 56.7% with (pre)diabetes). Concentrations of methionine, total homocysteine, cystathionine, total cysteine (tCys), total glutathione (tGSH), and taurine were measured in fasting plasma. Outcomes included measures of overall, peripheral and central adiposity, and liver fat. SCD activity was estimated by ratios of serum fatty acids as SCD16 and SCD18 indices. The associations between plasma SAAs and measures of adiposity or liver fat were examined with multiple linear regression analysis. Multiple mediation analysis was used to investigate whether the significant associations were mediated by SCD16 and SCD18 indices. RESULTS: Plasma tCys was positively associated with all adiposity measures (β ranged from 0.15 to 0.30). SCD16 significantly mediated all associations (proportion mediated ranged from 5.1% to 9.7%). Inconsistent mediation effects were found for SCD18. Despite a significant inverse association of plasma tGSH with all adiposity measures (β ranged from -0.08 to -0.16), no significant mediation effect was found. CONCLUSIONS: Plasma tCys may promote excessive body fat accumulation via upregulation of SCD activity.
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$a Adriaans, Bregje C $u Department of Internal Medicine, Maastricht University, Maastricht, The Netherlands (Drs Tore, Adriaans, Dagnelie, van Greevenbroek); CARIM, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands (Drs Tore, Adriaans, Kooi, Dagnelie, Eussen, van Greevenbroek)
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$a Olsen, Thomas $u Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway (Drs Olsen, Vinknes, Bastani, Refsum, Retterstøl, Stolt)
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$a Vinknes, Kathrine J $u Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway (Drs Olsen, Vinknes, Bastani, Refsum, Retterstøl, Stolt)
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$a Kooi, M Eline $u CARIM, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands (Drs Tore, Adriaans, Kooi, Dagnelie, Eussen, van Greevenbroek); Department of Radiology & Nuclear Medicine, Maastricht University Medical Center, Maastricht, The Netherlands (Dr Kooi)
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$a Elshorbagy, Amany K $u Department of Pharmacology, University of Oxford, Oxford, UK (Drs Elshorbagy, Refsum); Department of Physiology, Faculty of Medicine, University of Alexandria, Alexandria, Egypt (Dr Elshorbagy)
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$a Bastani, Nasser E $u Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway (Drs Olsen, Vinknes, Bastani, Refsum, Retterstøl, Stolt)
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$a Dagnelie, Pieter C $u Department of Internal Medicine, Maastricht University, Maastricht, The Netherlands (Drs Tore, Adriaans, Dagnelie, van Greevenbroek); CARIM, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands (Drs Tore, Adriaans, Kooi, Dagnelie, Eussen, van Greevenbroek)
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$a Eussen, Simone J P M $u CARIM, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands (Drs Tore, Adriaans, Kooi, Dagnelie, Eussen, van Greevenbroek); Department of Epidemiology, Maastricht University, Maastricht, The Netherlands (Dr Eussen); CAPHRI Care and Public Health Research Institute, Maastricht University, Maastricht, The Netherlands (Dr Eussen)
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$a Gundersen, Thomas E $u Vitas Analytical Services AS, Oslo, Norway (Dr Gundersen)
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$a Kožich, Viktor $u Department of Pediatrics and Inherited Metabolic Disorders, Charles University-First Faculty of Medicine, and General University Hospital in Prague, Prague, Czech Republic (Dr Kožich)
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$a Refsum, Helga $u Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway (Drs Olsen, Vinknes, Bastani, Refsum, Retterstøl, Stolt); Department of Pharmacology, University of Oxford, Oxford, UK (Drs Elshorbagy, Refsum)
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$a Retterstøl, Kjetil $u Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway (Drs Olsen, Vinknes, Bastani, Refsum, Retterstøl, Stolt); The Lipid Clinic, Oslo University Hospital, Norway (Dr Retterstøl)
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$a Stolt, Emma T K $u Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway (Drs Olsen, Vinknes, Bastani, Refsum, Retterstøl, Stolt)
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$a van Greevenbroek, Marleen M J $u Department of Internal Medicine, Maastricht University, Maastricht, The Netherlands (Drs Tore, Adriaans, Dagnelie, van Greevenbroek); CARIM, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands (Drs Tore, Adriaans, Kooi, Dagnelie, Eussen, van Greevenbroek)
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