This study was performed to investigate the effets of hesperidin extracted from tangerine peel on Cadmium (Cd) and lipid metabolism lipid peroxide formation, and antioxidative enzyme activities in rats. Forty-eight male Sprague-Dawley rats weighing 158.3$\pm$3.5g were blocked into eight groups according to body weight. Rats were raised for three weeks with diets containing 0 or 0.04%(w/w) cadmium chloride and 1%(w/w) extracted hesperidin from tangerine peel, commercial hesperidin or naringin. Food intake, weight gain and food efficiency ratio were significantly lower in the Cd-administered groups. The Cd concentrations in blood and liver and the Cd excretions in urine and feces were significantly higher in the Cd-administered groups. Among the Cd groups, blood Cd concentrations were decreased, fecal Cd excretions were increased, and Cd retenition ratios were decreased by feeding flavonoid diets. Plasma total lipid concentrations were significantly lower in the extracted hesperidin group, plasma triglyceride concentrations were significantly lower in the extracted hesperidin and naringin groups. Plasma HDL-cholesterol concentrations and HDL : total cholesterol ratios were increased by feeding flavonoids. Among the Cd groups, liver total lipid concentratons were decreased by feeding flavonoids. Fecal total lipid, fecal cholesterol, and fecal triglyceride excretions were significantly higher in the naringin group, and they were increased by feeding flavonoids among Cd groups. Thiobarbituric acid reactive substance concentrations in plasma and liver were higher in Cd groups, and were significantly decreased by feeding flavonoids. The activities of erythrocyte catalase, superoxide dismutase and glutathione peroxidase showed a tendency to increase by feeding. The activities of liver catalase, superoxide dismutase and glutathione peroxidase were not significantly affected by administering Cd or flavonoids. In conclusion, all flavonoids that were used in this experiment inhibited lipid peroxide formation in plasma and liver, but this effect was not caused by the increased in the activities of antioxidative enzymes.
Objective: High concentrate diets are widely used to satisfy high-yielding dairy cows; however, long-term feeding of high concentrate diets can cause subacute ruminal acidosis (SARA). The endocrine disturbance is one of the important reasons for metabolic disorders caused by SARA. However, there is no current report about thyroid hormones involved in liver metabolic disorders induced by a high concentrate diet. Methods: In this study, 12 mid-lactating dairy cows were randomly assigned to HC (high concentrate) group (60% concentrate of dry matter, n = 6) and LC (low concentrate) group (40% concentrate of dry matter, n = 6). All cows were slaughtered on the 21st day, and the samples of blood and liver were collected to analyze the blood biochemistry, histological changes, thyroid hormones, and the expression of genes and proteins. Results: Compared with LC group, HC group showed decreased serum triglyceride, free fatty acid, total cholesterol, low-density lipoprotein cholesterol, increased hepatic glycogen, and glucose. For glucose metabolism, the gene and protein expression of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase 1 in the liver were significantly up-regulated in HC group. For lipid metabolism, the expression of sterol regulatory element-binding protein 1, long-chain acyl-CoA synthetase 1, and fatty acid synthase in the liver was decreased in HC group, whereas carnitine palmitoyltransferase 1α and peroxisome proliferator activated receptor α were increased. Serum triiodothyronine, thyroxin, free triiodothyronine (FT3), and hepatic FT3 increased in HC group, accompanied by increased expression of thyroid hormone receptor (THR) in the liver. Conclusion: Taken together, thyroid hormones may increase hepatic gluconeogenesis, β-oxidation and reduce fatty acid synthesis through the THR pathway to participate in the metabolic disorders caused by a high concentrate diet.
The purpose of this thesis is to investigate whether taurine supplementation in combination with fructose improves both energy metabolism and exercise capacity. Eight collegiate female subjects were recruited for the study. Each subject went through threecross-over designs: control(fluid), fructose, and taurine plus fructose supplementation trials. Subjects received taurine supplementation 100 mg/kg a day for two weeks. After the supplementation, all subjects take 10% fructose at 15 min prior to exercise, immediately before exercise, and every 15 min during exercise. Subjects received 150 ml fluid as placebo during the same procedure. The subjects performed submaximal exercise at the exercise intensity of 60% for 45 min and then 80% of maximal oxygen uptake (VO2max) until exhaustion time. A 10ml blood sample was taken for measuring the level of glucose, ammonia, lactate, free fatty acids, and insulin every 15 min during exercise at 60% of VO2max. The blood glucose levels was significantly higher at 45 min and 50 min exercise after supplementation of fructose, and immediately before exercise and 50 min exercise after taurine plus fructose compared to the placebo trial. However, the values tended to be lower in taurine plus fructose supplementation compared to the fructose trial. The levels of both lactate and ammonia were significantly lower compared to the placebo, while the exhaustion time was significantly increased. The level of free-fatty acids was significantly lower at 30, 45, and 50 min after fructoseand fructose plus taurine supplementation compared to the placebo trial. The level of glucagon was significantly lower at 15, 30, 45, and 50 min after fructose and fructose plus taurine supplementation compared to the placebo trial. There was no differences in insulin concentration among three treatments. This thesis concludes that combined taurine and fructose supplementation prior to exercise may improve exercise tolerance time and energy metabolism, lowering the muscle fatigue factors such as lactate and ammonia.
The effect of cimetidine administration on the pharmacokinetic parameters of cyclosporine were determined in healthy voluteers. This study was performed in 10 volunteers of age ranged 22-48 years and body weight 48-62 kg. This study was performed with cross-over design. Mono cyclosporine and cyclosporine metabolites was extracted from whole blood analysed by fluororescence polarization immune assay (TDX-FLX, Abbott). After coadministration of cimetidine (300 mg) with cyclosporine (300 mg) orally, maximum concentration of mono cyclosporine was significantly increased $1221{\pm}143\;ng/ml\;to\;1562{\pm}184\;ng/ml$ (P<0.05), area under the time curve of cyclosporine (12 hr) also was significantly increased $7478{\pm}829\;ng/ml{\cdot}hr\;to\;9721{\pm}879\;ng/ml{\cdot}hr$ (P<0.05) and absolute baioavailability of cyclosporine was increased $50\pm5.6\%\;to\;57.6\pm6.1\%\;(P<0.05)$ compared to control group. The blood concentrations of cyclopsorine metabolites were significantly decrased (P<0.05) after coadministration of cimetidine. In cimetidine pretreated group, blood mono cyclosporine concentrations were increased significan시y $1220.0\pm203.00\;ng/ml\;to\;1510.0\pm204.00\;ng/ml$ compared with control group (P<0.05). In the mono cyclosporine pharmacokinetic parameter after oral administration absorption rate and maximum concentration were significantly higher in cimetidine coadministered and pretreated group than control group (P<0.05). The ratio of metabolites and mono cyclosporine concentrations was decreased significantly from $70.8\%\;in\;control\;to\;34.8\%$ in coadministration of cimetidine orally. As matter of facts these reults are considered to inhibition of cyclosporine hepatic metabolism and increasing of cyclosporine absorption rate in gastrointestinal tract because of maintaining cyclosporine stability in elevated gastric pH by cimetidine. We considered, it appeares that cimetidine increase bioavailability of cyclosporine by increasing oral absorption and by decreasing hepatic clearance. But the absorption and clearance of cyclosporine was highly variable individually, and therefore we consider that cyclosporine blood level monitoring would be essential in patients with cimetidine co-administration.
The definite mechanism in the control of triglyceride metabolism is not well understood. Nowadays, it has been known that the polymorphism of apolipoprotein C-III $Sst$ I was an important candidate for contributing to the control of triglyceride metabolism. In 298 Korean women aged 30 years or more, the genotypes of apolipoprotein C-III $Sst$ I were statistically compared with total blood cholesterol, triglyceride, high density lipoprotein, fasting blood sugar and hemoglobin A1c. Multiple logistic regression analysis was carried out to compare the odd-ratios of hypertriglyceridemia, hypercholesterolemia and diabetes mellitus with them. The differences among the polymorphic types ($S_1S_1$, $S_1S_2$, and $S_2S_2$) were not statistically significant in the distribution of triglyceride, total cholesterol, high density lipoprotein, fasting blood sugar, and hemoglobin A1c. There were not statistically significant in the odds ratios of the hypertriglyceridemia, hypercholesterolemia, and diabetes mellitus, neither. Those were not statistically significant. This study did not show that there was any association between the polymorphism of apolipoprotein C-III $Sst$ I and various laboratory values-total blood cholesterol, triglyceride, high density lipoprotein, fasting blood sugar and hemoglobin A1c.
The effects of dietary calcium levels on the blood pressure and calcium metabolism were investigated. Nine normotensive female college students having hypertention family history were participated in 4-week dietary expeiments. They were provided with either high Ca diet (HCa, average 797mg/day) or low Ca diet(LCa, average 225mg/day) during two weeks, each, consecutively. Sodium amounts of the body diets were 3566~4022mg/day, which were ordinary sodium intake levels in Korea. After the HCa, systolic blood pressures(SBR) in both seated and isogrip-seated postitions were decreased by about 2.5mgHg, comparing with those after the LCa(p<.05). Diastoilc blood pressures(DBP) were not changed by dietary calcium levels. Serum total Ca, ionized Ca, Mg and P levels and Ca/Mg ratio were not different between the HCa and the LCa. Serum parathyroid hormone(PTH) levels were similar between two diets, but individually in seven of nine subjects, the slightly lower values of PTH were observed after the HCa than after the LCa. Urinary excretion of Ca(p<.01), Mg(p<.05) and P(p<.1) were increased after the HCa comparing with the LCa, but Ca/Mg ratio were not different between the two diets. SBP was in positive correlations with boty urinary excretion of Ca(supine, r=.7356, p<.05) and urinary Ca/Mg ratio(isogrip-seated, r=.7483, p<.05). SBP was also negatively correlated with serum P level(supine, r=-.6930, p<.05) and DBP was in negative correlation with urinary P excretion(seated, r=-.8586, p<.01). Serum total and ionized Ca, Mg, Ca/Mg ratio were not significantly correlated with blood pressures.
The present study was designed to examine the effect of tested preparation, WY-91 (consisting of ginseng extract, ganoderma extract and Royal jelly) on alcohol-induced unusual metabolism(such as blood glucose(BG), triBlyceride(TG), and blood urea nitrogen(BUN) level in blood) and nrperinlental liver injury($CCl_4$ and high fat diet) in mice. WY-91 lowered the level of blood glucose (BG),triglyceride(TG) and blood urea nitrogen(BUN) induced by alcohol in a dose-dependent manner. This preparation could protect hepatic function from a damages caused by high fat diet and $CCl_4$ administration(p.o.).
The possible roles of spinal histamine receptors in the regulation of the blood glucose level were studied in ICR mice. Mice were intrathecally (i.t.) treated with histamine 1 (H1) receptor agonist (2-pyridylethylamine) or antagonist (cetirizine), histamine 2 (H2) receptor agonist (dimaprit) or antagonist (ranitidine), histamine 3 (H3) receptor agonist (${\alpha}$-methylhistamine) or antagonist (carcinine) and histamine 4 (H4) receptor agonist (VUF 8430) or antagonist (JNJ 7777120), and the blood glucose level was measured at 30, 60 and 120 min after i.t. administration. The i.t. injection with ${\alpha}$-methylhistamine, but not carcinine slightly caused an elevation of the blood glucose level. In addition, histamine H1, H2, and H4 receptor agonists and antagonists did not affect the blood glucose level. In D-glucose-fed model, i.t. pretreatment with cetirizine enhanced the blood glucose level, whereas 2-pyridylethylamine did not affect. The i.t. pretreatment with dimaprit, but not ranitidine, enhanced the blood glucose level in D-glucose-fed model. In addition, ${\alpha}$-methylhistamine, but not carcinine, slightly but significantly enhanced the blood glucose level D-glucose-fed model. Finally, i.t. pretreatment with JNJ 7777120, but not VUF 8430, slightly but significantly increased the blood glucose level. Although histamine receptors themselves located at the spinal cord do not exert any effect on the regulation of the blood glucose level, our results suggest that the activation of spinal histamine H2 receptors and the blockade of spinal histamine H1 or H3 receptors may play modulatory roles for up-regulation and down-regulation, respectively, of the blood glucose level in D-glucose fed model.
In the present study, the effect of intrathecal (i.t.) or intracerebroventricular (i.c.v.) administration with cholera toxin (CTX) on the blood glucose level was examined in ICR mice. The i.t. treatment with CTX alone for 24 h dose-dependently increased the blood glucose level. However, i.c.v. treatment with CTX for 24 h did not affect the blood glucose level. When mice were orally fed with D-glucose (2 g/kg), the blood glucose level reached to a maximum level at 30 min and almost returned to the control level at 120 min after D-glucose feeding. I.c.v. pretreatment with CTX increased the blood glucose level in a potentiative manner, whereas i.t. pretreatment with CTX increased the blood glucose level in an additive manner in a D-glucose fed group. In addition, the blood glucose level was increased in formalin-induced pain animal model. I.c.v. pretreatment with CTX enhanced the blood glucose level in a potentiative manner in formalin-induced pain animal model. On the other hand, i.t. pretreatment with CTX increased the blood glucose level in an additive manner in formalin-induced pain animal model. Our results suggest that CTX administered supraspinally or spinally differentially modulates the regulation of the blood glucose level in D-glucose fed model as well as in formalin-induced pain model.
The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
/
v.34
no.3
/
pp.70-79
/
2021
Objectives : The purpose of this study is to investigate the possibility of using herbal medicine for the management of psoriasis focusing on lipid metabolism. Methods : We reviewed studies about pathophysiology, and medical treatment of psoriasis, the relationship between psoriasis and metabolic syndrome and lipid metabolism, and herbal medicine on Pubmed and Google scholar. Results : Psoriasis is a chronic multi-organ inflammatory disease not limited to skin, and steroids, immuno-suppressants, and biological agents are used. It is known that psoriasis and metabolic syndrome act as mutual risk factors, and lipid metabolism are involved in psoriasis. The effects of various single herbal preparations and complex herbal extract, decoction on improving lipid metabolism have been consistently reported, and there was an improvement of psoriatic skin lesions and improvement of blood lipid levels through herbal medicine. Conclusions : Herbal medicine research in psoriasis has focused on the anti-inflammatory effect and the suppression effect of certain immune mediators. However, considering that psoriasis is affected by lipid metabolism and side effects of Western medicines, the use of herbal medicines for the purpose of controlling lipid metabolism in psoriasis is useful in aspects of reducing side effects of concurrent Western medicine, improving the severity of psoriasis, and managing metabolic risk factors.
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