Dietary Black Raspberry Seed Oil Ameliorates Inflammatory Activities in db/db Mice

The objective of this study was to evaluate the status of the markers related to inflammation in db/db mice fed black raspberry seed (BRS) oil, which is rich in α‐linolenic acid. Mice were divided into four groups: (1) C57BL/6 mice fed 16 % calories from soybean oil (normal CON); (2) C57BL/KsJ‐db/db mice fed 16 % calories from soybean oil (CON); (3) C57BL/KsJ‐db/db mice fed 8 % calories from soybean and 8 % calories from BRS oil (BRS 50 %); and (4) C57BL/KsJ‐db/db mice fed 16 % calories from BRS oil (BRS 100 %). After 10 weeks, n‐6/n‐3 fatty acid ratios were significantly (P < 0.05) lower in the livers and epididymal adipose tissues of the BRS 50 % and BRS 100 % mice than in the CON. Serum TNFα and IL‐6 were significantly (P < 0.05) lower in the BRS 50 % and BRS 100 % than in the CON. Serum IL‐10 was significantly (P < 0.05) higher in the BRS 100 % than the CON. In the liver and epididymal adipose tissue, mRNA levels of pro‐inflammatory markers in the BRS 50 % and BRS 100 % were lower than in the CON. Anti‐inflammatory markers were higher in the epididymal adipose tissues of the BRS 50 % and BRS 100 % than in the CON. In the epididymal adipose tissue, macrophage infiltration markers (F4/80 and CD68) and leptin mRNA were significantly (P < 0.05) lower in the BRS 50 % and BRS 100 % than in the CON. Results of this study suggest that BRS oil may have anti‐inflammatory effects in obese diabetic mice by ameliorating inflammatory responses.     

High-Fat Diet Alters Serum Fatty Acid Profiles in Obesity Prone Rats: Implications for In Vitro Studies

High‐fat diets (HFD) are commonly used in rodents to induce obesity, increase serum fatty acids and induce lipotoxicity in various organs. Invitro studies commonly utilize individual free fatty acids (FFA) to study lipid exposure in an effort to model what is occurring in vivo; however, these approaches are not physiological as tissues are exposed to multiple fatty acids in vivo. Here we characterize circulating lipids in obesity‐prone rats fed an HFD in both fasted and fed states with the goal of developing physiologically relevant fatty acid mixtures for subsequent in vitro studies. Rats were fed an HFD (60 % kcal fat) or a control diet (10 % kcal fat) for 3 weeks; liver tissue and both portal and systemic blood were collected. Fatty acid profiles and absolute concentrations of triglycerides (TAG) and FFA in the serum and TAG, diacylglycerol (DAG) and phospholipids in the liver were measured. Surprisingly, both systemic and portal serum TAG were ~40 % lower in HFD‐fed compared to controls. Overall, compared to the control diet, HFD feeding consistently induced an increase in the proportion of circulating polyunsaturated fatty acids (PUFA) with a concomitant decline in monounsaturated fatty acids (MUFA) and saturated fatty acids (SFA) in both serum TAG and FFA. The elevations of PUFA were mostly attributed to increases in n‐6 PUFA, linoleic acid and arachidonic acid. In conclusion, fatty acid mixtures enriched with linoleic and arachidonic acid in addition to SFA and MUFA should be utilized for in vitro studies attempting to model lipid exposures that occur during in vivo HFD conditions.     

Omega-3 PUFA of marine origin limit diet-induced obesity in mice by reducing cellularity of adipose tissue

Omega-3 PUFA of marine origin reduce adiposity in animals fed a high-fat diet. Our aim was to learn whether EPA and DHA could limit development of obesity and reduce cellularity of adipose tissue and whether other dietary FA could influence the effect of EPA/DHA. Weight gain induced by composite high-fat diet in C57BL/6J mice was limited when the content of EPA/DHA was increased from 1 to 12% (wt/wt) of dietary lipids. Accumulation of adipose tissue was reduced, especially of the epididymal fat. Low ratio of EPA to DHA promoted the effect. A higher dose of EPA/DHA was required to reduce adiposity when admixed to diets that did not promote obesity, the semisynthetic high-fat diets rich in EFA, either α-linolenic acid (ALA, 18∶3 n−3, the precursor of EPA and DHA) or linoleic (18∶2 n−6) acid. Quantification of adipose tissue DNA revealed that except for the diet rich in ALA the reduction of epididymal fat was associated with 34–50% depression of tissue cellularity, similar to the 30% caloric restriction in the case of the high-fat composite diet. Changes in plasma markers and adipose gene expression indicated improvement of lipid and glucose metabolism due to EPA/DHA even in the context of the diet rich in ALA. Our results document augmentation of the antiadipogenic effect of EPA/DHA during development of obesity and suggest that EPA/DHA could reduce accumulation of body fat by limiting both hypertrophy and hyperplasia of fat cells. Increased dietary intake of EPA/DHA may be beneficial regardless of the ALA intake.     

Effects of the ratio of polyunsaturated and monounsaturated fatty acid to saturated fatty acid on rat plasma and liver lipid concentrations

The effects of dietary monounsaturated fatty acid (MUFA) and polyunsaturated fatty acid+MUFA/saturated fatty acid (PUFA+MUFA/SFA) ratio on plasma and liver lipid concentrations were studied. In experiment I, when rats were fed with 40% fat (energy%, PUFA/SFA ratio 1.0) and 1% (w/w) cholesterol (C) diets for 21 d, a large amount of MUFA (28.1 energy%, PUFA+MUFA/SFA=5.7) in the diet was found to increase the plasma total C, triacylglycerol (TAG), and phospholipid (PL) as compared with the low-MUFA diet (7.0 energy%, PUFA+MUFA/SFA=1.4). The plasma very low density lipoprotein (VLDL)-C, VLDL-TAG, VLDL-PL, and low density lipoprotein (LDL)-C increased significantly in the high-MUFA diet group, but high density lipoprotein (HDL)-C did not change significantly. The high-MUFA diet resulted in greater accumulation of liver C but lesser accumulation of TAG. In experiment II, when dietary SFA was fixed at a certain level (13.2 energy%; PUFA+MUFA/SFA=2.0), rats given a larger amount of MUFA (23.1 energy%; PUFA/MUFA=0.2; MUFA/SFA=1.8) showed higher plasma and liver C levels than did the low-MUFA diet (7.7 energy%; PUFA/MUFA=2.5; MUFA/SFA=0.6). When PUFA was fixed at a certain level (24.4 energy%), there was not a significant difference in the plasma C level between the high-and low-MUFA dietary groups (PUFA+MUFA/SFA=4.8 and 8.4), but the higher PUFA+MUFA/SFA diet, which was high in MUFA/SFA ratio, significantly decreased the plasma HDL-C and TAG levels. However, when MUFA content was fixed at a certain level (16.4 energy%), no significant difference was observed between the two groups with different PUFA/SFA ratios of 0.2 and 4.1, but liver C level was raised in the higher PUFA/SFA diet. It appears that the PUFA/SFA ratio alone is unsuitable to predict the change of plasma C level, because a large amount of dietary MUFA may lead to an increase of plasma and liver lipids in rats. It seems that the prerequisites for keeping low plasma and liver C are (i) low MUFA/SFA ratio, (ii) high PUFA/MUFA ratio, and (iii) PUFA+MUFA/SFA ratio not to exceed 2.     

Dietary Monounsaturated Fatty Acids but not Saturated Fatty Acids Preserve the Insulin Signaling Pathway via IRS-1/PI3K in Rat Skeletal Muscle

Saturated fatty acids (SFA) and monounsaturated fatty acids (MUFA) show different effects on the development of insulin resistance. In this study, we compared the effect of dietary SFA and MUFA on the insulin signaling pathway in the skeletal muscle of a type 2 diabetic animal model. Twenty-nine-week-old male Otsuka Long-Evans Tokushima fatty (OLETF) rats were randomly divided into three groups and fed one of the following diets for 3 weeks; a normal chow diet, an SFA (lard oil) enriched or a MUFA (olive oil) enriched high-fat diet. The vastus lateralis muscle was used for analyses. Insulin tolerance test showed improved insulin sensitivity in rats fed the MUFA diet, as compared to those fed the SFA diet (p < 0.001). The SFA diet reduced IRS-1 expression and phosphorylated PI3K levels in skeletal muscle, as compared with a chow diet (p < 0.001, respectively). On the contrary, muscle IRS-2 expression and phosphorylated ERK1/2 was significantly increased in rats fed the SFA diet (p < 0.001, respectively). Membrane translocation of glucose transporter type 4 decreased in the skeletal muscle of rats fed the SFA diet, as compared to those fed a chow diet (p < 0.001). These changes in insulin signaling pathway in skeletal muscle were not observed in rats fed the MUFA diet. In conclusion, the beneficial effect of dietary MUFA on insulin sensitivity is associated with a conserved IRS-1/PI3K insulin signaling pathway which was altered by dietary SFA.     

Effects of conjugated linolenic acid and conjugated linoleic acid on lipid metabolism in mice

The effects of two isomers of conjugated linolenic acid (CLnA), α‐eleostearic acid (α‐ESA) and punicic acid (PA), on body fat and lipid metabolism were investigated, compared with a conjugated linoleic acid (CLA) mixture (primarily cis9,trans11‐ and trans10,cis12‐18:2) and α‐linolenic acid (ALA), a non‐conjugated octadecatrienoic acid, in the present study. ICR mice were fed either a control diet or one of four experimental diets supplemented with 1% α‐ESA, 1% PA, 1% CLA mixture and 1% ALA in the form of triacylglycerols (TAG) for 6 weeks. The weights of perirenal and epididymal adipose tissues were significantly decreased while the liver weight was significantly increased in mice fed CLA, compared with the control. In contrast to CLA, the tissue weights in α—ESA‐, PA‐ and ALA‐fed mice were not affected. No significant differences were observed in TAG, total cholesterol, high‐density lipoprotein and low‐density lipoprotein cholesterol levels among the five groups. The liver TAG level was significantly decreased in mice fed α‐ESA and PA while it was significantly increased in mice fed the CLA mixture. These results indicate that CLnA and CLA have differential effects on body fat mass and liver TAG levels in mice.     

Molecular Mechanisms for the Modulation of Selected Inflammatory Markers by Dietary Rice Bran Oil in Rats Fed Partially Hydrogenated Vegetable Fat

Industrially produced partially hydrogenated vegetable fat (PHVF) contains trans fatty acids (TFA) mostly comprising elaidic acid (EA, 18:1?9t). Though, the harmful effects of TFA on health have been repeatedly publicized, the fat containing TFA have been continued to be used as a cooking medium in many regions of the world. The adverse effects of PHVF on oxidative stress and inflammatory markers and the possible ameliorative action of rice bran oil (RBO) on these markers were evaluated. Weaning rats were fed a AIN‐93 purified diet supplemented with the following lipids: groundnut oil (GNO, 10 wt%), PHVF (10 wt%), RBO (10 wt%), PHVF blended with RBO at 2.5, 5.0 and 7.5 wt% levels. The final concentration of the lipids in the diet was maintained at 10 wt%. Rats were fed these diets for 60 days. They were sacrificed and analyzed for oxidative stress and inflammatory markers. The rats fed PHVF showed lower levels of lipid peroxidation and hepatic antioxidant enzymes. The rats fed PHVF‐containing diets showed enhanced levels of interleukin‐1β, C‐reactive proteins and also showed enhanced levels of paw inflammation when injected with carrageenan as compared to rats given GNO, RBO or PHVF blended with incremental amounts of RBO. The macrophages from rats fed diet containing PHVF showed up‐regulation in the expressions of cytosolic phospholipase A₂ (cPLA₂), nuclear factor‐κB p65, toll like receptor (TLR)‐2, TLR‐4 and down‐regulation in the expressions of peroxisome proliferator activated receptor gamma (PPAR)γ, adiponectin receptor (AdipoR)‐1 and AdipoR‐2 when compared to rats fed diet containing GNO, RBO and PHVF blended with RBO. It was concluded that dietary PHVF enhance pro‐inflammatory markers which can be reduced by judiciously blending PHVF with RBO.     

Different Ratios of Corn and Coconut Oil Blends in High-Fat Diets Influence Fat Deposition without Altering Metabolic Biomarkers in Male Rats

The effects of high-fat diets with the recommended dietary linoleic acid (LA) intake levels on health outcomes have not been studied extensively. This study investigated the effects of high-fat diets containing different weight ratios of coconut and corn oil with LA levels of <1.00% of energy (very low LA), 2.80% of energy (low LA), 5.80% of energy (moderate LA), and 9.70% of energy (high LA) on fat deposition and selected metabolic biomarkers of male Sprague-Dawley rats. Their initial and terminal body weights are recorded. Blood, adipose tissue, and liver samples are obtained for analysis after an 8-week feeding intervention. Compared with the very low-LA diet, the high-LA diet resulted in higher body weight gain and epididymal fat deposition. No significant differences are observed in liver-to-body weight ratio, blood glucose, visfatin, and leptin levels between the test diets. Serum tumor necrosis factor-alpha (TNF-α), insulin, and C-peptide levels do not significantly increase with the increase in dietary LA levels. High-LA diet results in higher LA levels in the liver and adipose tissue. It is concluded that a high-fat diet containing high LA levels induced body weight gain and epididymal fat deposition in rats but has no effect on selected metabolic biomarkers. Practical applications: Linoleic acid (LA) (C18:2) plays an important role as one of the nutritional elements to meet the daily essential fatty acid requirements. However, a full understanding is perplexed by the various ways that LA can be included in the diet when there is a recommendation to substitute saturated fatty acid (SFA), trans- or n-3 fatty acids intake. The data provide additional findings on the effects of excessive dietary intake of LA (C18:2) on fat deposition when different levels of SFAs are replaced.     

Dietary ALA,But not LNA,Increase Growth,Reduce Inflammatory Processes,and Increase Anti‐Oxidant Capacity in the Marine Finfish Larimichthys crocea

Whilst aquaculture feed is increasingly formulated with the inclusion of plant oils replacing fish oil, and increasing research effort has been invested in understanding the metabolic effects of reduced dietary n‐3 long chain poly unsaturated fatty acids (n‐3 LC‐PUFA), relatively little information is available on the potential direct metabolic roles of dietary alpha‐linolenic acid (ALA, 18:3n‐3) and alpha‐linolenic acid/linoleic acid (LNA, 18:2n‐6) ratio in cultured marine finfish species. In this study, four plant oil based diets, with varying ALA/LNA ratio (0.0, 0.5, 1.0 and 1.5) were fed to juvenile large yellow croakers (Larimichthys crocea) and compared to a fish oil‐based control diet (CD) to evaluate the resulting effects on growth, nonspecific immunity, anti‐oxidant capacity and related gene expression. High dietary LNA negatively impacted fish growth performance, nonspecific immunity and antioxidant capacity, but growth and immunity were maintained to levels comparable to CD by increasing the ratio of dietary ALA/LNA. The over‐expression of genes associated with inflammation (cyclooxygenase‐2 and interleukin‐1β) and fatty acid oxidation (carnitine palmitoyl transferase I and acyl CoA oxidase) in croakers fed high concentrations of LNA were reduced to levels comparable to those fed CD by increasing dietary ALA/LNA. This study showed that dietary ALA, by increasing the overall n‐3/n‐6 PUFA ratio, exerts direct anti‐inflammatory and antioxidant effects, similar to those exerted by dietary n‐3 LC‐PUFA.     

Dietary CLA Combined with Palm Oil or Ovine Fat Differentially Influences Fatty Acid Deposition in Tissues of Obese Zucker Rats

The effect of dietary conjugated linoleic acid (CLA) supplementation in combination with fat from vegetable versus animal origin on the fatty acid deposition, including that of individual 18:1 and 18:2 (conjugated and non-conjugated) isomers, in the liver and muscle of obese rats was investigated. For this purpose, 32 male Zucker rats were randomly assigned to one of four diets containing palm oil or ovine fat, supplemented or not with 1% of 1:1 cis(c)9,trans(t)11 and t10,c12 CLA isomers mixture. Total fatty acid content decreased in the liver and muscle of CLA-fed rats. In the liver, CLA increased saturated fatty acids (SFA) in 11.9% and decreased monounsaturated fatty acids (MUFA) in 6.5%. n-3 Polyunsaturated fatty acids (PUFA) relative proportions were increased in 30.6% by CLA when supplemented to the ovine fat diet. In the muscle, CLA did not affect SFA but decreased MUFA and PUFA percentages. The estimation of Δ9-indices 16 and 18 suggested that CLA inhibited the stearoyl-CoA desaturase activity in the liver (a decrease of 13–38%), in particular when supplemented to the ovine fat diet. Concerning CLA supplementation, the t10,c12 isomer percentage was 60–80% higher in the muscle than in the liver. It is of relevance that rats fed ovine fat, containing bio-formed CLA, had more c9,t11 CLA isomer deposited in both tissues than rats fed palm oil plus synthetic CLA. These results highlight the importance to further clarify the biological effects of consuming foods naturally enriched in CLA, alternatively to CLA dietary supplementation.     

Dietary Linoleic Acid Elevates the Endocannabinoids 2-AG and Anandamide and Promotes Weight Gain in Mice Fed a Low Fat Diet

Dietary intake of linoleic acid (LNA, 18:2n-6) has increased dramatically during the 20th century and is associated with greater prevalence of obesity. The endocannabinoid system is involved in regulation of energy balance and a sustained hyperactivity of the endocannabinoid system may contribute to obesity. Arachidonic acid (ARA, 20:4n-6) is the precursor for 2-AG and anandamide (AEA), and we sought to determine if low fat diets (LFD) could be made obesogenic by increasing the endocannabinoid precursor pool of ARA, causing excessive endocannabinoid signaling leading to weight gain and a metabolic profile associated with obesity. Mice (C57BL/6j, 6 weeks of age) were fed 1 en% LNA and 8 en% LNA in low fat (12.5 en%) and medium fat diets (MFD, 35 en%) for 16 weeks. We found that increasing dietary LNA from 1 to 8 en% in LFD and MFD significantly increased ARA in phospholipids (ARA–PL), elevated 2-AG and AEA in liver, elevated plasma leptin, and resulted in larger adipocytes and more macrophage infiltration in adipose tissue. In LFD, dietary LNA of 8 en% increased feed efficiency and caused greater weight gain than in an isocaloric reduction to 1 en% LNA. Increasing dietary LNA from 1 to 8 en% elevates liver endocannabinoid levels and increases the risk of developing obesity. Thus a high dietary content of LNA (8 en%) increases the adipogenic properties of a low fat diet.     

Mechanisms and Effect of Coptidis Rhizoma on Obesity-Induced Inflammation: In Silico and In Vivo Approaches

Obesity is characterized as a chronic, low-grade inflammation state accompanied by the infiltration of immune cells into adipose tissue and higher levels of inflammatory cytokines and chemokines. This study aimed to investigate the mechanisms and effects of Coptidis Rhizoma (CR) on obesity and its associated inflammation. First, we applied a network pharmacology strategy to search the target genes and pathways regulated by CR in obesity. Next, we performed in vivo experiments to confirm the antiobesity and anti-inflammatory effects of CR. Mice were assigned to five groups: normal chow (NC), control (high-fat diet (HFD)), HFD + CR 200 mg/kg, HFD + CR 400 mg/kg, and HFD + metformin 200 mg/kg. After 16 weeks of the experimental period, CR administration significantly reduced the weight of the body, epididymal fat, and liver; it also decreased insulin resistance, as well as the area under the curve of glucose in the oral glucose tolerance test and triglyceride in the oral fat tolerance test. We observed a decrease in adipose tissue macrophages (ATMs) and inflammatory M1 ATMs, as well as an increase in anti-inflammatory M2 ATMs. Gene expression levels of inflammatory cytokines and chemokines, including tumor necrosis factor-α, F4/80, and C-C motif chemokine (CCL)-2, CCL4, and CCL5, were suppressed in adipose tissue in the CR groups than levels in the control group. Additionally, histological analyses suggested decreased fat accumulation in the epididymal fat pad and liver in the CR groups than that in the control group. Taken together, these results suggest that CR has a therapeutic effect on obesity-induced inflammation, and it functions through the inhibition of macrophage-mediated inflammation in adipose tissue.     

Low Dietary c9t11-Conjugated Linoleic Acid Intake from Dairy Fat or Supplements Reduces Inflammation in Collagen-Induced Arthritis

Dietary cis‐9,trans‐11 (c9t11) conjugated linoleic acid (CLA) fed at 0.5 % w/w was previously shown to attenuate inflammation in the murine collagen‐induced (CA) arthritis model, and growing evidence implicates c9t11‐CLA as a major anti‐inflammatory component of dairy fat. To understand c9t11‐CLA's contribution to dairy fat's anti‐inflammatory action, the minimum amount of dietary c9t11‐CLA needed to reduce inflammation must be determined. This study had two objectives: (1) determine the minimum dietary anti‐inflammatory c9t11‐CLA intake level in the CA model, and (2) compare this to anti‐inflammatory effects of dairy fat (non‐enriched, naturally c9t11‐CLA‐enriched, or c9t11‐CLA‐supplemented). Mice received the following dietary fat treatments (w/w) post arthritis onset: corn oil (6 % CO), 0.125, 0.25, 0.375, and 0.5 % c9t11‐CLA, control butter (6 % CB), c9t11‐enriched butter (6 % EB), or c9t11‐CLA‐supplemented butter (6 % SB, containing 0.2 % c9t11‐CLA). Paw arthritic severity and pad swelling were scored and measured, respectively, over an 84‐day study period. All c9t11‐CLA and butter diets decreased the arthritic score (25–51 %, P < 0.01) and paw swelling (8–11 %, P < 0.01). Throughout the study, plasma tumor necrosis factor (TNFα) was elevated in CO‐fed arthritic mice compared to non‐arthritic (NA) mice but was reduced in 0.5 % c9t11‐CLA‐ and EB‐fed mice. Interleukin‐1β and IL‐6 were increased in arthritic CO‐fed mice compared to NA mice but were reduced in 0.5 % c9t11‐CLA‐ and EB‐fed mice through day 42. In conclusion, 0.125 % c9t11‐CLA reduced clinical arthritis as effectively as higher doses, and decreased arthritis in CB‐fed mice suggested that the minimal anti‐inflammatory levels of c9t11‐CLA might be below 0.125 %.     

The effect of fatty acid composition of rapeseed oil on plasma lipids and oxidative stability of low‐density lipoproteins in cholesterol‐fed hamsters

We studied the effect of four rapeseed oils with different fatty acid profiles on parameters implicated in the pathogenesis of atherosclerosis in humans in a model experiment with hamsters. The hamsters were divided into seven groups and fed a semi‐synthetic, cholesterol‐enriched diet (5 g/kg diet) containing 15% of the fat in question for a period of six weeks. The following rapeseed oils were used: (1) conventional rapeseed oil (6% saturated fatty acids [SFA], 64% monounsaturated fatty acids [MUFA], 18% linoleic acid [LA], 9% α‐linolenic acid [ALA]), (2) linoleic acid‐rich rapeseed oil (6% SFA, 61% MUFA, 28% LA, 2% ALA), (3) oleic acid‐rich rapeseed oil (6% SFA, 74% MUFA, 11% LA, 5% ALA), (4) myristic acid‐rich rapeseed oil (11% myristic acid, 35% SFA, 44% MUFA, 14% LA, 5% ALA). Sunflower oil, olive oil and lard were used as control fats. The concentrations of the lipids in the plasma, in the lipoprotein fractions and in the liver, the fatty acid composition of various tissues, the tocopherol status and the susceptibility of low‐density lipoproteins (LDL) to in vitro‐oxidation were determined. The concentrations of total cholesterol found in the plasma and in the LDL fraction and the ratios of LDL to HDL were similar after feeding the four different types of rapeseed oil, sunflower oil and olive oil. Lard produced the highest concentrations of cholesterol in plasma and the LDL fraction and the highest ratio of LDL to HDL. Feeding conventional, oleic acid‐ and myristic acid‐rich rapeseed oils resulted in markedly lower ratios of arachidonic to eicosapentaenoic acid in the lipids of the liver and the erythrocytes. This is considered beneficial for the formation of eicosanoids. The lag‐time before the onset of peroxidation of the LDL lipids, induced by copper ions, was not statistically significant between the seven hamster groups suggesting that the susceptibility of LDL to lipid peroxidation was similar after feeding all types of fat. Considering all parameters obtained in the used hamster model it is obvious that all four rapeseed oils are at least as favourable as olive oil or sunflower oil.     

Black Raspberry Seed Oil Improves Lipid Metabolism by Inhibiting Lipogenesis and Promoting Fatty‐Acid Oxidation in High‐Fat Diet‐Induced Obese Mice and db/db Mice

The objective of this study was to evaluate the beneficial effect of α‐linolenic acid‐rich black raspberry seed (BRS) oil on lipid metabolism in high‐fat diet (HFD)‐induced obese and db/db mice. Five‐week‐old C57BL/6 mice were fed diets consisting of 50% calories from lard, 5% from soybean, and 5% from corn oil (HFD), or 50% calories from lard and 10% from BRS oil (HFD + BRS oil diet) for 12 weeks. Six‐week‐old C57BL/KsJ‐db/db mice were fed diets consisting of 16% calories from soybean oil (standard diet), 8% from soybean, and 8% from BRS oil, or 16% from BRS oil for 10 weeks. The BRS oil diets lowered the levels of triacylglycerol, nonesterified fatty acids, and total cholesterol in serum and liver of both of the obese and db/db mice as compared with the HFD and standard diet, respectively. mRNA levels of lipogenesis markers including cluster of differentiation 36, fatty‐acid‐binding protein 1, sterol regulatory element binding protein 1c, fatty‐acid synthase, and solute carrier family 25 member 1 in the liver of the BRS oil groups were lower than those in the liver of the HFD and standard groups in the obese and db/db mice, respectively. On the other hand, fatty‐acid oxidation markers including carnitine palmitoyltransferase 1A, acyl‐CoA dehydrogenase, hydroxylacyl‐CoA dehydrogenase α, and acyl‐CoA oxidase in the liver of the BRS oil groups were higher than those in the liver of the HFD and standard groups in the obese and db/db mice, respectively. Peroxisome proliferator‐activated receptor α mRNA and protein levels increased in the liver and epididymal adipose tissue of the obese and db/db mice fed BRS oil compared with HFD and standard diet, respectively. BRS oil might improve lipid metabolism by inhibiting lipogenesis and promoting fatty‐acid oxidation in HFD‐induced obese and db/db mice.     

Dietary intakes and food sources of fatty acids for Belgian women, focused on n-6 and n-3 polyunsaturated fatty acids

The intake of fat, saturated and monounsaturated FA (SFA and MUFA), and omega-6 and omega-3 PUFA has been estimated in 641 Belgian women (age 18-39 y). Their food intake was recorded using a 2-d food diary. The PUFA included were linoleic (LA), alpha-linolenic (LNA), arachidonic (AA), eicosapentaeonoic (EPA), docosapentaenoic (DPA) and docosahexaenoic (DHA) acids. The mean total fat intake corresponded to 34.3% of total energy intake (E). The mean intake of the FA groups corresponded to 13.7%, 13.1%, and 6.0% of E, for SFA, MUFA, and PUFA, respectively. The mean intake of LA was 5.3% of E and of LNA was 0.6% of E, with a mean LA/LNA ratio of 8.7. The mean intake of AA was 0.03% of E. The mean intake of EPA, DPA, and DHA was 0.4%, 0.01%, and 0.06% of E, respectively. According to the Belgian recommendations, the total fat and SFA intake was too high for about three-quarters of the population. The mean LA and overall n-6 PUFA intake corresponded with the recommendation, with part of the population exceeding the upper level. Conversely, the population showed a large deficit for LNA and n-3 PUFA. The major food source for LA and LNA was fats and oils, followed by cereal products. The main sources of long-chain PUFA were fish and seafood, and meat, poultry, and eggs. From a public health perspective, it seems desirable to tackle the problem of low n-3 PUFA intake.     

Metformin Reduces Lipogenesis Markers in Obese Mice Fed a Low-Carbohydrate and High-Fat Diet

Lipogenesis is the process by which fatty acids are synthesized. In metabolic syndrome, an insulin resistant state along with high plasma levels of free fatty acids (FFA) and hyperglycemia may contribute to the lipogenic process. The aim of the present study was to investigate the effects of oral administration of metformin on the expression of lipogenic genes and glycemic profile in mice fed with low‐carbohydrate high‐fat diet by evaluating their metabolic profile. SWISS male mice were divided into 4 groups (N = 7) that were fed with standard (ST), standard plus metformin (ST + MET), low‐carbohydrate high‐fat diet (LCHFD) and low‐carbohydrate high‐fat diet plus metformin (LCHFD + MET) (100 mg kg^?1 diet) diets respectively. Food intake, body weight and blood parameters, such as glucose tolerance, insulin sensitivity, glucose, HDL‐c, total cholesterol, triglycerides, ASL and ALT levels were assessed. Histological analyses were performed on hematoxylin and eosin‐stained epididymal adipose tissue histological specimens. The expression levels of peroxisome proliferator‐activated receptor (PPARγ), sterol regulatory element‐binding protein 1 (SREBP1), fatty acid synthase (FAS) and acetyl‐CoA carboxylase (ACC), were assessed by RT‐PCR. This study showed that metformin decreased adipocyte area, body weight and food consumption in obese animals when compared to the standard group. Furthermore, the expression of lipogenic markers in adipose tissue were diminished in obese animals treated with metformin. This data showed that oral administration of metformin improved glucose and lipid metabolic parameters in white adipose tissue by reducing the expression of lipogenesis markers, suggesting an important clinical application of MET in treating obesity‐related diseases in metabolic syndrome.     

Dietary Monounsaturated Fatty Acids Are Protective Against Metabolic Syndrome and Cardiovascular Disease Risk Factors

Over 50 years of research has sought to define the role dietary fat plays in cardiovascular disease (CVD) risk. Although optimal dietary fat quantity has been keenly pursued over past decades, attention has recently centered on the value of dietary fat quality. The purpose of the present review is to provide a critical assessment of the current body of evidence surrounding efficacy of dietary monounsaturated fatty acids (MUFA) for reduction of traditional risk factors defining metabolic syndrome (MetS) and CVD. Due to existing and emerging research on health attributes of MUFA rich diets, and to the low prevalence of chronic disease in populations consuming MUFA rich Mediterranean diets, national dietary guidelines are increasingly recommending dietary MUFA, primarily at the expense of saturated fatty acids (SFA). Consumption of dietary MUFA promotes healthy blood lipid profiles, mediates blood pressure, improves insulin sensitivity and regulates glucose levels. Moreover, provocative newer data suggest a role for preferential oxidation and metabolism of dietary MUFA, influencing body composition and ameliorating the risk of obesity. Mounting epidemiological and human clinical trial data continue to demonstrate the cardioprotective activity of the MUFA content of dietary fat. As the debate on the optimal fatty acid composition of the diet continues, the benefit of increasing MUFA intakes, particularly as a substitute for dietary SFA, deserves considerable attention.     

The impact of dietary mono‐ and poly‐unsaturated fatty acids on risk factors for atherosclerosis in humans

The fatty acid composition of the diet has various effects on atherosclerosis risk factors. Dietary saturated fatty acids (SFA) and trans‐unsaturated fatty acids increase the low‐density lipoprotein (LDL)‐/high‐density lipoprotein (HDL)‐cholesterol ratio in serum, while these fats do not have a significant bearing on serum triglyceride levels. By contrast, dietary monounsaturated fatty acids (MUFA), n‐6 polyunsaturated fatty acids (PUFA), and α‐linolenic acid (C18:3n‐3) similarly reduce LDL cholesterol concentrations, while their influence on serum HDL cholesterol and triglycerides is not appreciable. Dietary long‐chain n‐3 PUFA slightly increase serum LDL cholesterol concentrations, but are nevertheless considered salubrious with regard to serum lipids due to the distinct triglyceride‐lowering effects. MUFA‐rich compared to n‐6 PUFA‐rich diets strongly reduce the in vitro oxidizability of LDL. The available studies on this subject also suggest that n‐3 PUFA in the small amounts usually present in the diet are not unduly harmful. These findings are consistent with reports from observational studies: the amount of SFA is positively and the amount of MUFA and n‐6 PUFA in the diet is inversely associated with the risk of cardiovascular disease in most epidemiological studies. The available studies have had an impact on current dietary guidelines, which unanimously recommend that most of the dietary fat should be in the form of MUFA, while the amount of SFA and trans fatty acids in the diet should be as low as possible.     

Positional analysis of triacylglycerols from bovine adipose tissue lipids varying in degree of unsaturation

The objective of this study was to demonstrate that changing the fatty acid composition of bovine adipose tissue concurrently changed (i) proportions of triacylglycerol species, (ii) fatty acid composition of triacylglycerol species, and (iii) positional distribution of the component fatty acids of the triacylglycerol species. To achieve this, we took advantage of adipose tissue lipids, from cattle fed in Australia and Japan, that varied widely in fatty acid composition and melting points. Treatment groups produced in Australia were cattle fed: a cornbased diet (MUFA1); a grain-based diet containing whole cottonseed (SFA); a grain-based diet containing protected cottonseed oil (PUFA); and a grain-based diet that resulted in high contents of trans fatty acids (TFA). Treatment groups produced in Japan (MUFA2 and MUFA3) were diets of unknown composition fed for over 300 d. The MUFA1, MUFA2, and MUFA3 samples all were rich in monounsaturated fatty acids, varying only in the proportions of the individual monounsaturates. The SFA, PUFA, and TFA samples had relatively high concentrations of stearic acid (18:0), PUFA, and TFA, respectively. Slip points (indicative of melting points) were 45.1, 41.5, 38.5, 30.7, 28.4, and 22.8°C, for the SFA, TFA, PUFA, MUFA1, MUFA2, and MUFA3 groups, respectively (P<0.05). Triacylglycerols were separated by high-performance liquid chromatography on a silver nitrate-impregnated column into sn-1,2,3-saturated fatty acid triacylglycerol (SSS); [triacylglycerols containing two saturated acids and one trans-monounsaturated fatty acid (SSMt sn-positions unknown)]; sn-1-saturated, 2-monounsaturated, 3-saturated triacylglycerol (SMS); sn-1-saturated, 2-monounsaturated, 3-trans-monounsaturated triacylglycerol (SMMt); sn-1-saturated, 2,3-monounsaturated fatty acid triacylglycerol (SMM); sn-1-saturated, 2-polyunsaturated, 3-trans-monounsaturated triacylglycerol; sn-1,2,3-monounsaturated fatty acid triacylglycerol (MMM); and sn-1-saturated, 2-polyunsaturated, 3-monounsaturated triacylglycerol. Fatty acid methyl esters of each triacylglycerol species also were determined, and further analysis indicated sn-2, and sn-1/3 positions. As the percentage oleic acid increased in the total lipid extract, the proportions of SMM and MMM increased (e.g., from 31.4 and 2.4% in the SFA group to 55.4 and 17.8% in the MUFA3 group). The elevated 18:0 in the SFA group (26%) was reflected in increased percentages of SSS and SSM, and caused an increase in the proportion of 18:0 in all triacylglycerol species relative to the other treatment groups. The percentage of 18:0 in the sn-1/3 positions was elevated markedly in the SMS fraction of the SFA group (to 44%); this would account for the high melting point of the fat of these animals. We conclude that long-term feeding of cattle is sufficient to produce significant alterations in fatty acid composition in bovine adipose tissue. Alterations in the fatty acid composition of bovine adipose tissue changed both the distribution and the composition of the triacylglycerol species, which, in turn, accounted for marked differences in melting points among treatment groups.