Nutritionally enriched 1,3-diacylglycerol-rich oil: Low calorie fat with hypolipidemic effects in rats.

An enzymatic process was developed for the preparation of a nutritionally enriched 1,3-diacylglycerol(DAG)-rich oil from a blend of refined sunflower and rice bran oils. The process involves hydrolysis of vegetable oil blend using Candida cylindracea followed by esterification with glycerol using Lipozyme RM1M. The resultant DAG-rich oil contains 84% of DAG (66% of 1,3-DAG, 18% of 1,2-DAG) and 16% of triacylglycerol (TAG) along with micro nutrients like γ-oryzanol, tocotrienols, tocopherols and phytosterols. Nutritional studies of the DAG-rich oil were conducted in Wistar rats and compared with sunflower oil (SFO). The calorific value of the DAG-rich oil was estimated to be 6.45 Kcals/g as against 9.25 Kcals/g for SFO. The serum and liver cholesterol and TAG levels in rats fed with 1,3-DAG-rich oil were found to be significantly reduced as compared to rats fed diet containing SFO. We conclude that 1,3-DAG-rich oil is a low calorie fat and exhibits hypolipidemic effects.

Down-regulation of NF-κB expression by n-3 fatty acid-rich linseed oil is modulated by PPARγ activation, eicosanoid cascade and secretion of cytokines by macrophages in rats fed partially hydrogenated vegetable fat.

PURPOSE: The industrially produced partially hydrogenated vegetable fat (PHVF) contains trans fatty acid mostly comprising of elaidic acid (18:1 ∆9t). PHVF is used as a cooking medium in Southeast Asian countries. The purpose of this study is to evaluate the effects of dietary PHVF on inflammatory mediators and possible ameliorative effects of n-3 fatty acid (α-linolenic acid, ALA)-rich linseed oil (LSO) on the inflammatory mediators. METHODS: Male Wistar weaning rats were fed AIN-93-purified diet supplemented with one of the following lipids for 60 days, groundnut oil (GNO, 10 wt%), PHVF (10 wt%), LSO (10 wt%), PHVF blended with LSO at 2.5, 5.0 and 7.5 wt% levels. The final fat level in the diet was maintained at 10 wt%. RESULTS: The macrophages from rats fed PHVF showed higher levels of total cholesterol and free cholesterol as compared to those from rats fed GNO and LSO. Macrophages from rats fed PHVF down-regulated the expression of PPARγ and up-regulated the expressions of cytosolic phospholipase A2, cyclooxygenase-2, 5-lipoxygenase and nuclear factor-kappa B p65. The macrophages from rats fed PHVF secreted higher levels of pro-inflammatory eicosanoids and cytokines. The rats fed PHVF blended with LSO at incremental amounts showed a significant reduction in the expressions of pro-inflammatory markers in dose-dependent manner. CONCLUSION: Detrimental effects of dietary PHVF in enhancing pro-inflammatory agents in rats could be significantly reduced by providing ALA (n-3 PUFA)-rich LSO.

Dietary gamma oryzanol plays a significant role in the anti-inflammatory activity of rice bran oil by decreasing pro-inflammatory mediators secreted by peritoneal macrophages of rats.

Ricebran oil (RBO) is promoted as heart friendly oil because of its ability to maintain serum lipids at desirable levels. Inflammation also plays an important role on cardiovascular health. The role of minor constituents present in unsaponifiable fraction (UF) of RBO on inflammatory markers is not well understood. To evaluate this, we have taken RBO with UF (RBO-N), RBO stripped of UF (RBO-MCR) and RBO-MCR supplemented with UF from RBO (UFRBO) or Gamma-Oryzanol (γ-ORY) were added in AIN-93 diets which was then fed to Wistar rats for a period of 60 days. Groundnut oil with UF (GNO-N), UF removed GNO (GNO-MCR) and GNO-MCR supplemented with UF from RBO or γ-ORY was also used for comparison. The peritoneal macrophages from the rats were activated and pro-inflammatory mediators such as Reactive Oxygen Species (ROS), eicosanoids, cytokines, hydrolytic enzymes of lysosomal origin were monitored. The results indicated that UF of RBO and γ-ORY supplemented in the dietary oils play a significant role in reducing the secretion of pro-inflammatory mediators by macrophages. Hence γ-ORY in RBO significantly contributed to the anti-inflammatory properties of RBO.

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-1ß, 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.

Diet containing partially hydrogenated vegetable fat enhances the carrageenan induced paw inflammation but not oxidative stress markers in liver of rats.

In the present study, we investigated the effect of feeding Partially hydrogenated vegetable fat (PHVF) on carrageenan induced paw inflammation and oxidative stress markers in liver of rats. In addition, the effect of feeding rats with Linseed Oil (LSO, α-linolenic acid, n-3 PUFA) or PHVF blended with incremental amounts of LSO on these markers were also monitored. Rats weighing 200 g were given 1 mL of different oils (PHVF, Groundnut Oil; GNO, Olive Oil; OO and LSO) per day for 15 days. Rats given PHVF showed higher levels of paw inflammation in response to carrageenan injection. Rats given LSO showed least amounts of paw inflammation when injected with carrageenan. A second set of experiment was conducted by feeding weaning rats with AIN-93 purified diet supplemented with PHVF or PHVF with incremental amounts of LSO for 60 days. The rats fed PHVF showed higher degree of carrageenan induced inflammation as compared to rats given GNO and LSO. However, the rats fed PHVF showed lower levels of lipid peroxides, protein carbonyls, 8-hydroxy guanine and antioxidant enzyme activities in liver homogenate as compared to those given LSO. In conclusion dietary PHVF rendered the rats prone to higher levels of carrageenan induced inflammation which can be reduced by giving PHVF blended with LSO. However, oxidative stress markers found to be higher levels in rats given LSO or PHVF blended with LSO as compared to rats given PHVF as sole source of fat.

Modulatory effects of alpha-linolenic acid on generation of reactive oxygen species in elaidic acid enriched peritoneal macrophages in rats.

Fatty acids are known to influence the ability of macrophages to generate reactive oxygen species (ROS). However the effect of elaidic acid (EA, 18:1 trans fatty acid) on ROS generation is not well studied. Rat peritoneal macrophages were enriched with elaidic acid by incubating the cells with 80 1M EA. The macrophages containing EA generated higher amounts of superoxide anion (O2*-), hydrogen peroxide (H2O2) and nitric oxide (NO) by 54, 123 and 237%, respectively as compared to control cells which did not contain EA. To study the competition of other C18 fatty acids with EA macrophages were incubated with EA along with stearic acid (18:0), oleic acid (18:1), linoleic acid (18:2) and alpha-linolenic acid (ALA, 18:3). ALA significantly reduced the incorporation of EA into macrophage lipids. This also significantly reduced the generation of O2*-, H2O2, NO by macrophages. Studies were also conducted by feeding rats with diet containing partially hydrogenated vegetable fat (PHVF) as a source for EA and linseed oil (LSO) as a source for ALA. The rats were fed AIN-93 diet containing PHVF with 17% EA and incremental amounts of linseed oil for 10 weeks. The peritoneal macrophages from rats fed partially hydrogenated vegetable fat generated higher levels of O2*-, H2O2, NO by 46, 161 and 76% respectively, when compared to rats fed control diets containing ground nut oil. Macrophages from rats fed PHVF with incremental amounts of LSO produced significantly lower levels ROS in a dose dependent manner. Thus ALA reduces the higher levels of ROS generated by macrophages containing EA.