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Diet Quality, Saturated Fat and Metabolic Syndrome.
Harrison, S, Couture, P, Lamarche, B
Nutrients. 2020;(11)
Abstract
Indices reflecting overall diet quality are used globally in research to predict the risk of various diseases and metabolic disorders such as metabolic syndrome (MetS). Such indices are built to measure adherence to current dietary guidelines or to best assess the diet-disease relationship. Although mostly food-based, dietary guidelines often include recommendations to limit saturated fatty acid (SFA) intake in order to prevent cardiovascular diseases. However, not all diet quality indices consider SFA in their definition of diet quality. Additionally, the relationship between SFA consumption and the development of MetS remains unclear. The purpose of this short review was to explore the association between MetS and various diet quality indices and dietary patterns, with a focus on how SFA contributes to these associations.
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Carbohydrate and fat intake associated with risk of metabolic diseases through epigenetics of CPT1A.
Lai, CQ, Parnell, LD, Smith, CE, Guo, T, Sayols-Baixeras, S, Aslibekyan, S, Tiwari, HK, Irvin, MR, Bender, C, Fei, D, et al
The American journal of clinical nutrition. 2020;(5):1200-1211
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Abstract
BACKGROUND Epigenome-wide association studies identified the cg00574958 DNA methylation site at the carnitine palmitoyltransferase-1A (CPT1A) gene to be associated with reduced risk of metabolic diseases (hypertriglyceridemia, obesity, type 2 diabetes, hypertension, metabolic syndrome), but the mechanism underlying these associations is unknown. OBJECTIVES We aimed to elucidate whether carbohydrate and fat intakes modulate cg00574958 methylation and the risk of metabolic diseases. METHODS We examined associations between carbohydrate (CHO) and fat (FAT) intake, as percentages of total diet energy, and the CHO/FAT ratio with CPT1A-cg00574958, and the risk of metabolic diseases in 3 populations (Genetics of Lipid Lowering Drugs and Diet Network, n = 978; Framingham Heart Study, n = 2331; and REgistre GIroní del COR study, n = 645) while adjusting for confounding factors. To understand possible causal effects of dietary intake on the risk of metabolic diseases, we performed meta-analysis, CPT1A transcription analysis, and mediation analysis with CHO and FAT intakes as exposures and cg00574958 methylation as the mediator. RESULTS We confirmed strong associations of cg00574958 methylation with metabolic phenotypes (BMI, triglyceride, glucose) and diseases in all 3 populations. Our results showed that CHO intake and CHO/FAT ratio were positively associated with cg00574958 methylation, whereas FAT intake was negatively correlated with cg00574958 methylation. Meta-analysis further confirmed this strong correlation, with β = 58.4 ± 7.27, P = 8.98 x 10-16 for CHO intake; β = -36.4 ± 5.95, P = 9.96 x 10-10 for FAT intake; and β = 3.30 ± 0.49, P = 1.48 x 10-11 for the CHO/FAT ratio. Furthermore, CPT1A mRNA expression was negatively associated with CHO intake, and positively associated with FAT intake, and metabolic phenotypes. Mediation analysis supports the hypothesis that CHO intake induces CPT1A methylation, hence reducing the risk of metabolic diseases, whereas FAT intake inhibits CPT1A methylation, thereby increasing the risk of metabolic diseases. CONCLUSIONS Our results suggest that the proportion of total energy supplied by CHO and FAT can have a causal effect on the risk of metabolic diseases via the epigenetic status of CPT1A.Study registration at https://www.clinicaltrials.gov/: the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN)-NCT01023750; and the Framingham Heart Study (FHS)-NCT00005121.
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Effects of a hypoenergetic diet rich in α-linolenic acid on fatty acid composition of serum phospholipids in overweight and obese patients with metabolic syndrome.
Egert, S, Baxheinrich, A, Lee-Barkey, YH, Tschoepe, D, Stehle, P, Stratmann, B, Wahrburg, U
Nutrition (Burbank, Los Angeles County, Calif.). 2018;:74-80
Abstract
OBJECTIVES Plant-derived α-linolenic acid (ALA) may exert cardioprotective effects. Dietary ALA can undergo desaturation and elongation to form long-chain ω-3 polyunsaturated fatty acids, but the extent to which this occurs in humans is unclear. The aim of the study was to examine the effects of an energy-restricted diet enriched with ALA on fatty acid composition of serum phospholipids in patients with metabolic syndrome. METHODS The present analysis compared the effects of a hypoenergetic diet high in ALA (3.4 g/d) with a control diet low in ALA (0.9 g/d) on fatty acid composition of serum phospholipids in 81 overweight or obese patients with features of metabolic syndrome. RESULTS After a 26-wk intervention, concentration of ALA in serum phospholipids remained constant in both diet groups. The control group had a significant decrease in serum phospholipid eicosapentaenoic acid concentration, although no significant intergroup difference was observed. Serum phospholipid docosahexaenoic acid concentration significantly decreased to a similar extent with both interventions. Additionally, both interventions significantly decreased serum phospholipid concentrations of palmitic acid, stearic acid, total saturated fatty acids, linoleic acid, total ω-6 and ω-3 polyunsaturated fatty acids, with no effect of diet group on these changes. Compared with the ALA diet, the control diet led to a significant increase in serum phospholipid oleic acid concentration. CONCLUSION Daily intake of 3.4 g of ALA during a 26-wk energy-restricted diet did not lead to an enrichment of serum phospholipids with ALA and did not increase eicosapentaenoic acid due to conversion. Additionally, dietary ALA was unable to compensate for a decrease in serum phospholipid docosahexaenoic acid.
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Short communication: Daily intake of 125 g of cheese for 2 weeks did not alter amount or distribution of serum lipids or desaturase indexes in healthy adults in an exploratory pilot study.
Høstmark, AT, Lunde, MSH, Hjellset, VT
Journal of dairy science. 2018;(11):9625-9629
Abstract
Regular cheese contains saturated fat, consumption of which may negatively influence the amount of serum lipids. The American Dietary Guidelines (https://health.gov/dietaryguidelines/2015/guidelines/) recommend consumption of low-fat food. However, we observed a negative association between cheese intake and serum triglycerides and a positive association with high-density lipoprotein cholesterol. Cheese intake was also inversely related to metabolic syndrome and blunted the harmful association of intake of soft drinks with serum lipids. Cheese contains calcium and factors that may inhibit desaturases, thereby partly explaining why cheese might not have negative effects on serum lipids. Thus, opposing forces seem to govern the cheese effect but will any of these prevail? In an exploratory pilot study, 17 healthy subjects participated in a 4-wk crossover trial without washout. During the first 2 wk, 9 subjects were randomly assigned to add 125 g/d of regular cheese to their habitual diet. After 2 wk, cheese intake was discontinued and the subjects were instructed to return to their habitual diet. The other 8 subjects followed their habitual diet during the first 2 wk, and then added 125 g/d of cheese for the next 2 wk. Mean values (mmol/L) before and after 2 wk on habitual (cheese) diet were as follows: serum triglycerides: 0.91 (0.89) and 0.95 (0.91); total cholesterol: 5.25 (5.16) and 5.08 (5.24); low-density lipoprotein cholesterol: 3.18 (3.17) and 3.09 (3.22); and high-density lipoprotein cholesterol: 1.71 (1.64) and 1.61 (1.66). The fatty acid pattern in total serum lipids and desaturase indexes did not change significantly in response to high cheese intake. Thus, an appreciable increase in daily cheese intake for 2 wk may not alter concentrations of serum lipids, estimates of desaturases, or the distribution of serum fatty acids.
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The Effects of High-Protein and High-Monounsaturated Fat Meals on Postprandial Lipids, Lipoprotein Particle Numbers, Cytokines, and Leptin Responses in Overweight/Obese Subjects.
Shah, M, Adams-Huet, B, Franklin, B, Phillips, M, Mitchell, J
Metabolic syndrome and related disorders. 2018;(3):150-158
Abstract
BACKGROUND Obesity is linked to dyslipidemia, proinflammatory state, and hyperleptinemia. The influence of high-protein (HP) versus high-monounsaturated fat (HMF) meals on postprandial lipids, lipoprotein particle numbers, cytokines, and leptin responses in overweight/obese (OW/O) subjects is unknown. METHODS Twenty-four OW/O participants consumed an HP (31.9% energy from protein) and HMF (35.2% fat and 20.7% monounsaturated fat) meal, of similar energy/carbohydrate content, in a random order. The outcome variables were assessed from blood samples collected in fasted and postprandial (3 hr) states. RESULTS Repeated measures analysis found significant (P < 0.05) meal condition by time interactions for triglycerides (TGs), very low-density lipoprotein particles (VLDLP), total high-density lipoprotein particles (T-HDLP), and the ratio of large-buoyant high-density lipoprotein 2b (LB-HDL2b) to T-HDLP, and meal effect on small-dense HDLP (SD-HDLP). Comparison of HP versus HMF condition showed significantly lower TG at 120 min [geometric mean (95% confidence interval, CI): 148 (125-175) vs. 194 (164-230) mg/dL] and 180 min [167 (138-203) vs. 230 (189-278) mg/dL] and VLDLP at 180 min [70.0 (58.2-84.3) vs. 88.0 (73.1-106) nmol/L]. HP versus HMF condition showed significantly lower LB-HDL2b/T-HDLP at 180 min [mean difference (95% CI): 0.021 (0.004-0.038)], and higher T-HDLP [671 (263-1079) nmol/L] and SD-HDLP [606 (292-920) nmol/L] at 120 min. Area under the curve was significantly lower for TG and higher for T-HDLP, SD-HDLP, and small-dense LDL III (SD-LDL III) in the HP condition. Cytokines and leptin were not different between conditions. CONCLUSION OW/O subjects had lower TG and VLDLP, but less favorable SD-LDL III, SD-HDLP, and LB-HDL2b/T-HDLP ratio responses to the HP versus HMF meals.