Effect of diarrhea on nutrient utilization in protein deficient or protein-calorie deficient rats

Diarrhea increases the effects of malnutrition. Accordingly, the effect of diarrhea on two types of malnutrition (protein deficiency and protein-calorie deficiency) was studied. The experiment included 42 young Sprague Dawley rats. The rats were distributed into three groups with 14 rats per group. During the first 16 of the experiment, the first group was fed a control diet ad libitum, the second received the same diet but with food intake reduced in 50% whereas the third group was offered a protein deficient diet. Thus, at the end of this period there were well-fed rats (control), as well as protein and protein-calorie malnourished rats. Then one half of the rats in each group were given lactose to produce diarrhea and all rats continued with their previously assigned diet and feeding regime during one more week. Therefore, during this period there were control rats, protein deficient rats and protein-calorie deficient rats with and without diarrhea. The results showed that diarrhea caused a substantial reduction in food intake and growth in the well-fed rats and also in the group fed the protein deficient diet. However, the protein-calorie deficient group did not reduce its intake nor its growth rate. As a result, diarrhea caused malnutrition in the control group and increased malnutrition in the protein deficient but it did not have an additional effect in the protein-calorie deficient rats. The apparent absorption of lipids and nitrogen measured in these rats showed that the absorption reduction caused by diarrhea was more pronounced in the protein deficient group. This group also had the lowest activities of intestinal disaccharidases. These results showed that diarrhea had a more detrimental effect in protein deficient than in protein-calorie deficient rats.     

Effect of EFA deficiency on lipid transport from liver

Studies are reported of the effect of an essential fatty acid (EFA) deficiency on synthesis of triglycerides (TG) and phospholipids (PL) and secretion of these compounds by livers of male Sprague-Dawley rats. Animals were fed a semipurified diet containing corn oil or hydrogenated coconut oil (HCO) as the sole source of fat or no fat from weaning to 20 weeks of age. Liver function of the animals in each group was compared by an isolated liver perfusion technique with perfusates containing erythrocytes and linoleate, and in vivo experiments via tail vein injection of palmitate-³H. Perfusion experiments showed that an EFA deficiency reduced the ability of the liver to secrete TG and PL. Accumulation of TG in the liver and its diminished secretion into the blood of EFA deficient animals were demonstrated by in vivo experiments with palmitate-³H. The rate of conversion of linoleate to arachidonate and synthesis of PL was greater in livers of EFA deficient rats than in the control, corn oil fed animals. The results suggest a relationship of EFA metabolism to lipid transport. One of five papers to be published from the Symposium “Lipid Transport” presented at the AOCS Meeting, New Orleans, April 1970.     

Activities of liver mixed function oxidase system in rats fedtrans fat

Rats were fed diets containing either camellia oil or partially hydrogenated corn oil, as a source ofcis ortrans octadecenoate, respectively, in the presence of adequate linoleic acid. After 35 days of feeding the diets, activities of several hepatic drug metabolizing enzymes as well as the content of hepatic microsomal cytochrome P-450 were determined. Geometrical difference in the dietary fat did not affect the amount of microsomal protein nor the content of cytochrome P-450. Also, activities of NADPH cytochrome C reductase, aminopyrine N-demethylase and biphenyl hydroxylase were approximately the same between two groups of rats. Aniline hydroxylase was slightly elevated in the rats fedtrans fat. It was concluded that the difference in the geometry of dietary fatty acids had little effect in modulating the hepatic mixed function oxidase system.     

Biosynthesis of brain sphingolipids and myelin accumulation in the mouse

Microsomal fractions were prepared from the brains of mice sacrificed at 13 are points between 5 and 48 days of age. Several enzymatic activities implicated in sphingolipid biosynthesis were assayed. The developmental pattern for the terminal step in galactosylceramide synthesis, transfer of galactose from UDP-galactose to ceramide, peaked sharply at 17–19 days of age. Thus maximal activity for biosynthesis of this relatively myelin specific lipid appears slightly before the time period of maximal rate of accumulation of myelin (21–23 days). These latter data were obtained by isolating myelin from mice at 10 age points from 9 to 45 days of age. A control enzymatic activity, transfer of glucose from UDP-glucose to ceramide to form glucosylceramide, was high at all age points with a broad peak between 20 and 35 days of age. Condensation of palmitoyl-CoA and serine to form ketodihydrosphingosine, a common precursor to both glucosyl- and galactosylceramide also followed a developmental pattern of high activity at all age points, but peaked slightly at ca. 10–12 days of age.     

Emodin prevents intrahepatic fat accumulation, inflammation and redox status imbalance during diet-induced hepatosteatosis in rats

High-fat and/or high-carbohydrate diets may predispose to several metabolic disturbances including liver fatty infiltration (hepatosteatosis) or be associated with necro-inflammation and fibrosis (steatohepatitis). Several studies have emphasized the hepatoprotective effect of some natural agents. In this study, we investigated the potential therapeutic effects of the treatment with emodin, an anthraquinone derivative with anti-oxidant and anti-cancer abilities, in rats developing diet-induced hepatosteatosis and steatohepatitis. Sprague-Dawley rats were fed a standard diet (SD) for 15 weeks, or a high-fat/high-fructose diet (HFD/HF). After 5 weeks, emodin was added to the drinking water of some of the SD and HFD/HF rats. The experiment ended after an additional 10 weeks. Emodin-treated HFD/HF rats were protected from hepatosteatosis and metabolic derangements usually observed in HFD/HF animals. Furthermore, emodin exerted anti-inflammatory activity by inhibiting the HFD/HF-induced increase of tumor necrosis factor (TNF)-α. Emodin also affected the hepatocytes glutathione homeostasis and levels of the HFD/HF-induced increase of glutathionylated/phosphorylated phosphatase and tensin homolog (PTEN). In conclusion, we demonstrated that a natural agent such as emodin can prevent hepatosteatosis, preserving liver from pro-inflammatory and pro-oxidant damage caused by HFD/HF diet. These findings are promising, proposing emodin as a possible hindrance to progression of hepatosteatosis into steatohepatitis.     

Activities of liver mitochondrial and peroxisomal fatty acid oxidation enzymes in rats fedtrans fat

The effect oftrans fat on the activities of liver mitochondrial and peroxisomal fatty acid oxidation enzymes was examined in various strains of rats. When Wistar and Sprague-Dawley rats were fed for 30 days diets containing either olive oil or partially hydrogenated corn oil as a source ofcis-ortrans-octadecenoate, respectively, the activities of various enzymes of mitochondrial and peroxisomal β-oxidation measured withcis- andtrans-9-octadecenoic acid as substratese showed little dietary fatdependent change. In Fischer 344 rats, feedingtrans fat for 15 mo increased only moderately various enzymes of β-oxidation except for carnitine acyltransferase. The rate of mitochondrial ketogenesis and the activity of carnitine acyltransferase measured withtrans-9-octadecenoic acid as a substrate were about half those with thecis-counterpart. Peroxisomes oxidizedtrans-9-octadecenoyl-CoA at a rate comparable to thecis-counterpart. It was concluded from this study and previous ones that the difference in the geometry of dietary fatty acid had only a marginal effect in modulating the hepatic fatty acid oxidation system, in spite of marked differences in the metabolic behavior ofcis-andtrans fatty acid in cell-free preparations and perfused liver.     

Endocrine control of fat mobilization in the isolated fat cells of cold-exposed rats

Adipose tissue in rats maintained at normal ambient temperature grows by a mixture of cell proliferation and lipid deposition in the early growth stage of the rat. In the mature rat, the tissue grows primarily by lipid deposition, mitotic activity being significantly decreased. When the rat is acclimated to 5 C, growth of adipose tissue is less than that of rats maintained at normal ambient temperature. Furthermore, growth of adipose tissue in the 5 C rat occurs through a mixture of cell proliferation and lipid deposition throughout the body weight range studied. The differences in tissue growth were taken into consideration in measuring the stimulatory effect of norepinephrine on lipolysis and reesterification of isolated fat cells. The results indicate that the cell size affects the lipolytic response; the larger the cell the less sensitive it is. Fat cells from cold-acclimated rats are more sensitive to the lipolytic action of norepinephrine, independent of differences in cell size. On the other hand, reesterification is not affected by cell size, nor by exposure of the rat to cold     

Dietary polyunsaturated fat in relation to mammary carcinogenesis in rats

High fat diets promote the development of mammary tumors induced in rats by 7,12-dimethylbenz(a)anthracene (DMBA), and polyunsaturated fats are more effective than saturated fats. This difference is related to the linoleic acid content of polyunsaturated vegetable oils, but the amount of linolealte required for maximum tumor promotion appears to be higher than indicated by earlier experiments. Comparison of the effects of a polyunsaturated vegetable oil (corn oil) containing linoleate with a fish oilo (menhaden oil) containing polyunsaturated fatty acids derived from linolenic acid showed that higher dietary mammary tumors, while corresponding levels of menhaden oil had an inhibitory effect. This is further evidence that promotion of mammary tumorigenesis by polyunsaturated vegetable oils may be mediated by prostaglandins or other biologically active eicosanoids derived from n−6 fatty acids.     

Intake of conjugated eicosapentaenoic acid suppresses lipid accumulation in liver and epididymal adipose tissue in rats

It has been reported that consumption of CLA and EPA alters lipid metabolism. CLA contains conjugated double bonds, and EPA is an n−3 PUFA. Based on the possibility that a molecule with both of these structures might have interesting physiological effects, we prepared conjugated FA from EPA by alkaline isomerization and examined the effects of the conjugated EPA (CEPA) on lipid metabolism in rats. Rats were fed by oral gavage every day for 4 wk with 200 mg of FA including linoleic acid, EPA, CLA, or CEPA. Compared with other groups, rats fed CEPA showed a significant weight loss in epididymal adipose tissue and significant decreases in the levels of liver TAG and total cholesterol (TC), indicating reduced accumulation of lipid in the liver and adipose tissue. The plasma levels of TAG, TC, FFA, and tumor necrosis factor-α in rats fed CEPA were reduced, as was the activity of the FA synthesis system in the liver, whereas the FA-β-oxidation system was activated by CEPA. These results suggest that intake of CEPA suppresses lipid accumulation in the liver and epididymal adipose tissue while increasing lipid catabolism in rats.     

Coenzyme q metabolism is disturbed in high fat diet-induced non alcoholic Fatty liver disease in rats

Oxidative stress is believed to be a major contributory factor in the development of non alcoholic fatty liver disease (NAFLD), the most common liver disorder worldwide. In this study, the effects of high fat diet-induced NAFLD on Coenzyme Q (CoQ) metabolism and plasma oxidative stress markers in rats were investigated. Rats were fed a standard low fat diet (control) or a high fat diet (57% metabolizable energy as fat) for 18 weeks. The concentrations of total (reduced + oxidized) CoQ9 were increased by >2 fold in the plasma of animals fed the high fat diet, while those of total CoQ10 were unchanged. Reduced CoQ levels were raised, but oxidized CoQ levels were not, thus the proportion in the reduced form was increased by about 75%. A higher percentage of plasma CoQ9 as compared to CoQ10 was in the reduced form in both control and high fat fed rats. Plasma protein thiol (SH) levels were decreased in the high fat-fed rats as compared to the control group, but concentrations of lipid hydroperoxides and low density lipoprotein (LDL) conjugated dienes were unchanged. These results indicate that high fat diet-induced NAFLD in rats is associated with altered CoQ metabolism and increased protein, but not lipid, oxidative stress.     

Dietary conjugated linolenic acid in relation to CLA differently modifies body fat mass and serum and liver lipid levels in rats

The present study compared the effect of dietary conjugated linolenic acid (CLNA) on body fat and serum and liver lipid levels with that of CLA in rats. FFA rich in linoleic acid, α-linolenic acid, CLA, or CLNA were used as experimental fats. Male Sprague-Dawley rats (4 wk old) were fed purified diets containing 1% of one of these experimental fats. After 4 wk of feeding, adipose tissue weights, serum and liver lipid concentrations, serum tumor necrosis factor (TNF)-α and leptin levels, and hepatic β-oxidation activities were measured. Compared with linoleic acid, CLA and, more potently, CLNA were found to reduce perirenal adipose tissue weight. The same trend was observed in the weight of epididymal adipose tissue. CLNA, but not CLA, was found to significantly increase serum and liver IG concentrations. Serum FFA concentration was also increased in the CLNA group more than in the other groups. The activity of β-oxidation in liver mitochondria and peroxisomes was significantly higher in the CLNA group than in the other groups. Thus, the amount of liver TG exceeded the ability of hepatic β-oxidation. Significant positive correlation was found between the adipose tissue weights and serum leptin levels in all animals (vs. perirenal: r=0.557, P<0.001; vs. epididymal: r=0.405, P<0.05). A less significant correlation was found between adipose tissue weights and serum TNF-α level (vs. perirenal: r=0.069, P<0.1; vs. epididymal: r=0.382, P<0.05). Although the mechanism for the specific effect of CLNA is not clear at present, these findings indicate that in rats CLNA modulated the body fat and TG metabolism differently from CLA.     

有限元分析软件Marc及其在橡胶材料分析中的应用

介绍了有限元分析软件Marc的组成及功能，并探讨了其在橡胶材料力学分析中的应用。Marc软件由求解器、前后处理图形对话界面、六面体网格划分器及与其它软件的接口等部分组成，可对各种结构的位移场、非结构的温度场、流场等进行分析，其非线性分析能力尤为突出。Marc软件为橡胶材料力学分析提供了Mooney，Ogden等多种材料模型，可进行橡胶材料形变、应力—应变分析，为结构设计提供依据。     

Liver lipid alterations in rats fed arginine deficient diets

Arginine deficiency is associated with a marked increase in liver lipids in the rat. Triglyceride accumulation accounts for most of the fatty infiltration. Cholesterol concentration per gram of liver increased approximately 280% above control rats receiving dietary arginine. The percentage of phospholipids was significantly decreased in the arginine-deficient rat liver compared to controls. The fatty acid composition revealed a significant reduction in the percentage of palmitic, palmitoleic, oleic, and linoleic acids. However, both stearic and arachidonic acids were increased approximately 250 and 160%, respectively, in arginine-deficient livers compared to controls. Arginine deficiency in the rat causes a marked alteration in lipid metabolism similar to that observed with orotic acid feeding. The similarities of arginine deficiency and orotic acid feeding are discussed.     

Composition and concentration of lipoproteins in the serum of normal rats and rats deficient in essential fatty acids

A comparison is made of the concentration and chemical composition of serum lipoproteins of normal rats and rats deficient in essential fatty acids. The concentration of very low density lipoproteins (VLDL) and of low density lipoproteins (LDL) in serum of deficient rats is about half that found in normal rats, but the concentration of high density lipoproteins (HDL) is higher than normal and they contain an increased amount of cholesterol esters. The proportion of cholesterol that is esterified is much greater than normal in the serum of deficient rats. The deficiency of essential fatty acids also appears to result in compensating changes occurring in the composition of serum lipoproteins. In both VLDL and LDL of deficient rats the proportion of protein is raised and that of phospholipid lowered compared to normal, while the proportions of trigly ceride and cholesterol esters are unchanged.     

Effect of ethanol on utilization of plasma free fatty acids for liver triacylglycerol synthesis and its relation to hepatic triacylglycerol accumulation in rats

The effect of 3 different single doses of ethanol on the liver triacylglycerol concentration and on the metabolism of intravenously injected¹⁴C-oleic acid in fasted rats was studied. All 3 doses (2,3.75, and 6 g ethanol/kg body wt_ caused a rapid increased in the liver triacylglycerol concentration during the first 5–6 hr after the ethanol was given. Until the plasma ethanol concentration had fallen to low values, the high liver triacylglycerol levels were raised and were independent of the ethanol dose given. The incorporation of radioactivity from intravenously injected¹⁴C-oleic acid into liver triacylglycerols was increased over control values to the same extent in all rats given ethanol as long as the plasma ethanol concentration was above a low level. High rates of ethanol oxidation and increased utilization of plasma free fatty acids for liver triacylglycerol synthesis were closely correlated with the development and maintenance of the ethanol induced liver triacylglycerol accumulation.     

Labeling of liver and plasma lecithins after injection of 1–2-14C-2-dimethylaminoethanol and14C-L-methionine-methyl to choline deficient rats

Groups of rats were fed a choline-deficient (CD) or a choline-supplemented (CS) diet for 15 hr. Labeling of liver and plasma cephalins and lecithins was followed with time after injection of¹⁴C-L-methionine-methyl or 1–2-¹⁴C-2-dimethylaminoethanol, either alone or together with³H-S-adenosyl-L-methionine-methyl. A reduced concentration of liver and plasma lecithins was found in CD rats. In the same animals, labeling of the phospholipid fractions was considerably greater and faster than in CS rats. Administration of choline to rats previously fed the CD diet resulted in both an increased concentration of liver and plasma lecithins and a reduction in the labeling of liver and plasma lecithins to levels seen in control rats. These results suggest that in CD rats, while the overall synthesis of lecithins may be reduced due to insufficient availability of choline, the synthesis of lecithins via stepwise methylation of cephalins may be increased.     

Cholesterol metabolism in relation to aging and dietary fat in rats and humans

A review of research in the authors' laboratories regarding effects of dietary fat polyunsaturation upon longevity in rats and some aspects of the regulation of cholesterol metabolism with regard to age of rats and humans is presented. The longevity of the rat was found to be enhanced by consumption of dietary fat providing a polyunsaturated to saturated fatty acid (P/S) ratio of 0.3 to 1, corresponding to about 5–12% of energy (en%) as linoleate, compared with less or more polyunsaturated fat, mechanisms of the effects of the fats upon cholesterol metabolism were studied. With advancing age, there seems to be a decline in the rate of catabolism of cholesterol, resulting in longer retention in the body of the rat. In the human, there seems to be a decline in regulation of uptake of cholesterol by leukocytes and, therefore, perhaps other tissues, resulting in increased synthesis of cholesterol by the peripheral tissues. Moderate rather than high dietary consumption of polyunsaturated fat seems to be favorable to metabolic processes contributing to longevity. Presented at the AOCS meeting in Chicago, May 1983.     

Effect of relative humidity on the oxidative and physical stability of encapsulated milk fat

Milk fat was used in this work as a model to study the effects of humidity and physical properties on lipid oxidation. Although milk fat is considered a relatively stable fat because of its low content of unsaturated FA, it can oxidize significantly under certain conditions, as observed, for example, in the case, of dairy-based powders. Humidity and physical properties have a profound influence on the oxidative stability of powders, containing fat, and these factors affect the surface and encapsulated fractions of the fat differently. To examine these effects, encapsulated milk fat powders were stored under conditions of controlled relative humidity. Oxidation of the encapsulated fat as assessed by measurements of PV, losses of FA, and hexanal production increased, with increasing relative humidity (RH). At higher RH, moisture penetrates into the hydrophilic wall, interacting with and plasticizing the components, thereby making them less effective as moisture and oxygen barriers. Total oxidation of the powders was strongly influenced by the extent of oxidation in the encapsulated fraction (>98% of total lipids) although the surface fat fraction was oxidized more rapidly. Better protection against oxidation was obtained when fats were encapsulated and stored at 14 and 44% RH than at 52% RH.     

Effect of dietary fat on diabetes-induced changes in liver microsomal fatty acid composition and glucose-6-phosphatase activity in rats

Experimental diabetes may manifest itself in a defect in liver microsomal fatty acid desaturation and increased activity of glucose-6-phosphatase (G-6-Pase). The present study was designed to determine whether these changes could be normalized by a change in the dietary fat consumed. Control and streptozotocin-induced diabetic rats were fed nutritionally adequate diets which varied in fatty acid composition. Fatty acid analysis of liver microsomal phospholipids revealed that non-diabetic control animals fed saturated fat (beef tallow) or a diet high in ω3 fatty acids (fish oil) exhibited a significantly higher level of 18∶2ω6 and a lower level of 20∶4ω6 in the phosphatidylcholine and phosphatidylethanolamine fractions compared with diabetic animals. Control and diabetic animals fed the high linoleic acid diet had similar levels of 18∶2ω6 in the microsomal phosphatidylcholine and phosphatidylserine fractions. Microsomal G-6-Pase activity was higher in diabetic than in control animals. Activity of G-6-Pase was lower in microsomes of control animals fed the soybean oil or the fish oil diet, but was not significantly reduced in diabetic animals fed high polyunsaturated fats. Blood glucose levels were similar in control groups fed the different diets, but the plasma hemoglobin A1c level was lower in diabetic animals fed the soybean oil diet. Cholesterol and triglyceride levels were lower in diabetic animals fed the fish oil-based diet. The results suggest that dietary fat manipulation has the potential to change at least some of the abnormalities in the microsomal membrane in experimental diabetes.