Abstract 3562: The Ala12 Variant of the PPARG Gene is Associated with Higher Polyunsaturated Fatty Acids in Adipose Tissue and Attenuates the Protective Effect of Polyunsaturated Fat Intake on the Risk of MI

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Edward Ruiz-Narvaez ◽  
Peter Kraft ◽  
Hannia Campos

Background: Intake of polyunsaturated fat is protective against development of coronary heart disease (CHD). Less is known about genetic variation modulating this association. The Ala12 allele of the PPARG gene decreases lipolysis of triacylglycerols in adipose tissue, resulting in accumulation of fatty acids in adipocytes. Objective: Determine whether the Pro12Ala polymorphism interacts with polyunsaturated fat intake to affect the risk of myocardial infarction (MI). Design: Cases (n=1805) with a first nonfatal acute MI and age, sex and area of residence matched population-based controls (n=1805) living in Costa Rica, were genotyped for the PPARG Pro12Ala genetic polymorphism. Polyunsaturated fat intake was determined by a validated food frequency questionnaire and by GC analysis in adipose tissue. Odds ratios (ORs) and 95% confidence intervals (95% CI) for MI were estimated using logistic regression. Results: The relative allele frequencies of the Ala12 allele were 10% in controls and 11% in cases. ORs (95% CI) for MI per each 5% increase of energy from polyunsaturated fat were 0.66 (0.53, 0.82) in Pro12/Pro12 subjects, and 0.93 (0.61, 1.42) in carriers of the Ala12 allele (p for interaction = 0.03). Increments (95% CI) of polyunsaturated fat in adipose tissue per 5% increment in dietary intake were 5.4% (4.9%, 5.9%) in Pro12/Pro12 homozygous, and 7.0% (6.0%, 8.0%) in carriers of the Ala12 variant (p for homogeneity of slopes = 0.02). Conclusions: The protective effect of polyunsaturated fat intake on MI is attenuated in carriers of the Ala12 allele of the PPARG gene.

2010 ◽  
Vol 105 (7) ◽  
pp. 1005-1011 ◽  
Author(s):  
Nicole J. W. de Wit ◽  
Hanneke Bosch-Vermeulen ◽  
Els Oosterink ◽  
Michael Müller ◽  
Roelof van der Meer

There is increased interest in the potential protective role of dietary Ca in the development of metabolic disorders related to the metabolic syndrome. Ca-induced intestinal precipitation of fatty acids and bile acids as well as systemic metabolic effects of Ca on adipose tissue is proposed to play a causal role. In this experiment, we have studied all these aspects to validate the suggested protective effect of Ca supplementation, independent of other dietary changes, on the development of diet-induced obesity and insulin resistance. In our diet intervention study, C57BL/6J mice were fed high-fat diets differing in Ca concentrations (50 v. 150 mmol/kg). Faecal excretion analyses showed an elevated precipitation of intestinal fatty acids (2·3-fold; P < 0·01) and bile acids (2-fold; P < 0·01) on the high-Ca diet. However, this only led to a slight reduction in fat absorption (from 98 to 95 %; P < 0·01), mainly in the distal small intestine as indicated by gene expression changes. We found no effect on body-weight gain. Lipolysis and lipogenesis-related parameters in adipose tissue also showed no significant changes on the high-Ca diet, indicating no systemic effects of dietary Ca on adiposity. Furthermore, early gene expression changes of intestinal signalling molecules predicted no protective effect of dietary Ca on the development of insulin resistance, which was confirmed by equal values for insulin sensitivity on both diets. Taken together, our data do not support the proposed protective effect of dietary Ca on the development of obesity and/or insulin resistance, despite a significant increase in faecal excretion of fatty acids and bile acids.


1980 ◽  
Vol 44 (3) ◽  
pp. 265-271 ◽  
Author(s):  
J. Shepherd ◽  
Jennifer M. Stewart ◽  
Janice G. Clark ◽  
Kay Carr

1. The early effects of a moderate polyunsaturated fat diet on the composition of circulating lipoproteins and adipose tissue fatty acids were measured in five healthy adults.2. The fatty acid content and gross composition of the three major plasma lipoprotein fractions altered within 7 d of treatment. The response of depot fat was slower but did show a significant and progressive change after 14 d on the diet.3. The efficiency of the moderate diet in changing the composition of the lipoproteins suggests that it should be equally dfective in altering their metabolic handling.


2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 861-861
Author(s):  
Jowy Seah Yi Hoong ◽  
Wee Siong Chew ◽  
Federico Torta ◽  
Chin Meng Khoo ◽  
Markus R Wenk ◽  
...  

Abstract Objectives Sphingolipid concentrations have been associated with risk of type 2 diabetes and cardiovascular diseases. Because sphingolipids can be synthesized de novo from saturated fatty acids (SFA), dietary fatty acids may affect plasma sphingolipid concentrations. We aimed to evaluate dietary fat and protein intakes in relation to circulating sphingolipid levels. Methods We used cross-sectional data from 2860 ethnic Chinese Singaporeans collected from 2004–2007. Nutrient intakes were estimated on the basis of a validated 159-item food frequency questionnaire. We quantified 79 molecularly distinct sphingolipids in a large-scale lipidomic evaluation from plasma samples. Results Higher saturated fat intake was associated with higher concentrations of 16:1; O2 sphingolipids including ceramides, monohexosylcermides, dihexosylceramides, sphingomyelins, and sphingosine 1-phosphates. Higher polyunsaturated fat intake was associated with lower plasma long-chain ceramides and long-chain monohexosylcermide concentrations. Protein intake was inversely associated with concentrations of most subclasses of sphingolipids, with the exception of sphingolipids containing a 16:1; O2 sphingoid base. Lower intake of saturated fat and higher intake of polyunsaturated fat and protein may decrease plasma concentrations of several sphingolipid classes. Conclusions These findings may represent a novel biological mechanism for the impact of nutrient intakes on cardio-metabolic health. Funding Sources This work was supported by the National Research Foundation Investigatorship grant (NRF-NRFI2015–05, to MRW), A*STAR (I1901E0040), and the National University Health System (NUHSRO/2014/085/AF-Partner/01, DRH). FT was supported by the NRF and A*STAR IAF-ICP I1901E0040.


2018 ◽  
Vol 88 (5-6) ◽  
pp. 263-269 ◽  
Author(s):  
Fariba Koohdani ◽  
Gity Sotoudeh ◽  
Zahra Kalantar ◽  
Anahita Mansoori

Abstract. Background: Peroxisome proliferator-activated receptor γ (PPARγ) Pro12Ala polymorphism (rs1801282) has been associated with metabolic syndrome components in some studies. Moreover, the PPARγ gene may mediate the physiological response to dietary fat intake in a ligand-dependent manner. Methods: Metabolic syndrome components (body mass index, waist circumference, and lipid profile) were determined in 290 type 2 diabetes mellitus patients in a cross-sectional study. DNA genotyping for determining PPARγ Pro12Ala polymorphism was conducted using the polymerase chain reaction-restriction length polymorphism method. A semi-quantitative food frequency questionnaire was used to assess the participants’ dietary intakes in the previous year. Results: There were significant differences between the two genotype groups of PPARγ Pro12Ala polymorphism, Ala carriers (Pro/Ala + Ala/Ala) versus non-Ala carriers (Pro/Pro), in terms of mean body mass index (p = 0.04) and waist circumference (p = 0.02). Below the median percentage of energy from monounsaturated and polyunsaturated fatty acids, Ala carriers had a higher body mass index (p = 0.01) compared to non-Ala carriers. Furthermore, a significant interaction between this single-nucleotide polymorphism and polyunsaturated fatty acids intake on serum triglyceride levels (p = 0.01) was seen, and in higher polyunsaturated fatty acids intake (≥ median) Ala carriers had lower triglyceride levels than non-Ala carriers (p = 0.007). Conclusions: The findings of the current study support a significant association between PPARγ Pro12Ala polymorphism and metabolic syndrome components, and they suggest that this polymorphism can modulate the biological response of dietary fat intake on body mass index and triglyceride levels.


1999 ◽  
Vol 150 (1) ◽  
pp. 75-87 ◽  
Author(s):  
L. F. Andersen ◽  
K. Solvoll ◽  
L. R. K. Johansson ◽  
I. Salminen ◽  
A. Aro ◽  
...  

2005 ◽  
Vol 93 (1) ◽  
pp. 115-121 ◽  
Author(s):  
M. Rosell ◽  
G. Johansson ◽  
L. Berglund ◽  
B. Vessby ◽  
U. de Faire ◽  
...  

The relative contents of the fatty acids 14: 0, 15: 0 and 17: 0 in serum and adipose tissue may be used as biological markers of dairy fat intake. However, the determinants of these fatty acids are not fully understood. This study investigates the relationship between these fatty acids and the intake of macronutrients and physical activity in a cross-sectional study of 301 healthy men aged 61–64 years. Dietary intake was assessed using a pre-coded 7 d food record, and physical activity during the previous year was recorded in an interview. Under-reporters of energy intake were identified by the Goldberg cut-off. Fatty acid composition was determined in serum phospholipids (PL) and subcutaneous adipose tissue (AT) from the upper buttock. The relative content of each of 14: 0, 15: 0 and 17: 0 in PL and AT was positively associated with the intake of dairy fat. In addition, all three fatty acids were inversely correlated with alcohol intake,Rranging from −0·28 to −0·53 (P<0·001). The results were not markedly affected when under-reporters (n88) were excluded from the analyses. In both PL and AT, the relative content of the fatty acids was approximately 5% higher in a group of high physical activity compared with a group of low physical activity, although significant trends were only seen for 14: 0 in PL and 17: 0 in AT. The findings suggest that adjustments should be made for alcohol intake when the fatty acids 14: 0, 15: 0 and 17: 0 are applied as markers for dairy fat intake.


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