Hepatic Subcellular Fractions Lipids in Rats Fed Millet (Sorghum vulgarie) at Different Protein Levels

Effect of feeding defatted millet (Sorghum vulgarie) flour at 5, 10 and 14.5% protein levels respectively for six weeks has been studied on rat liver mitochondrial, microsomal and supernatant fractions total lipids, cholesterol, triglycerides, total phospholipids, phosphatidyl choline and phosphatidyl ethanolamine. The results have been compared with rats fed casein at 10% level for the same period. The metabolism of liver subcellular fractions lipids of millet diet and casein diet fed rats has been studied by the incorporation of acetate-1-¹⁴C and . A significant increase in mitochondrial triglycerides of rats fed millet diet at 5 and 10% protein level, in microsomes of rats fed millet diet at 5, 10 and 15% protein levels and in supernatant fractions of rats fed millet diet at 5 and 15% protein levels was observed. A significant increase in total cholesterol in mitochondria and microsomes and a significant decrease in supernatant fraction of rats fed millet diet at 10% protein level was observed. A significant increase in mitochondrial total phospholipids, phosphatidyl choline and phosphatidyl ethanolamine in rats fed millet diet at 10% protein level and a decrease in these in rats fed millet diet at 5 per cent protein level was observed. In microsomes total phospholipids were increased in rats millet diet at 10% protein level and phosphatidyl choline was increased in rats fed millet diet at 15% protein level. Total phospholipids, phosphatidyl choline and phosphatidyl ethanolamine were significantly reduced in the supernatant fraction of rats fed millet at 10% protein level.

Incorporation of acetate-1-¹⁴C into nonsaponifiable fraction of mitochondria, microsomes and supernatant fractions of rats fed millet diet at 5 and 15 % protein levels was significantly greater, and in saponifiable fractions of the above subcellular fractions was greater in rats fed millet diet at 5 per cent protein level. The specific activity (counts/min/mg) of free cholesterol in mitochondria, microsomes and supernatant fractions of millet diet fed rats was significantly greater, whereas the specific activity of triglycerides was not significantly different from the controls. The acetate-1-¹⁴C specific activity of phosphatidyl choline and phosphatidyl ethanolamine was significantly greater in all the above subcellular fractions of millet diet fed rats (except of phosphatidyl choline in rats fed millet diet at 5 % protein level). The specific activities of phosphatidyl choline were significantly greater in mitochondria of rats fed millet diet at 5 % protein level and of phosphatidyl choline and phosphatidyl ethanolamine in microsomes and supernatant fractions of rats fed millet diet at 5 and 15% protein levels. The specific activities of phosphatidyl choline were significantly decreased in mitochondria and microsomes of rats fed millet diet at 10% protein level. The total acetate-1-¹⁴C activities (counts/min/g equivalent wet liver) of free and esterified cholesterol triglycerides, phosphatidyl choline and phosphatidyl ethanolamine showed that their synthesis from acetate-1-¹⁴C was either enhanced in millet diet fed rats or was comparable to the controls. The total activity of (counts/min/g equivalent wet liver) into phosphatidyl choline and phosphatidyl ethanolamine showed that their synthesis was decreased in microsomes of rats fed millet diet at 10% protein level, increased in rats fed millet diet at 5 and 15% protein levels.     

Effect of Retinol on Liver Lipid Metabolism of Rats

Effect of feeding 4.23, 16.94 and 27.53 mg of retinol daily for 10 days on the liver lipids of adult rats has been studied. Feeding of different amounts of retinol produced dose dependent toxicity symptoms in rats. Retinol feeding resulted in significant elevations of liver total lipids, total fatty acids, and glycerides, The amounts of liver esterified cholesterol were significantly raised in rats fed different amounts of retinol. Acetate-1-¹⁴C incorporation was increased in liver total cholesterol of rats fed 27.53 mg retinol and in free cholesterol of all retinol fed rats. Total ¹⁴C activity of hepatic triglycerides of retinol fed rats was the same as that of control, but their specific activity was decreased. Significant alterations were noted in phosphatidyl serine, lysophosphatidyl choline, lysophosphatidyl ethanolamine, sphingomyelin, phosphatidyl choline, phosphatidyl ethanolamine and phosphatidic acid and polyglycerophosphate fractions in liver rats fed different amounts of retinol.     

Effect of Feeding Millet (Sorghum vulgarie) Protein at Various Protein Levels on Adrenal Lipids of Rats

A significant increase in adrenal weight, total lipids, cholesterol phospholipids and glycerides (mono-and triglycerides) was observed in rats fed millet at 5, 10 and 15 % protein levels respectively for a period of six weeks as compared to rats fed casein at 10 per cent level. Increases in cholesterol were in both its free and esterified fraction. Adrenal phosphatidyl etha-nolamine was increased in all millet fed rats whereas phosphatidyl choline increased in M–15 % and decreased in M–5 % groups. Other phospholipid fractions viz. monophosphatidyl inositol, lysophosphatidyl ethanolamine, sphingomyeline, phosphatidic acid and polyglycerophosphatide also showed significant alterations in rats fed millet protein as compared to control. Incorporation of acetate–l–¹⁴C into adrenal lipids was lower and that of glucose–U–¹⁴C, palmitate–l–¹⁴C and NaH₂³²PO₄ was higher than the control.     

Effect of feeding protein deficient diet on phospholipid turnover and protein kinase C mediated protein phosphorylation in rat brain

Feeding of protein deficient diet is known to alter the transmembrane signalling in brain of rat by reducing total protein kinase C (PKC) activity. Phospholipid metabolism regulates the activation of PKC through generation of second messengers and the extent of PKC activation accordingly influences the magnitude of phosphorylation of its endogenous substrate proteins. Thus it was speculated that ingestion of protein deficient diet may modify the turnover rate of membrane phospholipids and magnitude of phosphorylation of endogenous substrate proteins of PKC. The experiments were conducted on rats fed on three different types of laboratory prepared diets viz. casein (20% casein), deficient (4% protein, rice flour as source of protein) and supplemented (deficient diet supplemented with L-lysine and DL-threonine) for 28 days. The metabolism of phosphoinositides (PIs) and phosphatidyl choline (PC) was studied by equilibrium labeling with [3H] myo inositol and [14C methyl] choline chloride respectively. The phosphorylation of endogenous substrate proteins of PKC was studied by using 32P-gamma-ATP followed by SDS-PAGE and autoradiography. The results suggest that in deficient group, there is an increased incorporation of [3H] myo inositol in PIs and inositol phosphate pool in comparison to the casein group. The phosphatidyl inositol (PI) turnover reduced, although there was a marginal increase in the phosphatidyl inositol monophosphate (PIP) and phosphatidyl inositol bis phosphate (PIP2). Supplementation of diet showed a reversal of the pattern towards control to a considerable extent. In the deficient group, PC metabolism showed an increased incorporation of [14C methyl] choline in choline phospholipids but decreased incorporation in phosphoryl choline in comparison with the casein group. The increase in total PC contents was significant but marginal in residue contents. The turnover rate of PC increased only marginally and that of residue declined. Supplementation of diet reduced the total contents of PC and residue, but the turnover rate of PC and residue remained still higher. Phosphorylation of endogenous proteins showed four different proteins of 78, 46, 33 and 16 kDa to be the substrates of PKC in casein group. In deficient group, phosphorylation of these proteins increased markedly while supplementation of diet had a reversing effect rendering the values to be intermediate between casein and the supplemented group. The changes in phospholipid metabolism and in phosphorylation of endogenous substrate proteins of PKC suggest that dietary protein deficiency causes alterations in transmembrane signalling mechanism in rat brain. These effects are partially reversed by improving the quality of proteins in the diet.     

Effect of Feeding Defatted Millet (Sorghum vulgarie) Flour at Different Protein Levels on Phospholipids of Rat Liver

Effect of feeding defatted millet flour at 5, 10 and 14.5 percent protein levels respectively to rats for 6 weeks has been studied on their liver phospholipids. Feeding of millet at these protein levels significantly increased liver total lipids and total glycerides as compared to control rats fed casein at 10 percent level. Liver phospholipids and phosphatidyl choline were significantly increased in rats fed millet at 10 and 14.5 percent protein levels whereas phosphatidyl ethanolamine was increased in all millet protein fed groups. Incorporation of (counts/liver/100 g body weight) into liver total phospholipids, phosphatidyl choline and phosphatidyl ethanolamine was significantly increased in M–5 and M–15% groups and it was decreased in phosphatidyl choline in rats of M–10% groups as compared to control. The effects of feeding millet on liver phospholipids are due to the quantity as well as quality of the millet protein.     

Incorporation of dietary [14C]arachidonic acid and [3H]eicosapentaenoic acid into tissue lipids during absorption of a fish oil emulsion.

A preferential incorporation of dietary arachidonic acid (20:4, n-6) into chyle lipoprotein phospholipids, a relative resistance of 20:4 esters of chyle triacylglycerol (TG) to hydrolysis by lipoprotein lipase, a preferential utilization of 20:4 for phospholipid acylation, and a low rate of oxidation of 20:4 are factors that may contribute to the differences seen in the incorporation into tissue lipids between absorbed 20:4 and the predominant dietary 16-18 carbon fatty acids. In this study we fed [14C]20:4 and [3H]eicosapentaenoic acid (20:5, n-3) as free fatty acids in a fish oil emulsion to rats and analyzed the radioactivity in different tissue lipids after 1, 2, and 4 h. The purpose was to examine the degree of similarity in the fate of the two major eicosanoid precursors during the absorption of a fish oil meal. The recovery after 2 and 4 h of 14C exceeded that of 3H in lipids of small intestine, serum, liver, heart, kidneys, and spleen. The differences increased with time, e.g., the liver contained 9.7 (+/- 0.7)% 3H and 17.9 (+/- 1.4)% of the 14C (P less than 0.001), and the upper half of the small intestine 10.0 (+/- 0.8)% of the 3H and 22.8 (+/- 1.1)% of the 14C (P less than 0.001) after 4 h. The 14C and 3H radioactivity per g tissue after 4 h ranked as follows: liver and brown adipose tissue greater than kidneys greater than heart, lungs, spleen, and serum greater than colon greater than white adipose tissue and testes, the differences between tissues being up to 50-fold. There were up to fourfold variations in the 14C/3H ratios between tissues after 4 h, the highest value being observed in the heart and the lowest in white adipose tissue. Of the radioactivity retained in liver and intestine, more 14C and 3H was in phospholipids and less in triacylglycerol (TG), the differences being largest in the liver, e.g., after 4 h 57.6 (+/- 0.8)% of the 14C and 29.9 (+/- 0.9)% of the 3H (P less than 0.001) in the liver was in phosphatidylcholine (PC). In both intestine and liver the highest 14C/3H ratios were found in phosphatidylinositiol (PI). Also phosphatidylethanolamine (PE) contained more 14C than 3H but the quantitative differences were relatively small after 4 h. In heart the proportions of 3H and 14C found in PE and PI did not differ, whereas more of the 14C was in PC and more of the 3H was in cardiolipin and phosphatidylserine.(ABSTRACT TRUNCATED AT 400 WORDS)     

Antihyperlipidemic effect of D-pinitol on streptozotocin-induced diabetic Wistar rats

D-pinitol (3-O-methyl-chiroinositol), an active principle of the traditional antidiabetic plant, Bougainvillea spectabilis, is claimed to exert insulin-like effects. This study was undertaken to evaluate the effect of D-pinitol on lipids and lipoproteins in streptozotocin (STZ)-induced diabetic Wistar rats. Rats were made type II diabetic by single intraperitoneal injection of STZ at a dose of 40 mg/kg body weight. STZ-induced diabetic rats showed significant (p < 0.05) increase in the levels of blood glucose and total cholesterol, triglycerides, free fatty acids, and phospholipids in serum, liver, kidney, heart, and brain. The levels of low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) cholesterol were significantly increased, and the level of high-density lipoprotein (HDL) cholesterol was significantly decreased in diabetic rats Oral administration of D-pinitol to STZ-induced diabetic rats showed significant (p < 0.05) decrease in the levels of blood glucose and total cholesterol, triglycerides, free fatty acids, and phospholipids in serum, liver, kidney, heart, and brain. The D-pinitol also lowered significantly (p < 0.05) LDL and VLDL cholesterol levels and increased significantly (p < 0.05) HDL cholesterol levels in the serum of diabetic rats. Thus, the present study clearly showed the antihyperlipidemic effect of D-pinitol in STZ-induced type II diabetic rats.     

Effect of aflatoxin B1 on lipids of rat tissues.

The effect of aflatoxin B1 on lipids of liver, kidney, adipose and plasma of rats was studied. A single dose administration (6 mg/kg body weight) increased liver and kidney weights and their total lipids within 24 h. Increase in liver lipids was confined mainly to phospholipid and cholesterol, whereas triglycerides showed a significant decrease. Adipose tissue triglycerides were, however, increased. Plasma showed decreases in triglycerides, free fatty acids and cholesterol. Incorporation studies with palmitate-1-14C revealed increased incorporation in adipose tissue lipids and decreased incorporation in liver and plasma lipids, thereby indicating an increased synthesis of lipids in adipose. Their mobilization to plasma was, however, inhibited, hence the low levels of triglyceride in liver. But the adrenals showed hypo-activity upon aflatoxin B1 administration.     

Effect of Dietary Composition on Lipids in Serum and in Liver of Rats Fed a Cystine-excess Diet

The effects of dietary composition on lipids in serum and in liver of rats fed with a cystine- excess diet were investigated.

When starch was used as the carbohydrate source, the addition of excess-cystine caused an increase in serum cholesterol and phospholipids, and hepatomegaly. Phospholipids in serum of rats fed with a cystine-excess diet containing 5% corn oil were higher than those with a cystine-excess diet that was low in corn oil (0.1 %). The addition of konjac mannan and pectin prevented hypercholesterolemia, and the rise in phospholipids in serum was prevented by the addition of konjac mannan.

Liver cholesterol (mg/liver/100 g of body wt.) increased in rats fed with a cystine-excess diet.

The addition of excess cystine to a diet containing sucrose as the carbohydrate source resulted in a marked increase of cholesterol in serum and liver, and a decrease of serum triglycerides.

The replacement of starch by sucrose in the cystine-excess diet increased liver cholesterol.

Lipids, cholesterol, phospholipids and triglycerides in the liver, but not phospholipids, when expressed as mg per g of liver for rats fed with the diets containing sucrose, increased when compared to those for rats fed with the diets containing starch. In contrast, serum triglycerides increased.     

Cholesterol gallstones in alloxan-diabetic mice

Normal and alloxan-diabetic male mice (Crj-ICR) were fed a diet containing 0.5% cholesterol for 5 and 10 weeks, and gallbladder bile was analyzed for cholesterol, phospholipids and bile acids, feces for sterols and bile acids, and plasma and liver for cholesterol, phospholipids, and triglycerides. Normal mice developed no gallstones but the diabetic mice developed cholesterol gallstones with an incidence of 70% by 5 weeks and 80% by 10 weeks after feeding of the cholesterol diet. Diabetic mice fed the ordinary diet also developed stones (23%) by 10 weeks. In the diabetic mice, the gallbladder was enlarged about threefold, and biliary lipid concentration, diet intake, and fecal excretion of sterols and bile acids increased but body weight decreased. Cholic acid and beta-muricholic acid comprised over 40% each of the total biliary bile acids in normal mice, but cholic acid increased to about 80% and beta-muricholic acid decreased to a few percent in the diabetic mice. Fecal excretion of bile acids increased after cholesterol feeding in both normal and diabetic mice, but the increased bile acid in the normal animals was beta-muricholic acid and that in the diabetic mice was deoxycholic acid. The mice that developed gallstones showed a marked increase in biliary cholesterol value and decreases in gallbladder bile and bile acid concentration, but no difference in biliary and fecal bile acid composition, bile acid synthesis, fecal sterols, or plasma and liver lipid levels. Cholesterol absorption was increased in the diabetic mice when examined by plasma 14C/3H ratio and fecal 14C-labeled sterol excretion after a single oral administration of [14C]cholesterol and a simultaneous intravenous injection of [3H]cholesterol. These data led to the conclusion that cholesterol gallstones developed in alloxan-diabetic mice fed excess cholesterol, due to the hyperphagia and the enhancement of cholesterol absorption caused by increases in the synthesis and secretion of cholic acid.     

Lipid metabolism in rabbits exposed to paraquat aerosol

In order to examine the effects of paraquat on pulmonary lipid metabolism rabbits were exposed to double distilled water by aerosol, or 250 mg paraquat in double distilled water. One hour prior to sacrifice, a group of rabbits were injected with [2?¹⁴C]-acetate. The levels of phospholipids, fatty acids, cholesterol, and triglycerides were determined as were their ¹⁴C-contents in the lung, broncoalveolar lavage fluid, serum, and liver. The serum of paraquat-exposed animals contained significantly increased levels of phospholipids, cholesterol, and triglycerides. Liver, lung, and bronchoalveolar lavage contained less than or equal to control levels of phospholipids, cholesterol, and triglycerides. Percent of palmitate in the hepatic fatty acid profile was slightly increased in liver but not in lung. The source of the increased lipids in the serum is unknown.     

Maturing patterns of organ weights in mice selected for rapid postweaning gain

Summary Correlated responses to selection for increased 3–6 week postweaning gain in male mice were estimated for seven internal organs (testes, spleen, liver, kidneys, heart, small intestine (S intest) and stomach) weighed at specific degrees of maturity in body weight (37.5, 50.0, 62.5, 75.0, 87.5 and 100%). Correlated responses in organ weights were generally large, but the magnitude and direction of response depended upon whether 1) comparisons were made at the same age, degree of maturity or body weight and 2) absolute or proportional organ weights were used. The selected line (M16) weighed more and had larger organ weights than controls (ICR) when compared at either the same degree of maturity or the same age, indicating positive genetic correlations between body weight and the respective organ weights. Positive correlated responses were found in spleen weight/body weight at all degrees of maturity and in liver and S intest weights as a proportion of body weight at some degrees of maturity. Testes, kidneys, heart and stomach weights as a proportion of body weight had negative correlated responses, though this was consistent only for kidneys across all degrees of maturity. Correlated responses in organ weights adjusted for body weight by covariance analysis were positive for spleen, S intest and stomach and negative for testes and kidneys. Based on the constrained quadratic model, degree of maturity in organ weight relative to degree of maturity in body weight responded positively for testes, kidneys and S intest and negatively for spleen and liver. Selection for increased growth caused negative correlated responses in allometric growth of testes, kidneys, S intest and stomach.Paper No. 10,545 of the Journal Series of the North Carolina Agricultural Research Service, Raleigh, 27695-7601. The use of trade names in this publication does not imply endorsement by the North Carolina Agricultural Research Service of the products named, nor criticism of similar ones not mentioned     

Hypolipidaemic efficacy of Capparis decidua fruit and shoot extracts in cholesterol fed rabbits

High fat diet caused significant (8-fold) increase in serum total cholesterol in rabbits. Administration of C. decidua fruit extract (50% ethanolic) at the dose of 500 mg/kg body weight significantly reduced serum total cholesterol (61%), LDL cholesterol (71%), triglycerides (32%) and phospholipids (25%). Similarly C. decidua shoot extract lowered serum total cholesterol (48%), LDL cholesterol (57%), triglycerides (38%) and phospholipids (36%).The cholesterol content of aorta was decreased by 44 and 28% in fruit and shoot extract treatment respectively. The HDL to total cholesterol ratio and atherogenic index was significantly decreased in plant extract treated groups suggesting antiatherosclerotic nature of these plant extract. These results reveal the hypolipidaemic potential of C. decidua fruit and shoot.     

Effect of acute hypobaric hypoxia on 32-P incorporation into phospholipids of alveolar surfactant, lung, liver and plasma of rat.

Exposure of adult rats to hypobaric hypoxia caused hypolipidemia, hypotriglyceridemia and hypophospholipidemia. Hypobaric hypoxia produced an increase in liver triglyceride and cholesterol levels and a decrease in lung triglyceride, total phospholipid and phosphatidyl choline. The proportion of phosphatidyl choline in the pulmonary surfactant fraction I phospholipids (responsible for reducing surface tension) decreased (55.2% as compared to 80.4% in control animals). Incorporation of 32-P into liver phosphatidyl ethanolamine was significantly increased, incorporation into lung phosphatidyl choline and phosphatidyl ethanolamine was increased whereas a decreased incorporation into plasma phosphatidyl choline was observed. The data suggest an enhanced lipid synthesis in liver with a probable impairment of mobilization into plasma.     

Hypervitaminosis A and Liver Phospholipids

Effect of daily oral feeding of 33 mg retinol for nine days on the liver phospholipids of rats has been studied. As early as two days after feeding retinol an increase in the amounts of liver triglycerides, proteins, phospholipids, and cholesterol was noted which kept increasing and reached the peak concentration 6 days after daily retinol feeding and thereafter a decrease in their amounts was noted. Hepatic phospholipid fractions viz. phosphatidyl choline, phosphatidyl ethanolamine, phosphatidic acid and polyglycerol phosphatide, phosphatidyl inositol, phosphatidyl serine, sphingomyelin, lysophosphatidyl ethanolamine and lysophos- phatidyl choline showed the same pattern. Labelling of these phospholipids with NaH₂³²PO₄ in rats fed daily 33 mg of retinol for a period of two days also exhibited the pattern which was observed in their amounts two days after daily feeding of retinol. The results suggest a close relationship between the metabolism of hepatic triglycerides and phospholipids of rats fed excessive amounts of retinol.     

CHANGES IN CEREBRAL CORTICAL LIPIDS IN COBALT-INDUCED EPILEPSY

Abstract– In control rats and in rats rendered epileptic by insertion of cobalt slivers into the cerebral cortex, total free fatty acids, free cholesterol, esterified cholesterol, triglycerides and phospholipids were measured in normal and lesion areas of cerebral cortex. The cortical lipid profile of the adult rat resembled that of the whole brain of very young rats rather than that of adult whole brain, with the principal differences from whole adult brain being lower total lipid content, increased proportions of phosphatidyl choline in the phospholipid fraction, and higher levels of cholesterol esters. Cobalt-induced epilepsy was associated with significant changes in cerebral cortical lipids in the area of the lesion and in the non-necrotic tissue adjacent to the lesion. The total lipid in the area of the lesion decreased sharply as a result of reductions in free cholesterol and total phospholipids. The levels of cholesterol esters and triglycerides increased in the area of the lesion, and cholesterol esters were also increased in the adjacent tissue. In addition there were decreases in the proportion of phosphatidyl ethanolamine in the phospholipids from the lesion site and adjacent tissue and decreases in the proportions of oleic, arachidonic and nervonic acids (unsaturated acids), and an increase in the proportions of lignoceric acid in the phospholipids. In the site of the lesion only, we observed a decrease in phospholipid palmitic acid and an appreciable increase in the proportions of an unidentified long-chained fatty acid.     

Lipid composition of gametes and embryos of the sea urchin Strongylocentrotus intermedius at early stages of development

The lipid composition of sea urchin gametes and embryos was examined in detail by micro thin-layer chromatography (tlc) and gas-liquid chromatography (glc). Lipids of unfertilized eggs contain 53.7% triglycerides, 33.2% phospholipids, and 9.4% cholesterol, while spermatozoa lipids consist of 65.0% phospholipids, 15.5% cholesterol, and no triglycerides. Phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidylserine (PS), phosphatidylinositol (PI), diphosphatidylglycerol (DPG), and lysophosphatidylcholine (LPC) were identified among the phospholipids of both eggs and spermatozoa. The major part of egg and embryo PE was present as plasmalogen. After fertilization and the first cleavage, phospholipid content decreased from 33.2 to 29.4%, but the amount of phospholipids returned to the 33.2% level by the blastula stage and reached 39.7% by the pluteus stage. Lipid class composition showed no qualitative changes during development, but concentrations of PE, PS, LPC, and cholesterol increased, while those of PC, PI, and triglycerides decreased during the process. The principal fatty acids of neutral and polar lipid fractions are 14:0, 16:0, 18:1, 18:4, 20:1, 20:4, and 20:5. Their relative content underwent some changes during development.     

Testosterone & lipid metabolism in rabbits.

Testosterone and lipid metabolism was studied in rabbits. The effect of orchidectomy in rabbits fed normal diets and of testosterone propionate administration to these animals on total cholesterol, phospholipids, and triglycerides of serum, liver, aortic arch, thoracic aorta, and abdominal aorta as well as the activity of lipoprotein lipase in the aortic segments and heart was investigated. With a few exceptions, total cholesterol,phospholipids, and triglycerides increased in these tissues in orchidectomized animals and testosterone counteracted this increase. 3 segments of the aorta revealed variations in response to lipids in the orchidectomized animals as well as in the testosterone administered. Lipoprotein lipase activity decreased in the heart and the 3 aortic segments on orchidectomy, and testosterone administration caused increased enzyme activity.     

Time-dependent effects of exposure to static magnetic field on glucose and lipid metabolism in rat

In the following study, we investigate the effects of static magnetic field (SMF) (128 mT, 1 h/day during 5 or 15 consecutive days) on anthropometric parameters, glucose and lipid metabolism in rats. Exposure to SMF during 5 days induced a decrease (-8%, p < 0.05) in relative liver weight and serum insulin concentration (-56%, p < 0.001), while blood glucose level was increased (+10%, p < 0.001). By contrast, the same treatment failed to alter body weight, relative kidney weight and levels of lactate, cholesterol, triglycerides and phospholipids. Exposure to SMF during 15 days induced a decrease (-15 %, p < 0.001) in body weight, liver weight (-15 %, p < 0.05), insulin concentration (-63%, p < 0.001), plasmatic lactate level (-55%, p < 0.05) and increased glucose (+24%, p < 0.001), cholesterol (+30%, p < 0.01,) and phospholipids levels (+58%, p < 0.001), whereas, triglycerides decreased (-28%, p < 0.001). These results showed that SMF effects on glucose and lipid metabolism are time-dependent.     

Preventive effect of naringin on lipids, lipoproteins and lipid metabolic enzymes in isoproterenol-induced myocardial infarction in Wistar rats

This study was designed to evaluate the preventive effect of naringin in isoproterenol (ISO)-induced myocardial infarction (MI) in rats. Rats were pretreated with naringin (10, 20, and 40 mg/kg body weight) orally for a period of 56 days. After the treatment period, ISO (85 mg/kg body weight) was administered subcutaneously to rats at an interval of 24 h for 2 days. There was a significant increase in the levels of total, ester, and free cholesterol, triglycerides (TG), and free fatty acids (FFA) in serum and heart and decrease in heart phospholipids (PL) in ISO-induced rats. Altered levels of lipoproteins and activities of 3-hydroxy-3-methylglutaryl-Coenzyme reductase A in liver and heart, lecithin cholesterol acyl transferase and lipoprotein lipase in plasma were also observed in ISO-induced rats. Pretreatment with naringin (10, 20, and 40 mg/kg) for a period of 56 days significantly decreased the levels of total, ester, and free cholesterol, TG, FFA in serum and heart and increased PL in heart. It also minimized the alterations in serum lipoproteins and lipid metabolic enzymes in ISO-induced rats. Thus, naringin has a lipid-lowering effect in ISO-induced MI rats.