China has richly and inexpensive fat and oils from animal and plants, but these resources could not get effectively utilization. In order to make the best of these resources, lipase-catalyzed acidolysis of lard with caprylic acid to produce functional lipid in solvent free system was investigated. Of the five lipases that were tested in the initial screening, immobilized lipase TL IM fromca T. languginosa resulted in the highest incorporation of capry lic acid into lard. This enzyme was further studied for the effect of enzyme load, substrate ratib, reaction time, reaction temperature and added water content on the incorporation of caprylic acid into lard. HPLC analyzed the products from the acidolysis reaction. The highest incorporation was attained at 20% enzyme load. Time course studied suggest that the incorporation of caprylic acid into lard was increased up to 38.77 mol% after 24h. Desirable mole ratio of substrates was 1:2 (lard: caprylic acid), caprylic acid incorporation up to 30.95 mol%. In the range of 45 - 60 degrees C , temperature had no significant effect on enzyme activity and caprylic acid incorporation changed little. When temperature was above 60 degrees C, incorporation of caprylic acid into lard was decreased. The highest incorporation of caprylic acid into lard 35.76 mol% was attained when added water content was 2.5%.
Caprylates ; chemistry ; Catalysis ; Chromatography, High Pressure Liquid ; Dietary Fats ; metabolism ; Enzymes, Immobilized ; metabolism ; Lipase ; metabolism ; Lipids ; chemical synthesis ; Solvents

According to the classic "diet-heart" hypothesis, high dietary intake of saturated fats and cholesterol combined with low intake of polyunsaturated fats can increase levels of serum cholesterol and lead to the development of atherogenic plaques and ultimately cardiovascular diseases. Recently, the beneficial health effects of omega-6 polyunsaturated fatty acids, particularly linoleic acid (LA), on cardiovascular health have been called into question with some scientists suggesting that consumption of LA should be reduced in Western countries. The focus of this critical review is on the controversy surrounding the effects of dietary intake of LA on cardiovascular health. Specifically, we critically examined the effects of both unadulterated and adulterated forms of LA on cardiovascular health outcomes based on findings from epidemiological studies and randomized controlled trials. Additionally, we address common concerns surrounding dietary intake of LA regarding its relationship with arachidonic acid, the ratio of omega-6 to omega-3 fatty acids, and its relationship with inflammation. Our critical review indicates that unadulterated forms of LA are cardioprotective and should be consumed as part of a healthy diet. In contrast, abundant evidence now indicates that adulterated forms of LA, predominantly hydrogenated vegetable oils, are atherogenic and should not be considered part of a healthy diet. The ability to adulterate the natural omega-6 fatty acid, LA, has contributed to mixed findings regarding the effects of this fatty acid on cardiovascular health. Thus, it is critical that the source of LA be taken into account when drawing conclusions about the physiological effects of this fatty acid. The findings of the present review are in line with current dietary recommendations of the American Heart Association.
Cardiovascular Diseases ; metabolism ; prevention & control ; Dietary Fats ; analysis ; metabolism ; Humans ; Linoleic Acid ; analysis ; metabolism ; Randomized Controlled Trials as Topic

The effect of alloxan-diabetic rat fed with normal, high fat, low protein and high protein diets on the rate of urea production and the activities of enzymes associated with the urea cycle (ornithine transcarbamoylase, E.C. 2.1.3.3, OTC; arginase, E.C. 3.5.5.1) have been studied in intact and isolated perfused liver. The amount of urea excretion was the highest in the high protein diet group. When each diet group was treated with alloxan, total urea excretion showed little differences between each diet group and its corresponding control group with the exception being in the normal diet group. However, the enzyme activity of OTC was increased significantly by alloxan treatment in low and high protein diet groups as compared to corresponding control groups. Similar results were obtained in arginase activity, although the magnitude of the change was less marked. In liver perfusion experiments on rats treated with alloxan, the amount of urea production and changes in OTC and arginase activity were very similar with those in the intact liver. These results suggest that alloxan treatment in normal diet group causes an increase in urea excretion both in intact and perfused liver regardless of changes in enzyme activities and total urea excretion, and enzyme activities are affected by changes in dietary components but the changes of enzyme activities may not correlate with total urea excretion.
Alloxan ; Animal ; Diabetes Mellitus, Experimental/metabolism* ; Dietary Fats/pharmacology* ; Dietary Proteins/pharmacology* ; In Vitro ; Liver/metabolism* ; Male ; Perfusion ; Rats ; Urea/metabolism* ; Urea/urine

We examined the effects of conjugated linoleic acid (CLA) on growth, fatty acid composition and enzyme activity of fatty acid oxidation in the liver of large yellow croaker. We divided 1600 fish (average initial weight 150 g) into 4 groups and reared them in 8 cages. Four dietary treatments were formulated to contain 0%, 1%, 2% and 4% (w/w) CLA, respectively. The fish were fed for 10 weeks ad libitum twice daily. We found that the dietary CLA had no effect on growth, biometric parameters and whole body proximate (P>0.05), but showed some significant effects on the fatty acid composition in both muscle and the liver. The activities of lipogenic enzymes were slightly depressed in fish fed with increasing levels of CLA when compared with control (P>0.05). Dietary CLA supplementation had no effects on liver lipid content, but significantly increased the contents of saturated fatty acids (SFA) and polyunsaturated fatty acids (PUFA) (P<0.05) and decreased monounsaturated fatty acid (MUFA) content in both muscle and the liver. Dietary CLA inclusion resulted in significant increases of the biologically active cis-9, trans-11 and trans-10, cis-12 isomers in both tissues (P<0.05). The total accumulation of CLA was higher in the liver (3.83%, w/w) than in muscle (3.77%, w/w) when fed with 4% (w/w) CLA. This study demonstrates that large yellow croakers are capable of absorbing and depositing CLA and long-chain n-3 PUFA in the liver and muscle, showing that this species fed with CLA could be an important human food source for these healthful fatty acids.
Animals ; Dietary Fats ; administration & dosage ; Dietary Supplements ; Fatty Acids ; metabolism ; Linoleic Acid ; administration & dosage ; Lipogenesis ; drug effects ; physiology ; Liver ; drug effects ; metabolism ; Perciformes ; growth & development ; metabolism

PURPOSE: Changes in human body composition can affect the accuracy of spine bone mineral density (BMD) measurements. The purpose of this study was to evaluate whether fat and water in the soft tissue of the abdomen influence lumbar spine BMD measurements obtained using dual energy X-ray absorptiometry (DXA). MATERIALS AND METHODS: Duplicate BMD measurements were carried out on healthy volunteers (10 men and 10 women) and the Hologic anthropomorphic spine phantom had on the same day before and after placement of following 3 materials in the abdominal area: lard 900 g, 1.5 cm thick; oil 1.4 liters in a vinyl bag; and water 1.2 liters in a vinyl bag. RESULTS: In the case of human participants, following the placement of exogenous water to mimic extracellular fluid (ECF), there was a significant decrease in lumbar spine BMD (-0.012 g/cm2, p=0.006), whereas the placement of exogenous lard and oil to mimic abdominal fat produced a slight increase in lumbar spine BMD (0.006 g/cm2, p=0.301; 0.008 g/cm2, p=0.250, respectively). The average percentage of lumbar spine BMD change with and without exogenous lard, oil, and water showed increase of 0.51%, and 0.67%, and decrease of 1.02%, respectively. Using the phantom, BMD decreased with the placement of both lard (-0.002 g/cm2, p=0.699) and water (-0.006 g/cm2, p=0.153); however, there was no difference in BMD after oil placement. CONCLUSION: These results suggest that in cases where changes in fat and ECF volume are similar, ECF exerts a greater influence than fat on DXA lumbar BMD measurements.
Absorptiometry, Photon ; Adult ; Bone Density/*drug effects ; Dietary Fats/pharmacology ; Fats/*pharmacology ; Female ; Humans ; Lumbar Vertebrae/*drug effects/*metabolism ; Male ; Water/*pharmacology

OBJECTIVETo create a rat insulin resistant fatty liver model.

METHODS14 male Wistar rats were randomly divided into a model and a control group. The model rats were fed a high-fat diet (45% of energy from fat) for 8 weeks, and the control group a standard diet (19% of energy from fat). Insulin sensitivity was measured with glucose infusion rate (GIR) by the euglycermic hyperinsulinemia clamp technique. The aminotransferase, triglyceride (TG), free fatty acid (FFA), superoxide dismutase (SOD) and malondialdehyde (MDA) were measured by biochemical methods, and insulin was measured by radioimmunoassay. The histological and ultrastructural changes of all rat livers were scored using light and electron microscopy.

RESULTSRats fed the high-fat diet developed panlobular macrovesicular steatosis, lobular inflammatory cell infiltration and abnormal mitochondria, whereas those fed the standard diet had normal livers. All model group rats had elevated levels of aminotransferase, TG, FFA, insulin and liver index, and low GIR. In addition, the high-fat diet increased MDA and decreased SOD.

CONCLUSIONA fatty liver and insulin resistance model was successfully developed in rats fed a high-fat diet for 8 weeks, which provided a useful experimental tool for elucidating pathogenesis and treatment of fatty liver.

Animals ; Dietary Fats ; administration & dosage ; Disease Models, Animal ; Fatty Liver ; metabolism ; physiopathology ; Insulin Resistance ; Male ; Random Allocation ; Rats ; Rats, Wistar

Gut microbiota play critical physiological roles in energy extraction from the intestine and in the control of systemic immunity, as well as local intestinal immunity. Disturbance of gut microbiota leads to the development of several diseases, such as colitis, inflammatory bowel diseases, metabolic disorders, cancer, etc. From a metabolic point of view, the gut is a large metabolic organ and one of the first to come into contact with dietary fats. Interestingly, excessive dietary fat has been incriminated as a primary culprit of metabolic syndrome and obesity. After intake of high-fat diet or Western diet, extensive changes in gut microbiota have been observed, which may be an underlying cause of alterations in whole body metabolism and nutrient homeostasis. Here, we summarize recent data on changes in the gut microbiota and immunity associated with dietary fat, as well as their relationships with the pathogenesis of metabolic syndrome. These findings may provide insight into the understanding of the complex pathophysiology related to the development of metabolic diseases and offer an opportunity to develop novel candidates for therapeutic agents.
Colitis ; Diet, High-Fat ; Diet, Western ; Dietary Fats* ; Gastrointestinal Microbiome* ; Homeostasis ; Inflammatory Bowel Diseases ; Intestines ; Metabolic Diseases ; Metabolism ; Obesity

OBJECTIVESTo explore the changes of hepatic gene expression during the course of nonalcoholic fatty liver disease (NAFLD) development in rats.

METHODSA rat model of NAFLD was developed by feeding the animals a high-fat diet for 24 weeks. Liver tissues of the model rats and the control rats were analyzed at different time points using rat U230A (Affymetrix GeneChip), which covers 15650 genes.

RESULTSCompared with the control rats, the number of genes expressed differently in the model group rats at 4 and 8 weeks was 426 and 540. The up-regulated genes among them were intracellular phosphorylase genes, metabolic enzyme genes, fatty acid binding protein genes, cytochrome P450 genes, cellular transcription and differentiation genes. The down-regulated genes were ionic channel genes, hormone receptor genes, and cytoskeleton genes. At the 12th week, the number of the genes expressed differently was 501, in which 352 were up-regulated genes, including genes related to inflammation and apoptosis such as interleukin and Toll-like receptor 4. At the 16th week, the number of the differently expressed genes was 665, with 430 up-regulated, such as those related to the inflammation and apoptosis genes and collagen I and fibrosis genes, however cell regeneration genes were down-regulated. At the 24th week the number was 663, of which fibroblast growth factor, transforming growth factor and insulin-like growth factor genes were up-regulated. Of all the differently expressed genes, the number of up-regulated genes was 128, including 10 lipogenic genes, 46 metabolic genes, 15 inflammation genes, 10 apoptosis genes, and 16 fibrosis genes; and the down-regulated genes were 52, including 6 hormone receptor genes, 5 cell regeneration genes and 11 electron transport genes.

CONCLUSIONThe changes of the hepatic gene expression of rats fed a fat-rich diet are related to the duration of the feeding, and are correlated with their histopathology in the livers.

Animals ; Dietary Fats ; Fatty Liver ; etiology ; genetics ; Gene Expression Profiling ; Liver ; metabolism ; Oligonucleotide Array Sequence Analysis ; Rats ; Rats, Sprague-Dawley

The purpose of the present study was to determine whether chronic high-fat diet (HF) induces insulin resistance independently of obesity. We randomly divided 40 rats into two groups and fed them either with a HF or with a high-carbohydrate diet (HC) for 8 weeks. Whole body glucose disappearance rate (Rd) was measured using a euglycemic hyperinsulinemic clamp. Firstly, we defined whether insulin resistance by HF was associated with obesity. Plasma glucose and triglyceride concentrations were significantly increased in HF. Rd was decreased (10.6+/-0.2 vs. 9.1+/-0.2 mg/kg/min in HC and HF, respectively) and the hepatic glucose output rate (HGO) was increased in HF (2.2+/-0.3 vs. 4.5+/-0.2 mg/kg/min in HC and HF, respectively). Rd was significantly correlated with %VF (p<0.01). These results implicate that visceral obesity is associated with insulin resistance induced by HF. In addition, to define whether dietary fat induces insulin resistance regardless of visceral obesity, we compared Rd and HGO between groups 1) after matching %VF in both groups and 2) using an ANCOVA to adjust for %VF. After matching %VF, Rd in HF was significantly decreased by 14% (p<0.001) and HGO was significantly increased by 110% (p<0.001). Furthermore, statistical analyses using an ANCOVA also showed Rd for HF was significantly decreased even after adjusting %VF. In conclusion, we suggest that dietary fat per se could induce insulin resistance in rats fed with chronic HF independently of obesity.
Adipose Tissue/*pathology ; Animal ; Dietary Carbohydrates/administration &age ; Dietary Fats/*administration &age ; Fatty Acids, Nonesterified/metabolism ; Female ; *Insulin Resistance ; Obesity/etiology ; Rats ; Rats, Sprague-Dawley ; Viscera

OBJECTIVETo determine the effect of hypercholsterolemia induced by a high-lipid diet on glomerulosclerosis.

METHODSTwenty nephrotic syndrome (NS) Wistar rats administrated adriamycin (ADR) with a single intravenous dose of 5 mg/kg body weight, were divided into the standard and high-lipid chow groups. Another 20 weight-matched non-NS rats that received a vehicle alone were grouped as control. Urinary protein excretion and serum cholesterol were assayed; image analysis and techniques of pathology, immunohistochemistry, and molecular biology were used to determine morphological changes in glomeruli and the production of glomerular mesangial matrices in different groups.

RESULTSThe serum total cholesterol level was significantly higher in rats with high-lipid chow in both non-NS [(2.2 +/- 0.3) g/L vs. (0.9 +/- 0.1) g/L, P < 0.01] and NS [(9.5 +/- 0.2) g/L vs. (2.3 +/- 0.3) g/L, P < 0.01]. The urinary protein excretion was significantly higher in the high-lipid diet rats than in standard chow rats [(76.2 +/- 24.2) mg/24h vs. (44.8 +/- 13.6) mg/24h, P < 0.05] in NS rats. Although increases in the mesangial matrix and mesangial cells were observed in rats with high-lipid diet in both NS and non-NS group, more obvious pathological changes were found in NS group, such as lipid deposits and foam cell formation in mesangial areas, and progressing to focal and segmental glomerulosclerosis in some glomeruli. The immunohistochemical asay showed that the production of 3 major components (collagen IV, fibronectin, and laminin) was increased in NS group, especially in the rats with high-lipid chow. The increased expression of laminin mRNA was also detected with slot blotting in both NS and non-NS rats with high-lipid chow, and it was more obvious in the rats with NS.

CONCLUSIONOur findings indicated that diet-induced hyperlipidemia can lead to over-production of mesangial matrix components, and further aggravate glomerulosclerosis in ADR-induced nephrosis.

Animals ; Dietary Fats ; pharmacology ; Doxorubicin ; Fibronectins ; metabolism ; Glomerular Mesangium ; metabolism ; pathology ; Hypercholesterolemia ; metabolism ; Laminin ; metabolism ; Male ; Nephrotic Syndrome ; chemically induced ; metabolism ; pathology ; Proteinuria ; urine ; Rats ; Rats, Wistar