• Journal of the East Asian Society of Dietary Life
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• v.15 no.6
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• pp.687-699
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• 2005

In order to investigate the effect of dietary zinc and phytic acid levels on protein metabolism in rats, male rats of Sprague-Dawley strains weighing approximately $60\~74g$ were fed different diets which contained 0, 0.35 and $1.05\%$ phytic acid each at 3 levels of zinc(0, 30 and 1,500 ppm zinc) for 28 days. Result obtained in this experiment are summarized as follows; 1. Body weight gait food consumption food efficiency ratio and protein efficiency ratio were lower in the rats fed zinc deficient diet(0 ppm zinc) than in those consuming 30 or 1,500 ppm dietary zinc, and the additional effect of phytic acid were not observed in all of then 2. Liver weight was lower in the rats fed 30 ppm zinc diet than in those fed 0 or 1,500 ppm-zinc diet but kidney and spleen weights were lower in the rats fed zinc deficient diet than in those fed 30 or 1,500 ppm-zinc diet Among organs measured only the liver appeared to be influenced by dietary phytic acid: the more the dietary phytic acid, the more the weight of liver, 3. Fecal nitrogen was decreased in the rats fed zinc deficient diet compared with those fed 30 or 1,500 ppm dietary zinc. Urinary nitrogen was increased in the rats fed $1.05\%$ dietary phytic acid compared with those fed 0.35 or $0\%$ dietary phytic acid Nitrogen retention of rat was influenced by neither dietary zinc nor phytic acid. 4. Urea nitrogen was decreased with increasing dietary zinc levels, and creatinine and uric acid levels were increased with increasing dietary zinc concentration or with additional quantity of phytic acid. Uric acid appeared to be influenced by zinc x phytic acid interaction; especially, the presence of phytic acid in the 30 ppm-zinc diet had significant effect on uric acid content. 5. Hemoglobin concentrations and hematocrit ratio were higher in the rats fed 30 ppm dietary zinc than in those fed 0 or 1,500 ppm-zinc diet Serum zinc concentration was increased with increasing dietary zinc levels. The content of total protein albumin and BUN and the ratio of albumin to globulin in serum, and protein content in liver were influenced by neither dietary zinc nor phytic acid.

• Molecules and Cells
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• v.46 no.8
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• pp.496-512
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• 2023

A fructose-enriched diet is thought to contribute to hepatic injury in developing non-alcoholic steatohepatitis (NASH). However, the cellular mechanism of fructose-induced hepatic damage remains poorly understood. This study aimed to determine whether fructose induces cell death in primary hepatocytes, and if so, to establish the underlying cellular mechanisms. Our results revealed that treatment with high fructose concentrations for 48 h induced mitochondria-mediated apoptotic death in mouse primary hepatocytes (MPHs). Endoplasmic reticulum stress responses were involved in fructose-induced death as the levels of phosho-eIF2α, phospho-C-Jun-N-terminal kinase (JNK), and C/EBP homologous protein (CHOP) increased, and a chemical chaperone tauroursodeoxycholic acid (TUDCA) prevented cell death. The impaired oxidation metabolism of fatty acids was also possibly involved in the fructose-induced toxicity as treatment with an AMP-activated kinase (AMPK) activator and a PPAR-α agonist significantly protected against fructose-induced death, while carnitine palmitoyl transferase I inhibitor exacerbated the toxicity. However, uric acid-mediated toxicity was not involved in fructose-induced death as uric acid was not toxic to MPHs, and the inhibition of xanthine oxidase (a key enzyme in uric acid synthesis) did not affect cell death. On the other hand, treatment with inhibitors of the nicotinamide adenine dinucleotide (NAD)⁺-consuming enzyme CD38 or CD38 gene knockdown significantly protected against fructose-induced toxicity in MPHs, and fructose treatment increased CD38 levels. These data suggest that CD38 upregulation plays a role in hepatic injury in the fructose-enriched diet-mediated NASH. Thus, CD38 inhibition may be a promising therapeutic strategy to prevent fructose-enriched diet-mediated NASH.

• Bulletin of the Korean Chemical Society
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• v.29 no.10
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• pp.1883-1884
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• 2008

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.149.1-149.1
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• 2003

Active ingredients, therapeutic and adverse effects of Aloe vera were comprehensively investigated. Aloe vera contains active components. including sugars, proteins, lipids, vitamins, minerals, phenolic compounds and other several compounds like phthalate esters, gibberellin, lectin-like substances, lignin, saponins, salicylic acid and uric acid. (omitted)

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.4
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• pp.1098-1101
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• 2004

This study was carried out to investigate the solubility of the ingredients of the kidney stone in the solution of the traditional oriental medicines. Calcium hydroxide, apatite and uric acid were chosen as the ingredients of the kidney stone. Plantaginis Semen, Lysimachiae Herba, Saururi Herba seu Rhizoma, Imperatae Rhizoma, Allium tuberosum Rottler were studied as the oriental medicines for the kidney stone. Calcium hydroxide had showed the very good solubility in the solution of Imperatae Rhizoma, the apatite had showed the good solubility in the solutions of Saururi Herba seu Rhizoma and Allium tuberosum Rottler. Uric acid had showed the mild solubility in the solution of Lysimachiae Herba and Saururi Herba seu Rhizoma.

• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.5
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• pp.1087-1091
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• 2007

In order to obtain practical application of Yiyiren-tang against gout disease, water extract of modified Gami-Yiyiren-tang(GYYT) added with Lonicera japonica is prepared through decoction and freeze drying. The effects were evaluated with blood sample from ICR mice treated with MSU intra-peritoneal injection 1 time a day, 3 days consecutively. The results were as follows. GYYT decreased C-reactive protein level and HDL cholesterol levels. But the creatinine, the LDL cholesterol levels, triglyceride and uric acid levels were not changed were decreased significantly. These results show that GYYT can be used effectively against the urate-related gout disease. But not better than effects of the Gami-daehwangmokdan-tang.

• YAKHAK HOEJI
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• v.23 no.3_4
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• pp.173-179
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• 1979

A dose, 1g/kg of ethanol produced experimental hyperuricemia in mouse. Ginseng saponins were tested for their ability to alter the hepatic xanthine oxidase activity and the blood level of uric acid in the ethanol-treated mouse. Intraperitoneal injection of ginseng saponin 4mg/kg markedly decreased the xanthine oxidase activity in the ethanol-treated mouse liver. It was also observed that ginseng saponin reduced the blood concentration of uric acid in experimentally induced hyperuricemia by alcohol treatment. In vitro, it was found that a low concentration of ginseng saponin in the reaction mixture incresed the hepatic xanthine oxidase activity, while a high concentration inhibited both enzyme preparations of normal and ethanol treated mice. In contrast with the xanthine oxidase, uricase activity was not influenced by ginseng saponin as well as in vivo. These results suggest there is a possibility that ginseng saponin may have some therapeutic effect on gout and other hyperuricemia syndrome.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2001.11a
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• pp.98-98
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• 2001

It has been suggested that hyperuricemia is related to the development of essential hypertension. Hypertensive patients with hyperuricemia has decreased glomerular filtration activity as compared to normotensive patients with hyperuricemia. These studies indicates uric acid concentrations in blood is associated with hypertension, Probenecid is an uricosuric agent which decreases uric acid reabsorption at the proximal tubule. Recently, we have shown that probenecid exerts anti-hypertensive action in Spontaneously Hypertensive Rats. Considering these results, I have designed a series of experiments to explore potential mechanism of antihypertensive action, of probenecid. In isolated rat thoracic aorta. probenecid significantly prevented phenylephrine-induced contraction of the blood vessel. When endothelium removed blood vessels were used, probenecid produced same effect as the intact blood vessels, indicating that probenecid directly act through the ${\alpha}$ -adrenergic receptor in vascular smooth muscles rather than through endothelium. These results suggest that one of the mechanism of antihypertensive effects of probenecid is due to the direct inhibition of ${\alpha}$ -adrenergic receptor in blood vessels.

• Journal of Genetic Medicine
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• v.10 no.1
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• pp.7-12
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• 2013

Familial Juvenile hyperuricemic nephropathy (FJHN) is a rare autosomal dominant disorder, characterized by early onset of hyperuricemia, gout and progressive kidney disease. Hyperuricemia prior to renal impairment and decreased fractional excretion of uric acid are hallmarks of FJHN. Renal dysfunction gradually appears early in life and results in end-stage renal disease usually between the ages of 20 and 70 years. FJHN is mostly caused by mutations in the uromodulin gene located at 16p12. The course of FJHN is highly variable. Treatment includes management for hyperuricemia, gout and progressive kidney disease. Individuals with gout have been usually treated with allopurinol. But controversy exists as to whether uric acid lowering therapy prevents the progression of chronic kidney disease.

• Journal of the East Asian Society of Dietary Life
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• v.7 no.1
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• pp.1-11
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• 1997

The purpose of this study was to describe the protein nutritional status of female collegians between nonvegetarian diet groups(14) and vegetarian diet groups(19). Daily intake, protein were calculated from food direct measurement. Urea/creatinine, muscle mass, fatique conditions and hematological parameter were calculated. Blood samples were analyzed for total protein, albumin ammonia, urea, uric acid, creatinine, BUN contents. The results obtained are summarized as following : 1) On total dietary intake, especially Fe, vitamin C, niacin intake, vegetarian groups were higher than non vegetarian groups. 2) On composition of EAA(essential amino acids), vegetarians were highter than non vegetarian of leucine contents, but were lower lysine and threonine contents. 3) On urea / creatinine excretion, vegetarians were higher than non begetarians. Muscle mass were non signicant, fatique condition, vegetarians were normal state. 4) Non vegetarians were increased serum albumin total protein, uric acid, ammonia but vegetarians were decreased BUN, ammonia after experimental diet intake. 5) In process of time after meal, non vegetarians were increased serum albumin total protein, BUN, but vegetarians were decreased ammonia.