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Proteome from patients with metabolic syndrome is regulated by quantity and quality of dietary lipids.

Rangel-Zúñiga OA, Camargo A, Marin C, Peña-Orihuela P, Pérez-Martínez P, Delgado-Lista J, González-Guardia L, Yubero-Serrano EM, Tinahones FJ, Malagón MM, Pérez-Jiménez F, Roche HM, López-Miranda J - BMC Genomics (2015)

Bottom Line: Its etiology is the result of a complex interaction between genetic and environmental factors, including dietary habits.The HSFA diet induced the expression of proteins responding to oxidative stress, degradation of ubiquitinated proteins and DNA repair.However, HMUFA, LFHCC and LFHCC n-3 diets down-regulated pro-inflammatory and oxidative stress-related proteins and DNA repairing proteins.

View Article: PubMed Central - PubMed

Affiliation: Lipids and Atherosclerosis Research Unit, IMIBIC/Reina Sofia University Hospital, University of Cordoba, Av. Menendez Pidal s/n. 14004, Córdoba, Spain. bb2razuo@uco.es.

ABSTRACT

Background: Metabolic syndrome is a multi-component disorder associated to a high risk of cardiovascular disease. Its etiology is the result of a complex interaction between genetic and environmental factors, including dietary habits. We aimed to identify the target proteins modulated by the long-term consumption of four diets differing in the quality and quantity of lipids in the whole proteome of peripheral blood mononuclear cells (PBMC).

Results: A randomized, controlled trial conducted within the LIPGENE study assigned 24 MetS patients for 12 weeks each to 1 of 4 diets: a) high-saturated fatty acid (HSFA), b) high-monounsaturated fatty acid (HMUFA), c) low-fat, high-complex carbohydrate diets supplemented with placebo (LFHCC) and d) low-fat, high-complex carbohydrate diets supplemented with long chain (LC) n-3 polyunsaturated fatty acids (PUFA) (LFHCC n-3). We analyzed the changes induced in the proteome of both nuclear and cytoplasmic fractions of PBMC using 2-D proteomic analysis. Sixty-seven proteins were differentially expressed after the long-term consumption of the four diets. The HSFA diet induced the expression of proteins responding to oxidative stress, degradation of ubiquitinated proteins and DNA repair. However, HMUFA, LFHCC and LFHCC n-3 diets down-regulated pro-inflammatory and oxidative stress-related proteins and DNA repairing proteins.

Conclusion: The long-term consumption of HSFA, compared to HMUFA, LFHCC and LFHCC n-3, seems to increase the cardiovascular disease (CVD) risk factors associated with metabolic syndrome, such as inflammation and oxidative stress, and seem lead to DNA damage as a consequence of high oxidative stress.

No MeSH data available.


Related in: MedlinePlus

Interaction between induced proteins at the long-term consumption of (a) HSFA and (b) HMUFA diets. Networks of differentially expressed proteins in the long-term ingestion of: a) HSFA, Saturated fatty acid diet; b) HMUFA, Monounsaturated fatty acid diet
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Fig1: Interaction between induced proteins at the long-term consumption of (a) HSFA and (b) HMUFA diets. Networks of differentially expressed proteins in the long-term ingestion of: a) HSFA, Saturated fatty acid diet; b) HMUFA, Monounsaturated fatty acid diet

Mentions: Our analysis also showed that the long-term consumption of the HSFA diet induced changes in proteins involved in five interaction networks (Fig. 1a), which are mainly related with the degradation of unfolding proteins (nuclear CHMP1.5), cell to cell signaling interaction (nuclear VASP and cytoplasmic TOM1), morphology and cardiovascular system development (nuclear ARPC2). Analysis of the biofunctions related with diseases and disorders showed that these proteins are included in neurological (p = 5.8E-04–1.2E-02) and infectious diseases (CHMP.5 and ACTB) (p = 8.5E-03 – 8.5E-03). Top canonical pathway analysis showed the interaction of three nuclear proteins ACTB, ARPC2 and VASP within the pathway Fcγ receptor-mediated phagocytosis in macrophages and monocytes [p = 1.55E-05; ratio 3/95 (0.032)].Fig. 1


Proteome from patients with metabolic syndrome is regulated by quantity and quality of dietary lipids.

Rangel-Zúñiga OA, Camargo A, Marin C, Peña-Orihuela P, Pérez-Martínez P, Delgado-Lista J, González-Guardia L, Yubero-Serrano EM, Tinahones FJ, Malagón MM, Pérez-Jiménez F, Roche HM, López-Miranda J - BMC Genomics (2015)

Interaction between induced proteins at the long-term consumption of (a) HSFA and (b) HMUFA diets. Networks of differentially expressed proteins in the long-term ingestion of: a) HSFA, Saturated fatty acid diet; b) HMUFA, Monounsaturated fatty acid diet
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4493955&req=5

Fig1: Interaction between induced proteins at the long-term consumption of (a) HSFA and (b) HMUFA diets. Networks of differentially expressed proteins in the long-term ingestion of: a) HSFA, Saturated fatty acid diet; b) HMUFA, Monounsaturated fatty acid diet
Mentions: Our analysis also showed that the long-term consumption of the HSFA diet induced changes in proteins involved in five interaction networks (Fig. 1a), which are mainly related with the degradation of unfolding proteins (nuclear CHMP1.5), cell to cell signaling interaction (nuclear VASP and cytoplasmic TOM1), morphology and cardiovascular system development (nuclear ARPC2). Analysis of the biofunctions related with diseases and disorders showed that these proteins are included in neurological (p = 5.8E-04–1.2E-02) and infectious diseases (CHMP.5 and ACTB) (p = 8.5E-03 – 8.5E-03). Top canonical pathway analysis showed the interaction of three nuclear proteins ACTB, ARPC2 and VASP within the pathway Fcγ receptor-mediated phagocytosis in macrophages and monocytes [p = 1.55E-05; ratio 3/95 (0.032)].Fig. 1

Bottom Line: Its etiology is the result of a complex interaction between genetic and environmental factors, including dietary habits.The HSFA diet induced the expression of proteins responding to oxidative stress, degradation of ubiquitinated proteins and DNA repair.However, HMUFA, LFHCC and LFHCC n-3 diets down-regulated pro-inflammatory and oxidative stress-related proteins and DNA repairing proteins.

View Article: PubMed Central - PubMed

Affiliation: Lipids and Atherosclerosis Research Unit, IMIBIC/Reina Sofia University Hospital, University of Cordoba, Av. Menendez Pidal s/n. 14004, Córdoba, Spain. bb2razuo@uco.es.

ABSTRACT

Background: Metabolic syndrome is a multi-component disorder associated to a high risk of cardiovascular disease. Its etiology is the result of a complex interaction between genetic and environmental factors, including dietary habits. We aimed to identify the target proteins modulated by the long-term consumption of four diets differing in the quality and quantity of lipids in the whole proteome of peripheral blood mononuclear cells (PBMC).

Results: A randomized, controlled trial conducted within the LIPGENE study assigned 24 MetS patients for 12 weeks each to 1 of 4 diets: a) high-saturated fatty acid (HSFA), b) high-monounsaturated fatty acid (HMUFA), c) low-fat, high-complex carbohydrate diets supplemented with placebo (LFHCC) and d) low-fat, high-complex carbohydrate diets supplemented with long chain (LC) n-3 polyunsaturated fatty acids (PUFA) (LFHCC n-3). We analyzed the changes induced in the proteome of both nuclear and cytoplasmic fractions of PBMC using 2-D proteomic analysis. Sixty-seven proteins were differentially expressed after the long-term consumption of the four diets. The HSFA diet induced the expression of proteins responding to oxidative stress, degradation of ubiquitinated proteins and DNA repair. However, HMUFA, LFHCC and LFHCC n-3 diets down-regulated pro-inflammatory and oxidative stress-related proteins and DNA repairing proteins.

Conclusion: The long-term consumption of HSFA, compared to HMUFA, LFHCC and LFHCC n-3, seems to increase the cardiovascular disease (CVD) risk factors associated with metabolic syndrome, such as inflammation and oxidative stress, and seem lead to DNA damage as a consequence of high oxidative stress.

No MeSH data available.


Related in: MedlinePlus