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The pandemic of obesity, type 2 diabetes mellitus T2DM and nonalcoholic fatty liver disease NAFLD has frequently been associated with dietary intake of saturated fats 1 and specifically with dietary palm oil PO 2.
According to current paradigms, chronic insulin resistance is the common feature of these diseases 34 and relates to intracellular concentrations of triglycerides TG and lipotoxins 5.
There is evidence that a chronic high-fat diet in mice and humans leads to insulin resistance via similar mechanisms 67. Chronic insulin resistance comprises not only impaired muscle insulin action but also increased rates of endogenous glucose production EGP and gluconeogenesis GNG in obese and T2DM patients 8 — Still, only a few studies have addressed the initial effects of high-fat loading using either intravenous or enteral administration of lipids.
These studies mainly focused on the role of skeletal muscle by assessing intramyocellular TG content 11substrate oxidation, glycogen synthesis 12or glucose disposal 13 — Studies using parenteral administration of unsaturated lipids 18 or high-calorie mixed meals yielded conflicting results with regard to hepatic energy metabolism.
One mixed-meal study found greater de novo lipogenesis without affecting hepatic glycogen metabolism 12while an intravenous lipid infusion study failed to detect any effect on hepatic insulin sensitivity Another study comparing subacute oral ingestion of fatty acids with different compositions found an increase in the glucose infusion rate only after polyunsaturated fatty acid ingestion To overcome possible limitations of the previous studies, such as the use of nonphysiological routes of lipid administration or mixed meals, which introduce protein and carbohydrates as confounders, we designed a translational study concept comprising a clinical trial involving healthy humans and a corresponding study involving nonobese nondiabetic mice.
The randomized crossover clinical trial examined the effects of a single oral challenge with PO, which is mainly composed of saturated fatty acids 2versus vehicle VCL ingestion on whole-body insulin sensitivity WBIS and hepatic insulin sensitivity.
Moreover, the contributions of hepatic glucose fluxes, i. In the mouse study, we examined the effects of a similar oral saturated fat challenge on insulin sensitivity and hepatic transcriptome changes. Studies in humans. A total of 14 young, lean, insulin-sensitive male volunteers Figure 1 and Table 1 received either an oral dose of PO ~1.
CONSORT flow diagram. Forty-four patients underwent screening, which included a medical history, BMI analyses, and bioimpedance and an oral glucose tolerance tests. Of the 44 participants, 19 did not meet the inclusion criteria, 2 declined to participate, and 2 were excluded for other reasons.
Twenty-one participants were allocated to receive the intervention, two of whom did not receive the allocated intervention. PO results in increased circulating TG, glucagon, and incretins.
Of note, FFA were increased at, and minutes. Blood glucose levels were not different between PO- and VCL-treated groups Figure 2E.
Time courses of circulating metabolites and hormones in humans. VCL gray triangles or PO black circles was administered at 0 minutes to lean, healthy men, and the hyperinsulinemic-euglycemic clamp was started at minutes.
TG circulating in plasma solid line and in chylomicrons dashed line. Circulating FFA B. Values represent the mean ± SEM. Large asterisks refer to AUC differences; small asterisks refer to differences per time point. PO induces insulin resistance at whole-body, liver, and adipose tissue levels. Insulin sensitivity was measured using hyperinsulinemic-euglycemic clamp tests in healthy humans.
Steady state was reached Supplemental Figure 1and pertinent parameters were analyzed during this time. Parameters of insulin resistance in human volunteers after VCL or PO during clamp experiments.
VCL, white bars; PO, black bars. A WBIS, reflected by the M value. B Rd and its components GOX and nonoxidative glucose disposal NOXGD. C EGP denoting hepatic insulin sensitivity at baseline — minafter PO or VCL ingestion minand under insulin-stimulated conditions during the clamp min.
D Insulin-induced EGP suppression as an indicator of hepatic insulin sensitivity. E Insulin-induced FFA suppression reflecting adipose tissue insulin sensitivity and F the percentage of insulin-induced TG suppression.
Data shown represent the mean ± SEM. P values were determined by 2-tailed t test and ANOVA. PO augments the contribution of GNG to EGP. In order to further analyze the PO-induced increase in EGP, we measured the contributions of gluconeogenic and glycogenolytic fluxes.
The contribution of glycogen cycling to total GP flux was negligible in both study arms Figure 4. Hepatic glucose fluxes in humans. Data represent the mean ± SEM. PO increases lipid oxidation rates. Resting energy expenditure REE and lipid oxidation LOX rates increased markedly at minutes after PO ingestion and remained elevated into the clamp at min after PO Figure 5, B and C.
GOX decreased during the clamp following PO ingestion compared with GOX after VCL ingestion Figure 5D. Time course of parameters of energy metabolism in lean, healthy volunteers after VCL and PO.
Parameters were obtained by performing an indirect calorimetry. The time points indicated are basal —5 minminutes after intervention, and minutes under insulin-stimulated conditions.
PO raises hepatic ATP and lipid content. Hepatocellular lipids and hepatic phosphorus-containing metabolites. Studies in mice.
: Fat intake and metabolism| Dietary fat intake and metabolic syndrome in adults: A systematic review | The dosage is another important factor. This study also found altered regulation of other putative cytoprotective mechanisms including the phospholipase C4 pathway, which is important for hepatic regeneration 54 , and PPARα, which serves as both a canonical pathway and an upstream regulator protecting against NAFLD progression Monounsaturated fats are called such because there is one slot along the carbon backbone or chain that can accommodate a hydrogen molecule. FIGURE 6. Coil loading was corrected via integration of the right-most peak of a 13 C-enriched sample of formic acid placed within the coil housing. Association of cholesterol with risk of pancreatic cancer: a meta-analysis. Saturated fat. |
| The effect of fat composition of the diet on energy metabolism | Harcombe Z. Therefore, the oral mefabolism of linoleic acid should not be restricted and metaboliam is Intxke to consume more n-3 Techniques for appetite management. Cite this article Leong, I. Schwartz K, Chang HT, Nikolai M, Pernicone J, Rhee S, Olson K, et al. Therefore, it was criticized as showing very small beneficial effects on body weight. Holme I. Angrisani L, Santonicola A, Iovino P, Formisano G, Buchwald H, Scopinaro N. |
| Fat Grams: How Much Fat Should You Eat Per Day? | However, in contrast with the present study, the diets used were not isocaloric, making it impossible to differentiate the effects of dietary caloric density from the effects of fat per se on energy intake. It is important to make this distinction because EBM argues that excess calories from all sources including fats and sugars are obesogenic 9 , Second, our expectation was that, because of their greater saturated fat content, consuming lard-based diets would be metabolically more detrimental than soy oil-based diets, especially when coupled with HFCS. However, we found that replacing soy oil with lard did not affect the metabolic phenotype of the mice. Others have also observed in rodents that the type of fat in the diet did not alter body weight and composition 39 , This indicates that total fat content is more important than the proportion of saturated fat for inducing detectable metabolic changes. The main limitations of this study include: a only simple sugars were used, and they were not compared with complex carbohydrates with low glycaemic index, b post prandial glycaemic and insulinemic response to experimental diets and the effects of insulin on glucose clearance, fat metabolism and appetite were not studied, c impact of diets on hypothalamic appetite and hedonic signalling was not examined, d diets with very high-fat content or high energy densities were not used, e cellulose content was adjusted to keep the diets isocaloric, f fructose and glucose were given only as solid diets, and not as liquid solutions, g metabolic effects of fat and sugars were not tested in pair feeding experiments, h single strain and single-sex of the mice was used, i mouse experiments were not repeated in thermoneutral conditions. The aim of this study was to interrogate the consequences of fat-sugar interaction. Thus, we used the monosaccharides found in major caloric sugars i. We have already compared the metabolic effects of simple sugars with glucose polymers starch and resistant starch in our previous work Although postprandial glucose and insulin levels were not specifically examined in response to experimental diets, data shown for glucose and insulin levels from fasting state and from oral glucose tolerance tests Fig. S3b, c is a good indicator of glucose metabolism. Further, hypothalamic appetite signalling and hedonic stimuli in response to experimental diets are most likely to reflect energy intake data Fig. Using large amounts of fat would have also meant using substantial amounts of cellulose to keep the diet isocaloric. This would have made dietary cellulose content a potentially important confounder when interpreting our data. There is evidence that fructose-containing sugars are more obesogenic when consumed via beverages Therefore, not testing metabolic outcomes when fructose is ingested in liquid form makes our findings less relevant to the role of sugary beverages in human obesity 17 , However, a direct experimental comparison of the metabolic effects of consuming fats and sugars in liquid form requires making mice drink large amounts of oil solutions which is challenging, and we were able to identify the ratio of fructose and glucose , which is obesogenic in the solid form. While pair feeding could provide additional information in separating the impact of nutrients from their caloric value, such studies often lead to extended periods of fasting in the pair-fed group as these mice tend to consume their food soon after it is made available Importantly, with the NG methodology, we can evaluate the impact of nutrients on metabolic phenotype at fixed levels of energy intakes e. However, not repeating our experiments in females, other strains of mice and under thermoneutral conditions is an important limitation of this work. Future research should examine if the metabolic effects observed in this study are dependent on the strain and sex of the mice as well as their housing temperatures. In conclusion, this study showed that in diets with a low-to-medium fat content, HFCS consumption led to greater food and energy intakes, body weights and adiposity when compared with consumption of glucose or fructose alone. However, with increasing fat intake, sugar-specific differences in metabolic effects became less pronounced, and there was a more generalised increase in body weight and adiposity, and greater impairment of glucose tolerance and insulin sensitivity. Using NG to disentangle the relative roles of fat and sugar intake in human data will further reconcile the differences between CIM and EBM as models of obesity. This study was approved by the institutional ethics committee at the University of Sydney. A detailed explanation of how to interpret nutritional geometry surfaces shown in the figures is available in supplementary materials. Male mice were chosen as they are more prone to diet-induced metabolic abnormalities than females Mice were acclimatised in the animal facility for 4 weeks while being fed regular brown chow. The ad libitum dietary intervention commenced when the mice became 8 weeks old. In vivo metabolic procedures, food intake, body weight measurements and animal tissue collections were performed as previously described Further details about the study design and animal numbers per diet are available in the Supplementary information. All 18 experimental diets were isocaloric with a net metabolisable energy of ~ Protein was sourced from casein and carbohydrate comprised of a mixture of the sources shown in Supplementary Data 1. The diets were kept isocaloric by altering their cellulose content. All 18 diets were manufactured by Specialty Feeds TM Glen Forrest, Western Australia with the following catalogue numbers: SF, SF, SF, SF, SF, SF, SF, SF, SF, SF, SF, SF, SF, SF, SF, SF, SF and SF MRI scanning of mice EchoMRI TM was used to determine the body composition fat and lean mass of mice. Conscious mice were analysed after weeks 5—6 and 12—14 on diets. Physical activity was measured by cumulative y-axis beam break counts. Data were analysed by using the CalR online tool Total AUC was calculated from blood glucose readings Higher AUC indicates worse glucose tolerance. An insulin tolerance test was performed at weeks 15—16 of dietary treatment. Mice were intraperitoneally injected with 0. Individual AUC was calculated from blood glucose readings. Higher AUC indicates lower insulin sensitivity. Blood samples were collected during GTTs, and insulin levels were quantified with the Ultrasensitive Insulin ELISA kit Crystal Chem. Plasma FGF21 was quantified with the mouse FGF21 ELISA kit Bio Vendor for blood samples collected at the end of dietary interventions. After harvesting, livers were fixed in formalin and embedded in paraffin. Triglyceride levels in plasma samples were analysed by a clinical chemistry analyser at the Charles Perkins Centre, University of Sydney. cDNA was then synthesised using the iScript Reverse Transcriptase enzyme and random hexamer primers Bio-Rad. cDNA was loaded in a well plate format with SYBR Green Bio-Rad fluorescent chemistry in a total 10 microlitres reaction volume with specific forward and reverse primers. Ribosomal protein gene Rpl13a was chosen as the housekeeping gene 47 after testing a fraction of samples for gene expression of actin, Rpl13a and cyclophilin. Ct values of housekeeping and candidate genes were determined, and their expression was calculated by the DDCt method. Primer sequences for Rpl13a 47 , Apob 48 , Khk isoform C 49 , Gpat3 50 , Acly 16 , Fasn 16 , Scd1 16 and Mcp1 51 were from previous publications. Liver triglyceride level was quantified as reported in previous studies 16 , A colourimetric assay was then used to quantify the triglyceride concentration with glycerol standards Precimat glycerol, Roche and the Triglyceride-GPO-PAP reagent Roche. Details of data analysis by the NG platform and its interpretation with general additive models GAMs were described previously 16 , 19 , For the NG-based analysis, GAMs with thin-plate splines were used to model the responses of mice over the nutrient-intake space in R version 4. Statistical outcomes retrieved from GAMs are provided in Supplementary Data. Scatter plots such as energy intake analysis were analysed by GAMs as well, fitting an interaction between a smooth term for dietary sugar content in one carbohydrate dimension and fat contents as three-level categorical factors and shown as scatterplots the dotted lines on scatterplots represent the standard error for the fitted values. All GAMs underwent model validation with analysis of the residuals. Data were log-transformed if needed. For histological studies, sections were given scores ranging from 0 to 3, and the scores were modelled with an ordinal regression proportional odds in R. For soy oil versus lard studies, data were analysed with ANOVA in GraphPad Prism software. Further information on research design is available in the Nature Portfolio Reporting Summary linked to this article. All data supporting the findings described in this article are available in the article and in the Supplementary Information and from the corresponding authors upon reasonable request. 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The role of low-fat diets in body weight control: a meta-analysis of ad libitum dietary intervention studies. Bueno, N. Very-low-carbohydrate ketogenic diet v. low-fat diet for long-term weight loss: a meta-analysis of randomised controlled trials. Effect of a plant-based, low-fat diet versus an animal-based, ketogenic diet on ad libitum energy intake. Olsen, N. Intake of calorically sweetened beverages and obesity. Hu, S. Dietary fat, but not protein or carbohydrate, regulates energy intake and causes adiposity in mice. Wang, X. Differential effects of high-fat-diet rich in lard oil or soybean oil on osteopontin expression and inflammation of adipose tissue in diet-induced obese rats. Lopez-Dominguez, J. The influence of dietary fat source on life span in calorie restricted mice. A Biol. Sundborn, G. Are liquid sugars different from solid sugar in their ability to cause metabolic syndrome? Our studies have identified a novel connection between enzymes involved in monounsaturated and polyunsaturated fatty acid synthesis and the control of hepatic glucose production and liver fat content. While these studies clarify molecular interactions between different metabolic pathways, they may also identify possible novel approaches to control certain diabetic complications. Other research in my laboratory has assessed the capacity of dietary omega-3 fatty acid supplementation to control high-fat, diet-induced, non-alcoholic fatty liver disease NAFLD. The incidence of NAFLD closely parallels the incidence of obesity in the U. NAFLD is a spectrum of diseases that span simple fatty liver benign steatosis to non-alcoholic steatohepatitis NASH. NASH is characterized as fatty liver with inflammation, fibrosis, oxidative stress, and hepatic damage. If left unchecked, NASH can progress to cirrhosis and liver cancer. Our recent studies have established that dietary omega-3 fatty acids found in fish oil eicosapentaenoic acid and docosahexaenoic acid can be used at clinically relevant levels of intake to attenuate multiple markers of NASH hepatosteatosis, inflammation, and fibrosis in a mouse model of high-fat, diet-induced NASH. Future studies will determine whether specific omega-3 fatty acids, either alone or in combination with other treatments, can be used in therapy to reduce hepatic damage associated with obesity-linked NASH. Donate Today! Lundsgaard, A. et al. Mechanisms preserving insulin action during high dietary fat intake. Cell Metab. Article PubMed Google Scholar. Download references. You can also search for this author in PubMed Google Scholar. Correspondence to Ivone Leong. Reprints and permissions. Leong, I. Metabolic adaptations to high-fat diet. Nat Rev Endocrinol 14 , Download citation. 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Fat intake and metabolism -
Characteristics of diet therapy should be simple, understandable, and long lasting for many subjects. For this purpose, physicians must keep studying nutritional science, and should be practicing healthy diet life by themselves.
Consuming healthy food by themselves will help to more confidently and comfortably recommend appropriate diet therapy to their patients.
In contrast to evidence levels in pharmacological therapy, there have been few trustworthy RCTs in nutrition, which thus has created substantial inconsistent understanding of diet therapy at present.
In the future, it is by far the most important task for related parties to be united to build up a foundation of high quality data of nutritional science. Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 3.
Edited by Akikazu Takada. Open access peer-reviewed chapter Effects and Issues of Diet Fat on Cardiovascular Metabolism Written By Yasuhiro Nishikawa.
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Impact of this chapter. Abstract Diet is a foundation of treatment for lifestyle-related diseases, such as high blood pressure, diabetes, and dyslipidemia.
Keywords saturated fat unsaturated fat complex and refined carbohydrate Mediterranean diet olive oil n-3 fish oil primary and secondary prevention LDL cholesterol antioxidant diet guidelines. Introduction Diet therapy has been disregarded in management of hyperlipidemia.
Table 1. b No restriction of fat intake, which is dependent upon individual preferences. c No restriction of fat intake, inconclusive for an ideal amount of total fat intake for people with diabetes; therefore, goals should be individualized.
d Not stated on intake of mono- and polyunsaturated fat. f Recommend intake of fish. g Recommend intake of fish.
h Recommend intake of fish. i No upper limit defined. However, should decrease as much as possible. j No upper limit. Complex Simple or refined Structure Polysaccharides Mono, disaccharides Taste No taste Sweet Digestion Slow Easy Blood sugar Slowly increases Rapidly increases Insulin response Low High Glycemic index Low High Satiety Longer Shorter Fiber High Low Body weight Loss Gain.
Table 2. Differences in two types of carbohydrate: complex vs. simple refined. Fat SFA MUFA PUFA n-3 PUFA n-6 Rapeseed oil g g 7. Table 3. Amounts of different fatty acids contained in several cooking oils, butter and foods.
Table 4. Control Intervention P To maintain desirable BW Step 1 Step 2 Energy, cal 0. Table 5. References 1. Collaborators TUBoD. The state of US health, — Burden of diseases, injuries, and risk factors among US States.
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Percent body fat was estimated using a single bioelectrical impedance analysis BIA, RJL Systems following a previously described validated protocol Lukaski et al. Abdominal adiposity was measured using the waist-to-height ratio WHtR. Waist circumference was measured at the level of the umbilicus during mid-respiration to the nearest 0.
Waist circumference was divided by averaged height to calculate WHtR with missing values at exam 6 being substituted using the mean values from exams 5 and 7. IL-6 and fibrinogen were measured with commercially available enzyme-linked immunoassay kits. We explored several potential confounding factors in the multivariable models.
Education level and physical activity were self-reported. Information on education was assessed at exam 2 and classified as high school or above vs. less than high school. Physical activity as assessed by a questionnaire at examination visit 5 Kannel and Sorlie, was used to calculate a baseline physical activity index by multiplying daily hours of moderate and vigorous activity by an appropriate weight based on oxygen consumption required for that level of exercise Kannel et al.
Cigarette smoking status and amount smoked were assessed at every exam by interview, and total pack-years of cigarette smoking were updated at each exam; we used updated data from the baseline exam visit exam 5 in these analyses. Age at menopause was assessed by interview at each exam exams until the occurrence of menopause.
The following dietary factors during exams were also explored as potential confounding variables: a energy-adjusted and weight-adjusted intakes of monounsaturated fat for total, omega-3, and omega-6 PUFA models , polyunsaturated fat for SFA and MUFA models , protein, and dietary fiber; b servings per day of foods such as fruits, vegetables, and dairy products, c energy intake kilocalories per day ; and d Healthy Eating Index HEI scores Krebs-Smith et al.
Given the strong interplay between fatty acid and carbohydrate metabolism, we also explored effect modification and confounding by energy-adjusted and body weight-adjusted carbohydrate intakes. Finally, we explored co-morbidities as of the baseline visit at exam 5 for these analyses, including prevalence of hypertension and diabetes status, as determined at each examination visit, as well as baseline lipid-lowering and antihypertensive medications use.
There were strong correlations between energy-adjusted vs. body weight-adjusted intakes among those with plausible intakes but weaker correlations among those with implausible energy intakes. Thus, we chose to adjust dietary fat intake for body weight rather than energy intake to minimize the impact of biased reporting of energy intake.
Non-normally distributed variables were log-transformed, including TG, IL-6, fibrinogen, and VLDL particle concentrations. Confounding was assessed by adding each factor one at a time to the age- and sex-adjusted models, then building the model forward by adding each individual confounder singly to the model and avoiding collinearity.
Sex-specific final models included age, weight-adjusted carbohydrate intakes, HEI scores, use of lipid-lowering medications, pack-years of cigarette smoking, baseline BMI, and prevalent diabetes. None of the other potential confounders altered the effect estimates and were thus dropped from the final models.
Statistical Analysis Systems software, version 9·4 SAS Institute, Cary, NC , was used to perform all analyses. Sex-specific characteristics according to categories of saturated fat intake are shown in Table 1.
Women and men with higher vs. lower saturated fat intakes were somewhat younger and had lower BMI and HEI scores at baseline. They also had higher intakes of dairy, nuts and seeds, but not higher intakes of fruits and vegetables, poultry, or fish.
Red meat intake was positively associated with saturated fat intake in both women and men. Further, women but not men in the highest intake category for saturated fat were slightly more likely to have a higher education level.
Men with higher saturated fat intakes were also much more likely to be current smokers TABLE 1. Sex-specific characteristics of participants according to weight-adjusted intakes of saturated fats.
Sex-specific baseline characteristics associated with categories of monounsaturated fat intake are shown in Supplementary Table S1. Results for both women and men are very similar to those for saturated fat intakes. Supplementary Table S2 shows the participant characteristics associated with intakes of total polyunsaturated fat.
Women, in particular, with higher intakes of polyunsaturated fat, had higher education levels. Both women and men with higher intakes of polyunsaturated fat had slightly higher mean diet quality scores on the HEI, higher intakes of fruits and vegetables, and higher intakes of all protein food sources.
Further, women and men with higher polyunsaturated fat consumption were substantially less likely to be current smokers i. Sex-specific adjusted mean levels of plasma lipids associated with intake categories of saturated and monounsaturated fats are shown in Figure 3 , and those for polyunsaturated fats including omega-3 and omega-6 PUFAs in Figure 4.
The final models were adjusted for age, weight-adjusted carbohydrate intakes, HEI scores, use of lipid-lowering medications, pack years of cigarette smoking, baseline BMI, and prevalent diabetes.
Higher intakes of saturated and monounsaturated fats were associated with higher adjusted mean levels of HDL-C, lower mean levels of TGs, and a lower TG:HDL ratio in both women and men.
Sex-specific differences were noted for the associations of polyunsaturated fats with lipid levels. In women, higher intakes of both omega-3s and omega-6s PUFAs were associated with lower TG:HDL ratio due mainly to higher HDL levels, while in men, only omega-3s led to a lower TG:HDL ratio.
There was no indication that dietary fat of any type was associated with higher mean LDL-C levels. FIGURE 3. Associations of saturated and monounsaturated fat intakes with blood levels of HDL-C A , fasting LDL-C B , log-transformed fasting TGs C , and TG:HDL ratio D in women and men.
All models were adjusted for age, weight-adjusted carbohydrate intakes, HEI scores, use of lipid-lowering medications, pack years of cigarette smoking, baseline BMI, and prevalent diabetes.
FIGURE 4. Associations of total, omega-3 and omega-6 polyunsaturated fat intakes on blood levels of HDL-C A , fasting LDL-C B , log-transformed fasting TGs C , and TG:HDL ratio D in women and men.
In addition to lipid levels, we also show cross-sectional sex-specific associations between dietary fats and adjusted mean lipoprotein particle sizes Figure 5 and concentrations Figure 6.
Overall, higher intakes of all types of dietary fat tended to be positively associated with HDL particle size in both women and men. However, higher intakes of saturated and monounsaturated fats were associated with beneficial higher mean LDL particle sizes in men only.
Regarding lipoprotein concentrations, higher intakes of saturated and monounsaturated fat intakes were favorably associated with all lipoprotein concentrations HDL, LDL, and VLDL in both women and men.
Women with higher intakes of polyunsaturated fats also had higher mean HDL and lower mean LDL and VLDL particle concentrations, while men had no different concentration levels between the intake categories of polyunsaturated fats. FIGURE 5.
Cross-sectional associations of dietary fat intakes on lipid particle sizes of HDL A , LDL B and VLDL C in women and men.
FIGURE 6. Cross-sectional associations of dietary fat intakes on lipid particle concentrations of HDL A , LDL B and VLDL C in women and men.
After adjusting for confounding by age, carbohydrate intakes, HEI scores, use of lipid-lowering medications, pack-years of cigarette smoking, and prevalent diabetes, these results show that higher vs.
lower intakes of any type of fat were associated with lower BMI levels, a lower percent body fat, and a smaller waist-to-height ratio in women. Only saturated fat was inversely associated with all three measures of adiposity in men. Finally, monounsaturated fats and omega-6 PUFAs were inversely associated with BMI among men Table 2.
TABLE 2. Sex-specific mean levels of adiposity associated with weight-adjusted intakes of dietary fats. There were no associations between saturated or monounsaturated fats and inflammatory biomarkers or fasting glucose among women.
However, among men, there was an inverse association between saturated fat consumption and log-transformed fibrinogen levels; among women, omega-3 PUFAs were inversely associated with IL There were no associations between any dietary fats and fasting glucose levels Table 3.
TABLE 3. Sex-specific mean levels of inflammatory biomarkers and fasting glucose levels associated with weight-adjusted intakes of dietary fats. In this US community-based cohort of mainly Caucasian women and men, we found no evidence to support an adverse relationship between any type of dietary fat and several cardiometabolic risk factors, including lipids, adiposity, inflammation, and glucose.
We found that saturated and monounsaturated fat intakes tended to be favorably associated with TG:HDL ratio in both women and men. However, sex-specific differences were noted for the associations of polyunsaturated fat intake on lipid levels. Women who consumed more omega-3 and omega-6 PUFAs had a lower mean TG:HDL ratio, while among men, only omega-3 PUFAs were inversely associated.
In addition to these associations with serum lipid levels, we also found that all types of dietary fat were associated with larger protective HDL particle sizes in both men and women. Women with higher intakes of all fat types also had higher concentrations of HDL particles, while for men, this was the case only in association with saturated and monounsaturated fats.
In general, dietary fats tended to be associated with lower LDL and VLDL particle concentrations. Once again, this was the case for all types of dietary fats among women, while in men, these findings were evident only in associations with saturated and monounsaturated fats.
We also noted that a higher intake of saturated fat was associated with less adiposity in both women and men. In addition, higher saturated fat intakes were associated with lower abdominal adiposity in both sexes, while unsaturated fat was only associated with less adiposity in women.
Lastly, there were a few differences in the associations between dietary fats and inflammatory markers between women and men. In women, there was some evidence of a beneficial association between polyunsaturated fat and IL-6 levels, whereas saturated fat was inversely associated with fibrinogen levels in men.
Our results contradict the long-held belief that high saturated fat is associated with an atherogenic lipid profile. The rationale for this was based on selected trials Hooper et al. The LIPGENE study, which is the largest diet intervention study among weight-stable individuals with metabolic syndrome from 18 European countries, also failed to show adverse associations with several lipid and apolipoprotein concentrations after reducing saturated fat intakes.
Authors suggested that the absence of a reduction in LDL was due to individuals with higher BMI exhibiting smaller than expected reductions in LDL-C in response to reductions in dietary saturated fat intakes Tierney et al. However, a subsequent randomized control trial of overweight and obese individuals without diabetes in the absence of weight loss showed that a high versus low saturated fat diet mainly from dairy sources had no differences in LDL, HDL, or TGs levels after adjustment for BMI Chiu et al.
Consistent with our results, the LIPGENE study also showed that high saturated or monounsaturated fat diets were associated with a lower atherogenic index Tierney et al.
In the present study, sex was an important determinant for the associations between polyunsaturated fats and lipid profiles. In women, omega-3 and omega-6 PUFAs were associated with higher mean levels of HDL and lower mean levels of TG:HDL ratio, while in men, omega-3s only led to a lower TG:HDL ratio because of concurrent higher HDL and lower TGs means.
Overall, information on the sex-specific differences in the associations of various types of fats on lipids is limited. Consistent with our results, in the LIPGENE study, omega-3 PUFA supplementation led to reduced TGs in men only.
Potential mechanisms could be the longer residence time of VLDL TGs in men enabling greater clearance by omega-3 PUFAs and greater metabolic utilization of long-chain omega-3s in men Tierney et al. Further, it is known that men tend to have higher concentrations of small dense LDL particles, higher LDL levels, and TG levels, all features of an atherogenic lipoprotein phenotype compared with that observed in premenopausal women Swiger et al.
A clinical trial showed that after excluding individuals with atherogenic lipoprotein profiles, increasing the dietary intake of omega-3s from foods led to a smaller proportion of small dense LDL particles and lower concentrations of TGs, particularly in men, after adjusting for baseline values.
The proportion of HDL 2 was also increased after increasing omega-3s in both women and men Griffin et al. Dietary fats have been associated with consuming energy-dense foods and, as a result, are hypothesized to increase body fat.
However, this hypothesis fails to consider the importance of mechanisms involved in fuel partitioning Manco et al. Our study differs from those of earlier studies. For example, a previous review suggested that the anti-obesity effects of omega-3s PUFAs were limited to men Buckley and Howe, However, in these current analyses, the associations between omega-3 PUFAs and body fat were stronger among women than among men.
Finally, our findings on the associations of unsaturated fats on measures of body fat support previous evidence showing that monounsaturated and polyunsaturated fat-enriched diets or meals may increase fat oxidation and energy expenditure while suppressing appetite and visceral fat deposition and beneficially modulate gut microbiota Buckley and Howe, ; Gillingham et al.
Lastly, in the LIPGENE study, leptin, a major appetite hormone, was not affected by diets high in any type of fat Tierney et al. In the current study, saturated and monounsaturated fats were inversely associated with fibrinogen levels in men, while omega-3 and omega-6s were inversely associated with IL-6 in women.
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CAS PubMed PubMed Central Google Scholar. Download references. was supported by a Peter Doherty Biomedical Research Fellowship from the National Health and Medical Research Council of Australia GNT This work was supported by a programme grant from the National Health and Medical Research Council GNT awarded to S.
and D. and their colleagues J. George, J. Gunton and H. Durrant-Whyte and a project grant from Diabetes Australia Y17G-WALJ awarded to J.
We thank P. Teixeira for administrative support; the Laboratory Animal Services at the University of Sydney for animal care and support; and W.
Potts from the Specialty Feeds company. Charles Perkins Centre, The University of Sydney, Sydney, NSW, Australia. Jibran A. Wali, Duan Ni, Harrison J. Facey, Tim Dodgson, Tamara J. Pulpitel, Alistair M. Faculty of Science, School of Life and Environmental Sciences, The University of Sydney, Sydney, NSW, Australia.
Wali, Tim Dodgson, Tamara J. School of Medical Sciences, Chronic Diseases Theme, Faculty of Medicine and Health, The University of Sydney, Sydney, NSW, Australia. Sydney Precision Data Science Centre, The University of Sydney, Sydney, NSW, Australia. Sydney Cytometry, The University of Sydney, Sydney, NSW, Australia.
You can also search for this author in PubMed Google Scholar. and J. conceived the study. and S. wrote the paper. reviewed the paper and provided intellectual input. and T. conducted mouse studies. and A. were involved in data analysis.
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Subjects Dietary carbohydrates Fat metabolism Fats Metabolic syndrome Obesity. Introduction The metabolic effects of dietary fats and sugars have been an area of great interest in obesity research 1 , 2 , 4. Results Study design Mice were fed ad libitum on one of 18 isocaloric ~ Full size image.
Discussion In this study, we used nutritional geometry to investigate how the dietary fat-sugar interaction influences metabolic status and if the consequences of this interaction are dependent on the type of sugar fructose vs glucose vs their mixtures and fat soy oil vs lard consumed.
Methods This study was approved by the institutional ethics committee at the University of Sydney. Interpretation of nutritional geometry surfaces A detailed explanation of how to interpret nutritional geometry surfaces shown in the figures is available in supplementary materials.
Body composition MRI scanning of mice EchoMRI TM was used to determine the body composition fat and lean mass of mice.
Insulin tolerance test An insulin tolerance test was performed at weeks 15—16 of dietary treatment. Insulin and FGF21 ELISA Blood samples were collected during GTTs, and insulin levels were quantified with the Ultrasensitive Insulin ELISA kit Crystal Chem.
Liver histology After harvesting, livers were fixed in formalin and embedded in paraffin. Plasma biochemistry Triglyceride levels in plasma samples were analysed by a clinical chemistry analyser at the Charles Perkins Centre, University of Sydney.
Liver triglyceride assay Liver triglyceride level was quantified as reported in previous studies 16 , Statistical analysis Details of data analysis by the NG platform and its interpretation with general additive models GAMs were described previously 16 , 19 , Reporting summary Further information on research design is available in the Nature Portfolio Reporting Summary linked to this article.
Data availability All data supporting the findings described in this article are available in the article and in the Supplementary Information and from the corresponding authors upon reasonable request.
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Background and aims: The metabolic syndrome MetS is Fat intake and metabolism cluster of imtake cardiovascular risk metablism. The role of specific dietary fats was reemphasized by dietary recommendations. Metaboilsm systematic review aims to Fxt evidence for Fat intake and metabolism Orange Salad Recipes of dietary fat intake metagolism MetS Whole food energy stimulant and reversion in adults. Methods and results: The MEDLINE database was used to search the existing literature. Thirty articles were selected 14 observational and 16 clinical trialsand we included information of dietary fat and fatty acids as well as MetS, body mass index, cholesterol, hypertension, and diabetes in adults. SFA intake was found to be positively associated with MetS components. Most of the observational reviewed studies found beneficial associations between MUFA and PUFA including n-3 and n-6 subtypes intake and MetS components.
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