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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) LFHCC and (b) LFHCC n-3 diets. Networks of differentially expressed proteins in the long-term ingestion of: a) LFHCC, Low fat, high-complex carbohydrate diet with placebo; b) LFHCC n-3, Low fat, high-complex carbohydrate diet with 1.24 g/d LC n-3 PUFA diet
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Fig2: Interaction between induced proteins at the long-term consumption of (a) LFHCC and (b) LFHCC n-3 diets. Networks of differentially expressed proteins in the long-term ingestion of: a) LFHCC, Low fat, high-complex carbohydrate diet with placebo; b) LFHCC n-3, Low fat, high-complex carbohydrate diet with 1.24 g/d LC n-3 PUFA diet

Mentions: Long-term consumption of the LFHCC diet showed significant changes in the proteins interlinked in one main network (Fig. 2a), that includes six molecules related with organism function (nuclear CAP, GSN, TPM, THBS1 and cytoplasmic GRB2, TBK1), tissue morphology, organism injury and abnormalities. Analysis of the molecular and cellular functions suggests that these proteins are involved in the carbohydrate metabolism, cell to cell signaling (THBS1 and GRB2) and cellular assembly and organization (nuclear GSN, CAP, THBS1, MYO1, TPM, and cytoplasmic GRB2, TBK). Our results showed that at the level of the biofunctions related with diseases and disorders, the changes induced by a chronic intake of the LFHCC diet are implicated in cardiovascular and metabolic diseases (TPM, GSN and THBS1). The canonical pathway analysis shows that the changes identified are related with actin cytoskeleton signaling (ACTB, GSN, GRB2) (p = 8.5E-04).Fig. 2


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) LFHCC and (b) LFHCC n-3 diets. Networks of differentially expressed proteins in the long-term ingestion of: a) LFHCC, Low fat, high-complex carbohydrate diet with placebo; b) LFHCC n-3, Low fat, high-complex carbohydrate diet with 1.24 g/d LC n-3 PUFA diet
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Fig2: Interaction between induced proteins at the long-term consumption of (a) LFHCC and (b) LFHCC n-3 diets. Networks of differentially expressed proteins in the long-term ingestion of: a) LFHCC, Low fat, high-complex carbohydrate diet with placebo; b) LFHCC n-3, Low fat, high-complex carbohydrate diet with 1.24 g/d LC n-3 PUFA diet
Mentions: Long-term consumption of the LFHCC diet showed significant changes in the proteins interlinked in one main network (Fig. 2a), that includes six molecules related with organism function (nuclear CAP, GSN, TPM, THBS1 and cytoplasmic GRB2, TBK1), tissue morphology, organism injury and abnormalities. Analysis of the molecular and cellular functions suggests that these proteins are involved in the carbohydrate metabolism, cell to cell signaling (THBS1 and GRB2) and cellular assembly and organization (nuclear GSN, CAP, THBS1, MYO1, TPM, and cytoplasmic GRB2, TBK). Our results showed that at the level of the biofunctions related with diseases and disorders, the changes induced by a chronic intake of the LFHCC diet are implicated in cardiovascular and metabolic diseases (TPM, GSN and THBS1). The canonical pathway analysis shows that the changes identified are related with actin cytoskeleton signaling (ACTB, GSN, GRB2) (p = 8.5E-04).Fig. 2

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