Dietary Monounsaturated Fatty Acids Research Articles

Causal association of monounsaturated fatty acids with rheumatoid arthritis but not osteoarthritis: A two-sample Mendelian randomization study

ObjectivesPrevious studies have indicated that dietary monounsaturated fatty acids (MUFAs) are associated with decreased risk of osteoarthritis (OA) and rheumatoid arthritis (RA). However, the causality of the observed associations is largely undetermined. We sought to ascertain the potential causal roles of two of the most common MUFAs, oleic acid and palmitoleic acid, in RA and OA risk using a two-sample Mendelian randomization approach. MethodsFor the outcomes, we used summary-level data for RA (14 361 people with RA and 43 923 controls) and OA (10 083 people with OA and 40 425 controls) from two genome-wide association studies in European ancestry. For the exposures, five single-nucleotide polymorphisms associated with palmitoleic acid and one associated with oleic acid with genome-wide significance (P < 5 × 10−8) were selected as instrumental variables. The causal effects were estimated using the inverse-variance weighted method with several sensitivity analyses. ResultsFor genetically predicted levels, an increase of one SD in palmitoleic acid (odds ratio, 0.24; 95% confidence interval, 0.10–0.59; P = 0.002) and oleic acid (odds ratio, 0.78; 95% confidence interval, 0.67–0.90; P < 0.001) was significantly associated with lower risk of RA. However, genetic predisposition to either of the two individual MUFAs was not associated with OA risk. Sensitivity analyses yielded similar results. ConclusionsOur Mendelian randomization analyses suggest a causal relationship between higher genetically predicted MUFA levels and lower risks of RA. However, the causality between MUFAs and OA cannot be inferred from this study. Further research is required to unravel the role of MUFA supplementation in arthritis prevention.

CLOCK Gene Variation Is Associated with the Incidence of Metabolic Syndrome Modulated by Monounsaturated Fatty Acids.

The circadian locomotor output cycles kaput (CLOCK) gene plays a crucial role in regulating circadian rhythms through its transcription factor gene product. The objective of this study was to investigate the association between CLOCK rs1801260 and the incidence of metabolic syndrome modulated by dietary monounsaturated fatty acid (MUFA) intake in Korean adults. Using a dataset from the Ansan-Ansung Cohort Study of the Korean Genome and Epidemiology Study, 3608 Korean adults were included after an average of nine years of follow-up. Men who were minor allele carriers (G allele) of CLOCK rs1801260 had a 18% higher incidence of metabolic syndrome than non-carriers [hazard ratio (HR), 1.18; 95% confidence interval (CI), 1.00–1.40; p Value = 0.047]. By dichotomizing dietary MUFA intake, we observed that men who were minor allele carriers (G allele) of CLOCK rs1801260 had a 42% increased incidence of metabolic syndrome when dietary MUFA intake was ≤3.5% (HR: 1.42, 95% CI 1.23–1.81; p Value = 0.004). No significant association was found between CLOCK rs1801260 and the incidence of metabolic syndrome modulated by dietary MUFA intake in women. CLOCK polymorphisms affected metabolic syndrome, modulated by dietary MUFA intake in men. These results suggest the significance of CLOCK genes in the pathogenesis of metabolic syndrome and the modulating role of dietary MUFA intake and provide new insights into the underlying mechanisms connecting the circadian system, dietary factors, and metabolic syndrome.

Transcriptome Response of genes mitigating Reactive Oxygen Species in Zebrafish (Danio rerio) Larvae during dietary lipid absorption.

The Mediterranean diet is associated with higher levels of polyunsaturated fatty acids (PUFAs) as well as lower incidences of cardiac disease and colon cancer (1). Due the presence of multiple double bonds, PUFAs such as alpha-linoleic acid (ALA), are thought to generate fewer harmful metabolites, specifically the Reactive Oxidative Species (ROS). Conversely, monounsaturated fatty acids (MUFAs) may lead to relatively increased ROS. In this study we compare two high-fat diets: the MUFA diet containing oleic acid (1 mM C18:1 plus 1 mM cholesterol) and the PUFA diet containing ALA (1 mM C18:3 plus 1 mM cholesterol). We compared gene expression from the dissected intestines of six days post-fertilization zebrafish (Danio rerio) larvae after feeding the PUFA and MUFA diets for 3 hours. We measured ROS response indirectly via the increased expression of ROS response genes (GSTO1, GSR, and cyp1a). Our preliminary results show upregulation of the ROS response genes GSTO1, GSR, and cyp1a in the presence of MUFA and await further replicates to become significant. . These data support the hypothesis that dietary fatty acid saturation plays a role in oxidative stress within enterocytes. In the future we plan to measure ROS responsiveness directly via respirometry. This work was supported by NIH Grant P20GM103434 to the West Virginia IDeA Network for Biomedical Research Excellence and NIH Grant P20GM103434 awarded to Bluefield State College and the McNair Scholars Program.

The association of dietary and plasma fatty acid composition with FTO gene expression in human visceral and subcutaneous adipose tissues.

The human obesity susceptibility gene, FTO, associates with body mass and obesity in humans through regulation of energy expenditure and intake. We aimed to determine how fatty acids in plasma and in diet associate with FTO gene expression in subcutaneous and visceral adipose tissues. In this study, 97 participants aged ≥ 18years were selected from patients admitted to the hospital for abdominal surgeries. Habitual dietary intake of participants was collected using a valid and reliable food frequency questionnaire (FFQ), from which the intake of fatty acids was quantified. Plasma fatty acids were assessed by gas-liquid chromatography. The mRNA expression of the FTO gene in visceral and subcutaneous adipose tissues obtained by biopsy was measured by Real-Time Quantitative Reverse Transcription PCR. Standardized β-coefficients were calculated by multivariable linear regression. After adjusting for age, homeostasis model insulin resistance index (HOMA-IR), and body mass index, total fatty acid intake was significantly associated with FTO gene expression in visceral (STZβ = 0.208, P = 0.037) and subcutaneous (STZβ = 0.236, P = 0.020) adipose tissues. Dietary intake of monounsaturated fatty acid (MUFA) and polyunsaturated fatty acids (PUFA) had positive significant associations with the expression of FTO in visceral (STZβ = 0.227, P = 0.023; STZβ = 0.346, P < 0.001, respectively) and subcutaneous (STZβ = 0.227, P = 0.026; STZβ = 0.274, P = 0.006, respectively) adipose tissues. There were no associations between plasma fatty acids and FTO mRNA expression in either subcutaneous or visceral adipose tissues. The weak association of dietary total fatty acids, MUFA, and PUFA with FTO gene expression in both adipose tissues may highlight the importance of dietary fatty acids composition along with total fat intake in relation to FTO gene expression.

The Association of Serum Levels of Leptin and Ghrelin with the Dietary Fat Content in Non-Obese Women with Polycystic Ovary Syndrome.

Women with polycystic ovary syndrome (PCOS) are at an increased risk of developing insulin resistance and abdominal obesity in the state of an improper diet balance. Leptin is a peptide considered to be a satiety hormone that plays an important role in the long-term energy balance, whereas ghrelin is a hormone that controls short-term appetite regulation and is considered a hunger hormone. The aim of the present study was to assess the relationship between serum leptin and ghrelin concentrations and the dietary macronutrient content in PCOS women. We examined 73 subjects: 39 women diagnosed with PCOS by the Rotterdam criteria and 34 healthy controls, matched by the body mass index. The subjects completed a consecutive three-day dietary diary to identify the macronutrient and micronutrient intake. Serum concentrations of leptin and total ghrelin were measured and homeostasis model assessment of insulin resistance (HOMA-IR) was calculated. The studied groups did not differ significantly in terms of the intake of macronutrients (proteins, fats, and carbohydrates) and serum concentrations of ghrelin and leptin (all p > 0.05). In the PCOS group, the serum leptin concentration positively correlated with the intake of total fat (r = 0.36, p = 0.02), total cholesterol (r = −0.36, p = 0.02), saturated fatty acids (r = 0.43, p < 0.01), and monounsaturated fatty acids (MUFA) (r = 0.37, p = 0.02), whereas the serum ghrelin concentration correlated in an inverse manner with the intake of total fat (r = −0.37, p = 0.02), MUFA (r = −0.37, p = 0.02), polyunsaturated fatty acids (r = −0.34, p = 0.03), and long chain polyunsaturated fatty acids (r = −0.38, p = 0.02). In this group, we also found a negative association of HOMA-IR with serum ghrelin levels (r = −0.4, p = 0.03) and a positive relationship with the serum leptin concentration (r = 0.5, p < 0.01) and relationships between HOMA-IR and total dietary fat (r = 0.38, p = 0.03) and MUFA (r = 0.35, p = 0.04) intake. In PCOS women, dietary components such as the total fat and type of dietary fat and HOMA-IR are positively connected to serum leptin concentrations and negatively connected to serum ghrelin concentrations, which may influence the energy balance.

Effects of a multifactorial ecosustainable isocaloric diet on liver fat in patients with type 2 diabetes: randomized clinical trial

IntroductionTreatment options for non-alcoholic fatty liver disease (NAFLD) in patients with type 2 diabetes (T2D) are still a matter of debate. We compared the effects of a diet including different...

Postprandial triglyceride-rich lipoproteins promote M1/M2 microglia polarization in a fatty-acid-dependent manner

Inhibiting M1 microglia phenotype while stimulating the M2 microglia has been suggested as a potential therapeutic approach for the treatment of neuroinflammatory diseases. Our hypothesis is that the type of dietary fatty acids (FAs) into human postprandial triglyceride-rich lipoproteins (TRLs) could modulate the plasticity of microglia. We isolated TRLs at the postprandial hypertriglyceridemic peak from blood samples of healthy volunteers after the ingestion of a meal rich in saturated FAs (SFAs), monounsaturated FAs (MUFAs) or MUFAs plus omega-3 long-chain polyunsaturated FAs. We observed that postprandial TRL-MUFAs enhance M2 microglia polarization, whereas postprandial TRL-SFAs made polarized microglia prone to an M1 phenotype. In addition, in contrast to dietary SFAs, dietary MUFAs primed for a reduced proinflammatory profile in the brain of mice fed with the different FA-enriched diets. Our study underlines a role of postprandial TRLs as a metabolic entity in regulating the plasticity of microglia and brings an understanding of the mechanisms by which dietary FAs are environmental factors fostering the innate immune responsiveness. These exciting findings open opportunities for developing nutraceutical strategies with olive oil as the principal source of MUFAs, notably oleic acid, to prevent development and progression of neuroinflammation-related diseases.

Protective Effects of Dietary MUFAs Mediating Metabolites against Hypertension Risk in the Korean Genome and Epidemiology Study.

Background and Aims: Metabolites related to dietary factors can be used to identify biological markers to prevent metabolic disease. However, most studies have been conducted in the United States and Europe, and those in the Asian region are limited. We investigated the effects of dietary monounsaturated fatty acids (MUFAs) and metabolites on new-onset hypertension in the Korean Genome and Epidemiology Study. Method and Results: A total of 1529 subjects without hypertension were divided into tertiles of dietary MUFAs intake. After a 4-year follow-up, 135 serum metabolites were measured using the AbsoluteIDQ p180 kit. During the 4-year follow-up period, 193 new-onset hypertension incidences were observed. The highest MUFAs intake group was inversely associated with the risk of hypertension compared with the lowest MUFAs intake group (odds ratio (OR) = 0.49, (95% confidence interval (CI) = 0.29–0.82)). Of the 135 metabolites, eight were significantly associated with MUFAs intake. Phosphatidylcholine-diacyl (PC aa) C 38:1 and hydroxysphingomyelin (SM OH) C 16:1 were associated with a decrease in hypertension risk (PC aa C 38:1, OR = 0.60 (95% CI = 0.37–0.96); SM OH C 16:1, OR = 0.42 (95% CI = 0.20–0.90)). The highest MUFAs intake group had a significantly decreased risk of hypertension, even considering PC aa C 38:1 and SM (OH) C 16:1 as a mediator. Conclusion: We confirmed that dietary MUFAs intake, and PC aa C 38:1 and SM (OH) C 16:1 had protective effects against hypertension. Furthermore, high MUFAs intake combined with PC aa C 38:1 and SM (OH) C 16:1 has the most significant effect on reducing the risk hypertension.

Dietary Intake of Fatty Acids, Total Cholesterol, and Stomach Cancer in a Chinese Population.

To investigate the associations between dietary fatty acids and cholesterol consumption and stomach cancer (SC), we analyzed data from a population-based case-control study with a total of 1900 SC cases and 6532 controls. Dietary data and other risk or protective factors were collected by face-to-face interviews in Jiangsu Province, China, from 2003 to 2010. Adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using multiple unconditional logistic regression models and an energy-adjusted method. The joint associations between dietary factors and known risk factors on SC were examined. We observed positive associations between dietary saturated fatty acids (SFAs), monounsaturated fatty acids (MUFAs), and total cholesterol and the development of SC, comparing the highest versus lowest quarters. Increased intakes of dietary SFAs (p-trend = 0.005; aOR, 1.11; 95% CI, 1.01–1.22 with a 7 g/day increase as a continuous variable) and total cholesterol (p-trend < 0.001; aOR, 1.13; 95% CI, 1.06–1.22 with a 250 mg/day increase as a continuous variable) were monotonically associated with elevated odds of developing SC. Our results indicate that dietary SFAs, MUFAs, and total cholesterol are associated with stomach cancer, which might provide a potential dietary intervention for stomach cancer prevention.

Associations of Monounsaturated Fatty Acids From Plant and Animal Sources With Total and Cause-Specific Mortality in Two US Prospective Cohort Studies.

Dietary monounsaturated fatty acids (MUFAs) can come from both plant and animal sources with divergent nutrient profiles that may potentially obscure the associations of total MUFAs with chronic diseases. To investigate the associations of cis-MUFA intake from plant (MUFA-P) and animal (MUFA-A) sources with total and cause-specific mortality. We followed 63 412 women from the NHS (Nurses' Health Study; 1990-2012) and 29 966 men from the HPFS (Health Professionals Follow-Up Study; 1990-2012). MUFA-Ps and MUFA-As were calculated based on data collected through validated food frequency questionnaires administered every 4 years and updated food composition databases. During 1 896 864 person-years of follow-up, 20 672 deaths occurred. Total MUFAs and MUFA-Ps were inversely associated with total mortality after adjusting for potential confounders, whereas MUFA-As were associated with higher mortality. When MUFA-Ps were modeled to isocalorically replace other macronutrients, hazard ratios (HRs, 95% CIs) of total mortality were 0.84 (0.77-0.92; P<0.001) for replacing saturated fatty acids, 5% of energy); 0.86 (0.82-0.91; P<0.001) for replacing refined carbohydrates (5% energy); 0.91 (0.85-0.97; P<0.001) for replacing trans fats (2% energy), and 0.77 (0.71-0.82; P<0.001) for replacing MUFA-As (5% energy). For isocalorically replacing MUFA-As with MUFA-Ps, HRs (95% CIs) were 0.74 (0.64-0.86; P<0.001) for cardiovascular mortality; 0.73 (0.65-0.82; P<0.001) for cancer mortality, and 0.82 (0.73-0.91; P<0.001) for mortality because of other causes. Higher intake of MUFA-Ps was associated with lower total mortality, and MUFA-As intake was associated with higher mortality. Significantly lower mortality risk was observed when saturated fatty acids, refined carbohydrates, or trans fats were replaced by MUFA-Ps, but not MUFA-As. These data suggest that other constituents in animal foods, such as saturated fatty acids, may confound the associations for MUFAs when they are primarily derived from animal products. More evidence is needed to elucidate the differential associations of MUFA-Ps and MUFA-As with mortality.

Disentangling the Effects of Monounsaturated Fatty Acids from Other Components of a Mediterranean Diet on Serum Metabolite Profiles: A Randomized Fully Controlled Dietary Intervention in Healthy Subjects at Risk of the Metabolic Syndrome.

ScopeThe Mediterranean (MED) diet has been associated with a decreased risk of cardiovascular diseases. It is unclear whether this health effect can be mainly contributed to high intakes of monounsaturated fatty acids (MUFA), characteristic for the MED diet, or whether other components of a MED diet also play an important role.Methods and ResultsA randomized fully controlled parallel trial is performed to examine the effects of the consumption of a saturated fatty acid rich diet, a MUFA‐rich diet, or a MED diet for 8 weeks on metabolite profiles, in 47 subjects at risk of the metabolic syndrome. A total of 162 serum metabolites are assessed before and after the intervention by using a targeted NMR platform. Fifty‐two metabolites are changed during the intervention (false discovery rate [FDR] p < 0.05). Both the MUFA and MED diet decrease exactly the same fractions of LDL, including particle number, lipid, phospholipid, and free cholesterol fraction (FDR p < 0.05). The MED diet additionally decreases the larger subclasses of very‐low‐density lipoprotein (VLDL), related VLDL fractions, VLDL‐triglycerides, and serum‐triglycerides (FDR p < 0.05).ConclusionThe findings clearly demonstrate that the MUFA component is responsible for reducing LDL subclasses and fractions, and therefore causes an antiatherogenic lipid profile. Interestingly, consumption of the other components in the MED diet show additional health effects.

Role of Dietary Macronutrients and Fatty Acids in Obesity and Metabolic Risk in Older Adults.

The aim of the study was to examine the role of dietary consumption of different types of fatty acids on metabolic risk factors and regional fat deposition in older men and women. We hypothesized that saturated fatty acid (SFA) intake, monounsaturated fatty acid (MUFA) and low intake of polyunsaturated fatty acids (PUFA) would be associated with markers of insulin resistance, hyperlipidemia, and hypertriglyceridemia. Sedentary, overweight and obese (body mass index: 29–48 kg/m2) adults (N=20) aged 45–78 years underwent two-hour oral glucose tolerance test, blood draw, DXA scan, and completed seven-day diet records. Subjects had low fitness levels (VO2 max=23.5 ± 2.4 mL/kg/min) and high total body fat (43.5 ± 1.7%). The average macronutrient composition of the diet was high in fat as a percent of total kcal (35.5%). The ratio of MUFA to PUFA was associated with serum cholesterol (r=0.48, P=0.03) and tended to be associated with higher fasting glucose (r=0.42, P=0.06) and glucose at 120 min (r=0.43, P=0.06). PUFA intake as a percentage of fat intake was associated with lower serum cholesterol (r=−0.44, P=0.05). Therefore, dietary MUFA intake unbalanced by PUFA may confer increased risk for diabetes among obese, sedentary individuals. Future investigation of food sources, or context of dietary lipids, could lead to individualized dietary recommendations to promote healthy eating habits and potentially alter metabolic risk.

Appetite responses to high-fat diets rich in mono-unsaturated versus poly-unsaturated fats

BackgroundModifying the type of dietary fat consumed may impact appetite, therefore having implications in weight management. ObjectiveTo test the effects of a 5-day, high-fat diet rich in poly-unsaturated fatty acids (PUFAs) and a diet rich in mono-unsaturated fatty acids (MUFAs) on markers of appetite. MethodsFifteen normal weight men participated in a randomized cross-over design with two controlled feeding trials (3d lead-in diet, pre-diet visit, 5d PUFA- or MUFA-rich diet, post-diet visit). The 5d diets (50% fat) were rich in either PUFA (25% of energy) or MUFA (25% of energy). At pre- and post-diet visits, subjects consumed breakfast and lunch test meals, rich in the FA corresponding to the 5-day diet. Fasting and postprandial subjective ratings of appetite were determined and blood draws were performed for 4h after each meal to determine changes in appetite hormones. An ad libitum buffet meal was given at the end of pre- and post-diet visits. ResultsAcutely, at the pre-diet visit, the PUFA-rich meal resulted in lower ghrelin (hunger hormone) (iAUC: -350.85 ± 60.70 vs. −233.16 ± 61.42 pg/ml/8h, for PUFA vs. MUFA, respectively; p < 0.05) and higher CCK (satiation hormone) (iAUC: 238.09 ± 46.07 vs. 196.84 ± 33.92 pM/8h, for PUFA vs. MUFA, respectively; p < 0.05). No other acute meal challenge differences were found. The 5d high PUFA diet resulted in lower hunger ratings (iAUC: -172.06 ± 40.59 vs. −274.46 ± 41.47 mm/8h, for pre-to post-diet, respectively; p < 0.05). However, energy intake, ratings of fullness, or PYY did not change from pre-to post-diet for either MUFA or PUFA, and no other changes were observed with the MUFA diet. ConclusionsAcutely, a PUFA-rich meal results in ghrelin suppression and higher CCK. After a 5-day high-fat diet, PUFAs suppressed postprandial hunger while MUFAs did not change any measures of appetite.

Potential contribution of monounsaturated fatty acids to cardiovascular risk in chronic kidney disease.

INTRODUCTION Patients with chronic kidney disease (CKD) are particularly susceptible to cardiovascular disease (CVD). Increased synthesis of endogenous monounsaturated fatty acids (MUFAs) by stearoyl-CoA desaturase-1 (SCD1) might predispose to cardiovascular complications. OBJECTIVES The aim of this study was to examine the serum MUFA content in patients at subsequent stages of CKD, and to evaluate associations between MUFA content and SCD1 activity, patients' diet, and cardiovascular risk. PATIENTS AND METHODS Serum fatty acid composition was evaluated in 177 patients with subsequent stages of CKD (1-2, 3a, 3b, 4-5, hemodialysis, peritoneal dialysis, and after kidney transplantation), and in 30 healthy controls. Gas chromatography-mass spectrometry was used for the measurement. RESULTS Serum MUFA content was shown to increase with subsequent stages of CKD and to be correlated with various risk factors of CVD, including serum triacylglycerols, HDL cholesterol (P <0.01), and high-sensitivity C-reactive protein (P <0.05). Moreover, also the prevalence of CVD was shown to increase with CKD progression. Estimated SCD1 activity was associated with serum MUFA content (P <0.01), but no association was found between dietary MUFA intake and serum MUFA levels. CONCLUSIONS Our results indicate that the elevation of serum MUFA levels in CKD patients may contribute to an increased risk of CVD during CKD progression, mainly due to increased endogenous MUFA synthesis by SCD1.

Saturated lipids are more effective than others in juvenile California yellowtail feeds—Understanding and harnessing LC-PUFA sparing for fish oil replacement

Diet-to-tissue transfer of long-chain polyunsaturated fatty acids (LC-PUFAs) is more efficient when diets contain saturated fatty acid (SFA) or monounsaturated fatty acid (MUFA)-rich alternative lipids. This mechanism, the omega-3 or LC-PUFA “sparing effect”, encourages more efficient metabolism of the limited LC-PUFAs available in terms of their important physiological functions and tissue retention, and the likelihood of successful fish oil sparing (i.e. complete fish oil replacement maintaining growth and tissue fatty acid profile). However, it is still unclear whether dietary SFAs and MUFAs are equivalent or interact synergistically or antagonistically in this context. Accordingly, we compared production performance and tissue fatty acid composition of California Yellowtail fed diets containing fish oil (rich in LC-PUFAs) or soybean oil (rich in C18 PUFAs), partially hydrogenated soybean oil (rich in MUFAs), fully hydrogenated soybean oil (rich in SFAs), or blends of these soybean oils. After 10 weeks, production performance was not affected by dietary lipid source or fatty acid composition, and tissue fatty acid profiles generally mimicked dietary fatty acid composition. However, tissues of fish fed SFA-rich lipids exhibited the greatest similarity to those fed fish oil, and fillets of fish fed fully hydrogenated soybean oil had significantly higher levels of LC-PUFAs (43.9 g LC-PUFA /100 g fatty acid methyl esters; FAMEs) than those fed any of the other diets (22.5–36.9 g LC-PUFA /100 g FAMEs), including the LC-PUFA-rich fish oil-based feed (39.8 g LC-PUFA /100 g FAMEs). Power regression analyses demonstrated a stronger positive relationship between dietary SFAs with fillet LC-PUFA deposition (r2 = 0.73) than dietary MUFAs (r2 = 0.09), whereas dietary C18 PUFAs were observed to have a negative relationship with fillet LC-PUFA content (r2 = 0.85). These trends were also observed in liver and eye tissues, and to a lesser extent in brain tissue. Multiple linear regression analyses demonstrated a stronger relationship between dietary levels of PUFAs and SFAs and tissue fatty acid profile composition, including LC-PUFA content, than dietary levels of PUFAs and MUFAs. Fillet lipid content varied significantly, with the FISH and C18 PUFA SOY diets displaying the highest levels. The same pattern was observed for liver lipid content, but not significantly. Our findings suggest that SFAs are the primary drivers of LC-PUFA sparing, whereas MUFAs exert a weaker independent sparing effect and appear to diminish the sparing effect of dietary SFAs when MUFAs were also present.

Replacing Fish Oil with Hydrogenated Soybean Oils in Feeds for Yellowtail

AbstractTo assess the relative merits of monounsaturated fatty acid (MUFA)‐rich versus saturated fatty acid (SFA)‐rich lipids as alternatives to fish oil in aquafeeds, diets formulated for Yellowtail Seriola dorsalis—containing menhaden fish oil, fully hydrogenated soybean oil (high SFA content), partially hydrogenated soybean oil (high MUFA content), or blends of these soy‐derived lipids (20/80, 40/60, 60/40, or 80/20)—were tested in a 7‐week feeding trial. Juvenile fish (~11 g) were stocked in a semi‐closed recirculating aquaculture system (15 fish/tank), diets were randomly assigned to tanks in triplicate (N = 3), and fish were fed in slight excess of estimated apparent satiation. Growth performance did not vary based on dietary SFA versus MUFA content, but performance was inferior among fish fed the soybean oil‐based feeds relative to those fed the fish oil‐based feed: weight gain was 714–770% versus 848%; specific growth rate was 4.03–4.16% versus 4.32% body weight/d; and feed conversion ratio was 1.30–1.38 versus 1.27. Generally, fillet fatty acid composition mirrored dietary composition except that the fillets of fish fed diets containing primarily fully hydrogenated soybean oil contained fewer SFAs and more long‐chain polyunsaturated fatty acids (LC‐PUFAs) than one would expect based on dietary fatty acid profiles. Fillets of fish that were fed partially hydrogenated soybean oil contained trans‐fatty acids (0.02–0.06 g of trans fats per 100 g of fillet) but only at trace levels. Liver fatty acid profiles were less affected by dietary lipid source, but where differences existed, they followed patterns similar to those observed in fillets. Results suggest that blends of fully and partially hydrogenated soybean oils may yield slightly higher growth performance and fillet lipid content without accumulating enough trans fats to negatively affect consumers. Diets containing only fully hydrogenated soybean oil may slightly reduce lipid digestion in Yellowtail, but they mitigate LC‐PUFA loss associated with fish oil sparing.

The effects of various diets on glycemic outcomes during pregnancy: A systematic review and network meta-analysis.

AimsEvidence to support dietary modifications to improve glycemia during pregnancy is limited, and the benefits of diet beyond limiting gestational weight gain is unclear. Therefore, a systematic review and network meta-analysis of randomized trials was conducted to compare the effects of various common diets, stratified by the addition of gestational weight gain advice, on fasting glucose and insulin, hemoglobin A1c (HbA1c), and homeostatic model assessment for insulin resistance (HOMA-IR) in pregnant women.MethodsMEDLINE, EMBASE, Cochrane database, and reference lists of published studies were searched through April 2017. Randomized trials directly comparing two or more diets for ≥2-weeks were eligible. Bayesian network meta-analysis was performed for fasting glucose. Owing to a lack of similar dietary comparisons, a standard pairwise meta-analysis for the other glycemic outcomes was performed. The certainty of the pooled effect estimates was assessed using the GRADE tool.ResultsTwenty-one trials (1,865 participants) were included. In general, when given alongside gestational weight gain advice, fasting glucose improved in most diets compared to diets that gave gestational weight gain advice only. However, fasting glucose increased in high unsaturated or monounsaturated fatty acids diets. In the absence of gestational weight gain advice, fasting glucose improved in DASH-style diets compared to standard of care. Although most were non-significant, similar trends were observed for these same diets for the other glycemic outcomes. Dietary comparisons ranged from moderate to very low in quality of evidence.Conclusion/InterpretationAlongside with gestational weight gain advice, most diets, with the exception of a high unsaturated or a high monounsaturated fatty acid diet, demonstrated a fasting glucose improvement compared with gestational weight gain advice only. When gestational weight gain advice was not given, the DASH-style diet appeared optimal on fasting glucose. However, a small number of trials were identified and most dietary comparisons were underpowered to detect differences in glycemic outcomes. Further studies that are high in quality and adequately powered are needed to confirm these findings.RegistrationPROSPERO CRD42015026008

Mono-unsaturated fatty acids link H3K4me3 modifiers to C. elegans lifespan

SummaryChromatin and metabolic states both influence lifespan, but how they interact in lifespan regulation is largely unknown. The COMPASS chromatin complex, which trimethylates lysine 4 on histone H3 (H3K4me3), regulates lifespan in C. elegans. However, the mechanism by which H3K4me3 modifiers impact longevity, and whether it involves metabolic changes, remain unclear. Here we find that H3K4me3-methyltransferase deficiency, which extends lifespan, promotes fat accumulation with a specific enrichment of mono-unsaturated fatty acids (MUFAs). This fat metabolism switch in H3K4me3-methyltransferase deficient animals is mediated at least in part by downregulation of germline targets, including S6 kinase, and by activation of an intestinal transcriptional network that upregulates delta-9 fatty acid desaturases. Interestingly, MUFA accumulation is necessary for the lifespan extension of H3K4me3-methyltransferase deficient worms, and dietary MUFAs are sufficient to extend lifespan. Given the conservation of lipid metabolism, dietary or endogenous MUFAs could extend lifespan and healthspan in other species, including mammals.

Comparison of the impact of SFAs from cheese and butter on cardiometabolic risk factors: a randomized controlled trial1–3

Background: Controversies persist concerning the association between intake of dietary saturated fatty acids (SFAs) and cardiovascular disease risk.Objective: We compared the impact of consuming equal amounts of SFAs from cheese and butter on cardiometabolic risk factors.Design: In a multicenter, crossover, randomized controlled trial, 92 men and women with abdominal obesity and relatively low HDL-cholesterol concentrations were assigned to sequences of 5 predetermined isoenergetic diets of 4 wk each separated by 4-wk washouts: 2 diets rich in SFAs (12.4–12.6% of calories) from either cheese or butter; a monounsaturated fatty acid (MUFA)–rich diet (SFAs: 5.8%, MUFAs: 19.6%); a polyunsaturated fatty acid (PUFA)–rich diet (SFAs: 5.8%, PUFAs: 11.5%); and a low-fat, high-carbohydrate diet (fat: 25%, SFAs: 5.8%).Results: Serum HDL-cholesterol concentrations were similar after the cheese and butter diets but were significantly higher than after the carbohydrate diet (+3.8% and +4.7%, respectively; P < 0.05 for both). LDL-cholesterol concentrations after the cheese diet were lower than after the butter diet (−3.3%, P < 0.05) but were higher than after the carbohydrate (+2.6%), MUFA (+5.3%), and PUFA (+12.3%) diets (P < 0.05 for all). LDL-cholesterol concentrations after the butter diet also increased significantly (from +6.1% to +16.2%, P < 0.05) compared with the carbohydrate, MUFA, and PUFA diets. The LDL-cholesterol response to treatment was significantly modified by baseline values (P-interaction = 0.02), with the increase in LDL cholesterol being significantly greater with butter than with cheese only among individuals with high baseline LDL-cholesterol concentrations. There was no significant difference between all diets on inflammation markers, blood pressure, and insulin-glucose homeostasis.Conclusions: The results of our study suggest that the consumption of SFAs from cheese and butter has similar effects on HDL cholesterol but differentially modifies LDL-cholesterol concentrations compared with the effects of carbohydrates, MUFAs, and PUFAs, particularly in individuals with high LDL cholesterol. In contrast, SFAs from either cheese or butter have no significant effects on several other nonlipid cardiometabolic risk factors. This trial was registered at http://clinicaltrials.gov as NCT02106208.

The Relationship Between Dietary Intake and Fasting Blood Glucose in Individuals with Pre‐Diabetes

BackgroundResearch has indicated that there may be a positive association between increased proportions of monounsaturated fatty acid (MUFA) intake and improved blood glucose levels. There has also been literature indicating there may be a link between intake of micronutrients such as iron, selenium, magnesium, vitamin E, and zinc and blood glucose levels. Using the validated Vioscreen food frequency questionnaire (FFQ), the current study aims to outline the relationship between various micronutrients and fasting blood glucose (FBG) levels as a marker of insulin resistance in individuals with pre‐diabetes.ObjectiveTo outline the effect of dietary micronutrients on FBG in individuals with pre‐diabetes using the Vioscreen FFQ.MethodsAll participants completed the Vioscreen FFQ. Participants were required to be fasting for at least 8 hours before blood glucose test was performed. Fasting blood glucose was compared with dietary intake of iron, selenium, magnesium, vitamin E, zinc, MUFAs, polyunsaturated fatty acids (PUFAs), and saturated fatty acids (SFAs).ResultsA univariate regression analysis of FBG compared with intake of different micronutrients gathered via Vioscreen FFQ showed a number of correlations.There was a statically significant negative correlation between fasting blood glucose (FBG) and dietary intake of total cholesterol (r=−0.12, p=0.02), iron (r=−0.48, p=0.04), selenium (r=−0.56, p=0.01), magnesium (r=−0.5, p=0.02), zinc (r=−0.45, p=0.04), MUFAs (r=−0.61, p=0.01), saturated fatty acids (SFA) (r=−0.58, p=0.01), and polyunsaturated fatty acids (PUFA) (r=−0.41, p=0.04).A negative correlation was present between FBG and vitamin E, however the finding did not reach significance (r=−0.282, p=0.17).ConclusionsData gathered from the Vioscreen FFQ suggests that there are significant correlations present between certain micronutrients and FBG levels for individuals with pre‐diabetes. These results indicate that increasing the amount of dietary iron, selenium, magnesium, zinc, MUFAs, SFAs, and PUFAs may be a valid dietary intervention for the treatment and maintenance of pre‐diabetes. A noteworthy finding of this study was the negative relationship between PUFAs (r=−0.41, p=0.04), MUFAs (r=−0.61, p=0.01), and SFAs (r=−0.58, p=0.01). This finding supports the theory of a high fat, low carbohydrate diet as an intervention for the maintenance of blood glucose levels in those with insulin resistance. It is particularly interesting that increased proportions of dietary SFA were associated with lower FBG levels, considering current 2015 U.S. Dietary Guidelines suggest limiting saturated fat in the diet. It must be noted however, that the sample size used was fairly small with 10 participants. This limitation indicates more research must be done to clarify the specific relationship, and mechanism in which the micronutrients tested affect FBG levels.Support or Funding InformationViterbo University Summer Undergraduate Research FellowshipTexas Pecan Growers Association