Dietary saturated fat, gender and genetic variation at the TCF7L2 locus predict the development of metabolic syndrome

Phillips, Catherine M.; Goumidi, Louisa; Bertrais, Sandrine; Field, Martyn R.; McManus, Ross; Herçberg, Serge; Lairon, Denis; Planells, Richard; Roche, Helen M.

doi:10.1016/j.jnutbio.2010.11.020

Cited by 55 publications

(75 citation statements)

References 39 publications

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“…Dietary fat is an important environmental factor, wherein excessive exposure plays a key role in the development of MetS (33)(34)(35)(36)(37)(38). Recently, we reported novel modulation of MetS risk conferred by the TCF7L2 genotype by dietary SFA (39). A cross-sectional analysis of the influence of dietary factors and physical activity on BMI according to the FTO rs9939609 genotype indicated that high-fat diets increase obesity risk (20,21).…”

Section: Discussionmentioning

confidence: 97%

High Dietary Saturated Fat Intake Accentuates Obesity Risk Associated with the Fat Mass and Obesity-Associated Gene in Adults

Phillips

Kesse‐Guyot

McManus

et al. 2012

The Journal of Nutrition

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139

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Fat mass and obesity-associated (FTO) is the strongest genetic determinant of obesity identified to date. Dietary fat is a key environmental factor that may interact with genotype to affect risk of obesity and metabolic syndrome (MetS). This study investigated associations among FTO rs9939609, obesity measures, and MetS phenotypes in adults and determined potential modulation by dietary fat intake at baseline and after a 7.5-y follow-up when MetS cases and controls were selected. FTO rs9939609 genotype, biochemical, dietary, and lifestyle measurements were determined in the LIPGENE-SU.VI.MAX study (n = 1754). FTO rs9939609 A allele carriers had a higher risk of being overweight or obese [OR = 1.66 (95% CI: 1.07, 2.57); P = 0.02] and of having a larger abdominal circumference [OR = 1.42 (95% CI: 1.01, 1.99); P = 0.04] compared with the TT homozygotes. These associations were independent of physical activity and energy intake and were maintained over the follow-up period, particularly in the MetS individuals. High dietary SFA intake (≥ 15.5% energy) and a low dietary PUFA:SFA intake ratio (<0.38) further accentuated the risk of having a BMI ≥ 25 kg/m(2) and being abdominally obese. Non-risk allele carriers appeared to be unresponsive to dietary SFA intake or to the dietary PUFA:SFA intake ratio with respect to obesity measures. In conclusion, FTO rs9939609 was associated with obesity measures, especially in those with the MetS, which was further exacerbated by high dietary SFA intake at baseline and 7.5 y later. These data indicate important novel modulation of genetic risk by dietary fat exposure in individuals with increased cardiometabolic risk.

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Section: Discussionmentioning

confidence: 97%

High Dietary Saturated Fat Intake Accentuates Obesity Risk Associated with the Fat Mass and Obesity-Associated Gene in Adults

Phillips

Kesse‐Guyot

McManus

et al. 2012

The Journal of Nutrition

Self Cite

139

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“…In our studies to elucidate the potential mechanisms involved in MetS-related periodontitis, we focused on saturated fatty acids (SFAs), since a clinical study with a large number of patients (n = 1,754) showed that high dietary saturated fat (>15.5% energy) exacerbated MetS risk (odds ratio, 2.35; P = 0.005; Phillips et al 2012). PA, as the most abundant SFA, has been shown to play an important role in SFA-induced insulin resistance and inflammation (Maloney et al 2009;Coll et al 2010;Igoillo-Esteve et al 2010).…”

Section: Discussionmentioning

confidence: 99%

Metabolic Syndrome Exacerbates Inflammation and Bone Loss in Periodontitis

Zhang

et al. 2014

J Dent Res

111

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Clinical studies have shown that metabolic syndrome (MetS) is associated with increased risk of developing periodontitis. However, the underlying mechanisms remain largely unknown. Since it is known that lipopolysaccharide (LPS)-activated toll-like receptor 4 signaling pathways play a crucial role in periodontitis, we hypothesized that MetS enhances LPS-induced periodontal inflammation and alveolar bone loss. In this study, we induced MetS in C57BL/6 mice by feeding them high-fat diet (HFD), and we induced periodontitis by periodontal injection of Aggregatibacter actinomycetemcomitans LPS. We found that mice fed a HFD had significantly increased body weight, plasma lipids, insulin, and insulin resistance when compared with mice fed regular chow, indicating that the mice developed MetS. We also found that a HFD markedly increased LPSinduced alveolar bone loss, osteoclastogenesis, and inflammatory infiltration. Analysis of gene expression in periodontal tissue revealed that HFD and LPS injection cooperatively stimulated expression of cytokines that are known to be involved in periodontal tissue inflammation and osteoclastogenesis-such as interleukin 6, monocyte-chemotactic protein 1, receptor activator of nuclear factor kappa-B ligand, and macrophage colony-stimulating factor. To further understand the potential mechanisms involved in MetS-boosted tissue inflammation, our in vitro studies showed that palmitic acid-the most abundant saturated fatty acid (SFA) and the major SFA in the HFD used in our animal study-potently enhanced LPS-induced proinflammatory gene expression in macrophages. In sum, this study demonstrated that MetS was associated with increased periodontal inflammation and alveolar bone loss in an LPS-induced periodontitis animal model. This study also suggests that SFA palmitic acid may play an important role in MetS-associated periodontitis by enhancing LPS-induced expression of inflammatory cytokines in macrophages.

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“…In humans, there is an association between high-SFA and/or low-UFA concentrations and infl ammation ( 54,55 ) or metabolic syndrome ( 54 ). In some studies, these parameters can predict metabolic syndrome development ( 56,57 ). Assays on small groups of people described a decrease of infl ammatory gene expression ( 31 ) and an improvement of insulin sensitivity ( 58 ) after UFA-rich diet.…”

Section: Ufas Reduce Il-1 ␤ Processing But Not Transcriptionmentioning

confidence: 99%

Unsaturated fatty acids prevent activation of NLRP3 inflammasome in human monocytes/macrophages

L’homme¹,

Esser

Riva

et al. 2013

Journal of Lipid Research

134

104

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Dietary saturated fat, gender and genetic variation at the TCF7L2 locus predict the development of metabolic syndrome

Cited by 55 publications

References 39 publications

High Dietary Saturated Fat Intake Accentuates Obesity Risk Associated with the Fat Mass and Obesity-Associated Gene in Adults

High Dietary Saturated Fat Intake Accentuates Obesity Risk Associated with the Fat Mass and Obesity-Associated Gene in Adults

Metabolic Syndrome Exacerbates Inflammation and Bone Loss in Periodontitis

Unsaturated fatty acids prevent activation of NLRP3 inflammasome in human monocytes/macrophages

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