Lipoprotein lipase variants interact with polyunsaturated fatty acids for obesity traits in women: Replication in two populations

Ma, Yuru; Tucker, Katherine L.; Smith, Caren E.; Lee, Y.C.; Huang, Tao; Richardson, Kris; Parnell, Laurence D.; Lai, Chao‐Qiang; Young, Kristin L.; Justice, Anne E.; Shao, Yaming; North, Kari E.; Ordovás, José M.

doi:10.1016/j.numecd.2014.07.003

Cited by 12 publications

(8 citation statements)

References 28 publications

(31 reference statements)

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“…Finally, dietary FA have been found to modulate the association between body composition and many genetic variants of obesity-related genes [111,[135][136][137][138][139][140][141], Table 1 summarizes available evidence on dietary fatty acid-adipogenic gene interactions. The data show promising evidence of interactions between dietary FA and several polymorphisms located in genes that can co-ordinate the adipogenesis process either via a metabolically-evident pathway such as PPARγ or via a suggested mechanism such as Circadian Locomotor Output Cycles Kaput.…”

Section: The Interaction Between Fat Quality and Single Nucleotide Pomentioning

confidence: 99%

Dietary Fatty Acid Composition Modulates Obesity and Interacts with Obesity‐Related Genes

Hammad

Jones

2017

Lipids

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The prevalence of obesity is skyrocketing worldwide. The scientific evidence has associated obesity risk with many independent factors including the quality of dietary fat and genetics. Dietary fat exists as the main focus of dietary guidelines targeting obesity reduction. To prevent/minimize the adipogenic effect of dietary fatty acids (FA), intakes of long-chain saturated- and trans-FA should be reduced and substituted with unsaturated FA. The optimal proportions of dietary unsaturated FA are yet to be defined, along with a particular emphasis on the need to achieve a balanced ratio of n-3:n-6 polyunsaturated FA and to increase monounsaturated FA consumption at the expense of saturated FA. However, inter-individual variability in weight loss in response to a dietary intervention is evident, which highlights the importance of exploring gene-nutrient interactions that can further modulate the risk for obesity development. The quality of dietary fat was found to modulate obesity development by interacting with genes involved in fatty acid metabolism, adipogenesis, and the endocannabinoid system. This review summarizes the current knowledge on the effect of the quality of dietary fat on obesity phenotype and obesity-related genes. The evidence is not only supporting the modulatory effect of fat quality on obesity development but also presenting a number of interactions between obesity-related genes and the quality of dietary fat. The identified gene-FA interaction may have a clinical importance and holds a promise for the possibility of using genetically targeted dietary interventions to reduce obesity risk in the future.

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Section: The Interaction Between Fat Quality and Single Nucleotide Pomentioning

confidence: 99%

Dietary Fatty Acid Composition Modulates Obesity and Interacts with Obesity‐Related Genes

Hammad

Jones

2017

Lipids

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“…However, the POUNDS LOST dietary conditions varied in total fat content, and the researchers did not account for the dietary fat composition (SFA, MUFA, PUFA) of the diets. The type and amount of dietary fat intake is evidenced to interact with genetic variants to influence blood lipid profiles [ 97 , 98 , 99 , 100 ].…”

Section: Nutrient-gene Interactions and Dyslipidemiamentioning

confidence: 99%

Nutrigenetic Contributions to Dyslipidemia: A Focus on Physiologically Relevant Pathways of Lipid and Lipoprotein Metabolism

2018

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Cardiovascular disease (CVD) remains the number one cause of death worldwide, and dyslipidemia is a major predictor of CVD mortality. Elevated lipid concentrations are the result of multiple genetic and environmental factors. Over 150 genetic loci have been associated with blood lipid levels. However, not all variants are present in pathways relevant to the pathophysiology of dyslipidemia. The study of these physiologically relevant variants can provide mechanistic understanding of dyslipidemia and identify potential novel therapeutic targets. Additionally, dietary fatty acids have been evidenced to exert both positive and negative effects on lipid profiles. The metabolism of both dietary and endogenously synthesized lipids can be affected by individual genetic variation to produce elevated lipid concentrations. This review will explore the genetic, dietary, and nutrigenetic contributions to dyslipidemia.

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“…Abnormalities in lipid metabolism have been linked to the development of obesity, and lipoprotein lipase (LPL), a key enzyme in lipid metabolism, contributes to the development of obesity through its role in the partitioning of lipids to different tissues [10][11][12]. Cholesteryl ester transfer protein (CETP), mainly expressed in adipose tissue, is also a major enzyme in lipid metabolism, which mediates the transport of cholesteryl esters and triglycerides (TG) between high-density lipoprotein cholesterol (HDL) and apolipoprotein B (ApoB)-containing lipoproteins such as very-low-density lipoprotein (VLDL) [13].…”

Section: Introductionmentioning

confidence: 99%

Impact of Lipid Genetic Risk Score and Saturated Fatty Acid Intake on Central Obesity in an Asian Indian Population

et al. 2022

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Abnormalities in lipid metabolism have been linked to the development of obesity. We used a nutrigenetic approach to establish a link between lipids and obesity in Asian Indians, who are known to have a high prevalence of central obesity and dyslipidaemia. A sample of 497 Asian Indian individuals (260 with type 2 diabetes and 237 with normal glucose tolerance) (mean age: 44 ± 10 years) were randomly chosen from the Chennai Urban Rural Epidemiological Study (CURES). Dietary intake was assessed using a previously validated questionnaire. A genetic risk score (GRS) was constructed based on cholesteryl ester transfer protein (CETP) and lipoprotein lipase (LPL) genetic variants. There was a significant interaction between GRS and saturated fatty acid (SFA) intake on waist circumference (WC) (Pinteraction = 0.006). Individuals with a low SFA intake (≤23.2 g/day), despite carrying ≥ 2 risk alleles, had a smaller WC compared to individuals carrying < 2 risk alleles (Beta = −0.01 cm; p = 0.03). For those individuals carrying ≥ 2 risk alleles, a high SFA intake (>23.2 g/day) was significantly associated with a larger WC than a low SFA intake (≤23.2 g/day) (Beta = 0.02 cm, p = 0.02). There were no significant interactions between GRS and other dietary factors on any of the measured outcomes. We conclude that a diet low in SFA might help reduce the genetic risk of central obesity confirmed by CETP and LPL genetic variants. Conversely, a high SFA diet increases the genetic risk of central obesity in Asian Indians.

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Lipoprotein lipase variants interact with polyunsaturated fatty acids for obesity traits in women: Replication in two populations

Cited by 12 publications

References 28 publications

Dietary Fatty Acid Composition Modulates Obesity and Interacts with Obesity‐Related Genes

Dietary Fatty Acid Composition Modulates Obesity and Interacts with Obesity‐Related Genes

Nutrigenetic Contributions to Dyslipidemia: A Focus on Physiologically Relevant Pathways of Lipid and Lipoprotein Metabolism

Impact of Lipid Genetic Risk Score and Saturated Fatty Acid Intake on Central Obesity in an Asian Indian Population

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