• Childhood Kidney Diseases
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• v.8 no.2
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• pp.195-204
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• 2004

Purpose: Hypophosphatemic rickets is a hereditary disease, characterized by hypophosphatemia due to renal phosphate wasting, impaired renal production of 1,25-dihydroxyvitamin $D_3$, rachitic bone deformities and impaired growth. The purpose of this study is to provide clinical profiles of patients with hypophosphatemic rickets in our hospital. Methods: Between July 1983 and February 2004, 56 patients were diagnosed as having hypophosphatemic rickets. The medical records of these patients were reviewed retrospectively. Clinical manifestations, family histories, laboratory data, treatment outcomes were described. Results: Fifty six patients were enrolled in this study. The average age at symptom onset and diagnosis were 20 months and 5 years respectively. Fourteen patients had family histories. The main clinical manifestations were bow legs and short stature. There was a significant negative correlation between the ages and the height z-scores at the time of diagnosis(r=-0.47, P=0.005). Initial laboratory data showed normocalcemia, hypophosphatemia, elevated serum alkaline phosphatase, decreased tubular reabsorption of phosphate and a normal range of 1,25-dihydroxyvitamin $D_3$ Radiographic examinations of bone revealed fraying, widening and cupping of the metaphyseal ends. Treatment consisted of Joulie solution and vitamin D metabolites, and resulted in improved biochemical and radiographic findings. However, height z-scores remained essentially unchanged(P=0.224). Complications of treatment were frequently observed, including hyperparathyroidism, nephrocalcinosis, and hypercalciuria. Sixteen patients had corrective osteotomy and 4 of them underwent leg lengthening together. Conclusion: There was a gap of several years between the onset of symptoms and the diagnosis. Early treatment seems to be essential to growth. For the earlier treatment, the offsprings of affected parents should be followed up closely.

• Nutritional Sciences
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• v.7 no.4
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• pp.208-213
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• 2004

In this study, we examined the effects of dietary 1,3-diacylglycerol (DG) compared to conventional triacylglycerol (TG) oil on the postprandial response of total and chylomicron TG, glucose, insulin, and free fatty acid (FFA). This study was conducted using a cross-over design. Ninety subjects participated in the high-fat meal tolerance test where they were randomly assigned to consume two experimental sandwiches containing mayonnaise with TG or DG oil with a seven-day interval. Blood samples were collected before ingestion and at 2, 3, 4 and 6 hr time point after ingestion and analyzed for total and chylomicron TG, glucose, insulin, FFA and phospholipid fatty acid composition. Both TG and DG ingestion had similar effects on postprandial TG response, but a different response from chylomicron TG. Compared with the TG group, TG levels were significantly lower only at 6 hr time point in the DG group. On the other hand, chylomicron TG rose steeply at 2 hr time point and decreased faster in this group. Also, the adjusted value to fasting levels was the same as the unadjusted level. Fasting levels and net differences in insulin were significantly lower at 3 hr time point where chylomicron TG levels were significantly lower in the DG group. But those of glucose and FFA in the TG and DG groups did not differ significantly. Fasting and postprandial levels of fatty acid composition in serum phospholipids in the two groups did not differ significantly. In conclusion, this study indicated that one could reduce the magnitude of postprandial lipemia without influencing glucose metabolism by consumning DG oil as a substitute for TG oil. Based on the correlation of coronary artery disease and postprandial lipemia, dietary DG ingestion might have a beneficial effect in treating such a disease. Further studies are required to clarify the long-tenn effects of dietary DG on blood lipid levels in humans.

• Journal of the Korea Society of Computer and Information
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• v.26 no.8
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• pp.197-207
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• 2021

Relationship between bone mineral density (BMD) and type 2 diabetes is still inconsistent. Recently, many epidemiologic data show that fracture risk is increased in type 2 diabetic patients regardless of BMD status. In this study, we used nation-wide data from 2008 to 2011 Korea National Health and Nutrition Examination Survey (KNHANES) to analyze the BMD status in patients with type 2 diabetes compared to non-diabetics. We included subjects aged 50 years or older in men (N=2,959, 2,430 without diabetes, 529 with type 2 diabetes) and postmenopausal women (N=2,902, 2,479 without diabetes, 423 with type 2 diabetes). Subjects with history of medication for osteoporosis or with illness or malignancy affecting bone metabolism were excluded. Data of anthropometric measurements and demographic characteristics were collected by trained examiner. Serum was separated from peripheral venous blood samples obtained after 8 hours of fasting. BMD was measured at lumbar spine and femur using dual-energy X-ray absorptiometry (DXA). There was a significant positive association between lumbar spine BMD and type 2 diabetes after adjusting age, gender, body mass index, monthly house income, education level, physical activity, daily calcium intake and vitamin D concentration by multiple regression analysis in all subjects. In the subgroup analysis by gender, this association was maintained both in male and female after adjusting those confounding factors. However, femur BMD was not different between type 2 diabetic and non-diabetic subjects. In conclusion, lumbar spine BMD was significantly higher in type 2 diabetic patients aged 50 years or more in men and postmenopausal women compared to non-diabetic subjects.

• Journal of Yeungnam Medical Science
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• v.18 no.2
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• pp.226-238
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• 2001

Background: Anemia in chronic renal failure plays an important role in increasing morbidity of dialysis patients. The causes of the anemia are multifactorial. With using of erythropoietin(EPO) most of uremia-induced anemia can be overcome. However, about 10% of renal failure patients shows EPO-resistant anemia. Hyporesponsiveness to EPO has been related to many factors: iron deficiency, aluminum intoxication, inflammations, malignancies and secondary hyperparathyroidism. So I evaluated the improvement of EPO responsiveness after correction of above several factors. Materials and Methods: Seventy-two patients on hemodialysis over 6 months were treated with intravenous ascorbic acid(IVAA, 300 mg t.i.w. for 12 weeks), After administration of IVAA for 12 weeks, patients were classified into several groups according to iron status, serum aluminum levels and i-PTH levels. Indivisualized treatments were performed: increased iron supplement for absolute iron deficiency, active vitamin D3 for secondary hyperparathyroidism and desferrioxamine(DFO, 5 mg/kg t.i.w.) for aluminum intoxication or hyperferritinemia. Results: 1) Result of IVAA therapy for 12 weeks on all patients(n=72). Hemoglobin levels at 2, 4, 6 week were significantly elevated compared to baseline, but those of hemoglobin at 8, 10, 12 week were not significantly different. 2) Result of IVAA therapy for 20 weeks on patients with 100 ${\mu}g/l$ ${\leq}$ ferritin < 500 ${\mu}g/l$ and transferrin saturation(Tsat) below 30%(n=30). After treatment of IV AA for 12 weeks, patients were evaluated the response of therapy according to iron status. Patients with 100 ${\mu}g/l$ ${\leq}$ ferritin < 500 ${\mu}g/l$ and Tsat below 30% showed the most effective response. These patients were treated further for 8 weeks. Hemoglobin levels at 2, 4 week were significantly increased compared to baseline with significantly reduced doses of EPO at 2, 4, 6, 10, 12, 16, 20 week. Concomitantly significantly improvement of Tsat at 2, 6, 16, 20 week compared to baseline were identified. 3) Result of IVAA therapy for 12 weeks followed by DFO therapy for 8 weeks on patients with serum aluminum above 4 ${\mu}g/l$(n=12) Hemoglobin levels were not significantly increased during IVAA therapy for 12 weeks but dosages of EPO were significantly decreased at 2, 4, 6, 8 week during DFO therapy compared to pre-treatment status. Conclusion: IVAA can be helpful for the treatment of the anemia caused by functional iron deficiency and can reduce the dosage of EPO for anemia correction. And administration of low dose DFO, in cases of increased serum aluminum level, can reduce the requirement of EPO.

• Proceedings of the Korean Nutrition Society Conference
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• 1995.11b
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• pp.11-34
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• 1995

Growth hormone (GH) plays a key role in regulating postnatal growth and can stimulate growth of animals by acting directly on specific receptors on the plasma membrane of tissues or indirectly through stimulating insulin-like growth factor (IGF)-I synthesis and secretion by the liver and other tissues. IGF-I and IGF-Ⅱ are polypeptides with structural similarity with proinsulin that stimulate cell proliferation by endocrine, paracrine and autocrine mechanisms. The initial event in the metabolic action of IGFs on target cells appears to be their binding to specific receptors on the plasma membrane. Current evidence indicates that the mitogenic actions of both IGFs are mediated primarily by binding to the type I IGF receptors, and that IGF action is also mediated by interactions with IGF-binding proteins (IGFBPs). Six distinct IGFBPs have been identified that are characterized by cell-specific interaction, transcriptional and post-translational regulation by many different effectors, and the ability to either potentiate or inhibit IGF actions. Nutritional deficiencies can have their devastating consequence during growth. Although IGF-I is the major mediator of GH's action on somatic growth, nutritional status of an organism is a critical regulator of IGF-I and IGFBPs. Various nutrient deficiencies result in decreased serum IGF-I levels and altered IGFBP levels, but the blood levels of GH are generally unchanged or elevated in malnutrition. Effects of protein, energy, vitamin C and D, and zinc on serum IGF and IGFBP levels and tissue mRNA levels were reviewed in the text. Multiple factors are involved in the regulation of intestinal epithelial cell growth and differentiation. Among these factors the nutritional status of individuals is the most important. The intestinal epithelium is an important site for mitogenic action of the IGFs in vivo, with exogenous IGF-I stimulating mucosal hyperplasia. Therefore, the IGF system appears to provide and important mechanism linking nutrition and the proliferation of intestinal epithelial cells. In order to study the detailed mechanisms by which intestinal mucosa is regulated, we have utilized IEC-6 cells, an intestinal epithelial cell line and Caco-2 cells, a human colon adenocarcinoma cell line. Like intestinal crypt cells analyzed in vivo or freshly isolated intestinal epithelial cells, IEC-6 cells and Caco-2 cells possess abundant quatities of both type Ⅰ and type Ⅱ IGF receptors. Exogenous IGFs stimulate, whereas addition of IGFBP-2 inhibits IEC-6 cell proliferation. To investigate whether endogenously secreted IGFBP-2 inhibit proliferation, IEC-6 cells were transfected with a full-length rat IGFBP-2 cDNA anti-sense expression construct. IEC-6 cells transfected with anti-sense IGFBP-2 protein in medium. These cells grew at a rate faster than the control cells indicating that endogenous IGFBP-2 inhibits proliferation of IEC-6 cells, probably by sequestering IGFs. IEC-6 cells express many characteristics of enterocyte, but do not undergo differentiation. On the other hand, Caco-2 cells undergo a spontaneous enterocyte differentiation. On the other hand, Caco-2 cells undergo a spontaneous enterocyte differentiation after reaching confluency. We have demonstrated that Caco-2 cells produce IGF-Ⅱ, IGFBP-2, IGFBP-3, and an as yet unidentified 31,000 Mr IGFBP, and that both mRNA and peptide secretion of IGFBP-2 and IGFBP-3 increased, but IGFBP-4 mRNA and protein secretion decreased after the cells reached confluency. These changes occurred in parallel to and were coincident with differentiation of the cells, as measured by expression of sucrase-isomaltase. In addition, Caco-2 cell clones forced to overexpress IGFBP-4 by transfection with a rat IGFBP-4 cDNA construct exhibited a significantly slower growth rate under serum-free conditions and had increased expression of sucrase-isomaltase compared with vector control cells. These results indicate that IGFBP-4 inhibits proliferation and stimulates differentiation of Caco-2 cells, probably by inhibiting the mitogenic actions of IGFs.

• Korean Journal of Poultry Science
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• v.42 no.1
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• pp.33-40
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• 2015

This study was conducted to investigate the effects of dietary quercetin on growth performance, blood biochemical parameters, immunoglobulin, and blood antioxidant activity in broiler chickens. Three hundred twenty one-day old Ross broilers were divided 8 treatments (C(-), basal diet; C(+), basal diet with antibiotics; vitamin E 20 IU; vitamin E 200 IU; quercetin 20 ppm; quercetin 200 ppm; methoxylated quercetin 20 ppm; methoxylated quercetin 200 ppm) with 4 replicates and 10 birds per replicate. Birds were reared for 35 days and their feed intake and weight gain were measured weekly. At 35d, eight birds of average weight from each replicate were selected for blood collection and analysis. Weight gain of birds in the groups fed quercetin was higher when compare to NC but there was no significant difference. In the serum, creatinine, BUN and AST in quercetin groups significantly decreased compared to those of control (NC and PC) (P<0.05). The contents of IgA and IgM were significantly lower in quercetin groups than those of NC (P<0.05). SOD like activity and MDA content tended to decrease in quercetin groups, however, there was no significant difference among treatments. In conclusion, supplemental quercetin to poultry diet could be positive aspect on performance and blood metabolites. Optimum adding levels was more than 20 ppm.

• The Korean Journal of Pharmacology
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• v.32 no.3
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• pp.407-416
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• 1996

The reactive intermediates formed during the metabolism of therapeutic agents, toxicants and carcinogens by cytochromes P450 are frequently capable of covalently binding to tissue macromolecules and causing tissue damage. It has been shown that YH439, a congener of malotilate, is effective in suppressing hepatic P450 2E1 expression. The present study was designed to further establish the mechanistic basis of YH439 protection against toxicant by assessing its effects against chemical-mediated potentiated hepatotoxicity. Retinoyl palmitate (Vit-A) pretreatment of rats for 7 days substantially enhanced carbon tetrachloride hepatotoxicity, as supported by an ${\sim}5-fold$ increase in serum alanine aminotransferase (ALT) activity, as compared to $CCl_4$ treatment alone. The elevation of ALT activity due to Vit-A was completely blocked by the treatment of $GdCl_3$ a selective inhibitor of Kupffer cell activity. Concomitant pretreatment of rats with both YH439 and Vit-A resulted in a 94% decrease in Vit-A-potentiated $CCl_4$ hepatotoxicity. YH439 was also effective against propyl sulfide-potentiated $CCl_4-induced$ hepatotoxicity. Whereas propyl sulfide (50 mg/kg, 7d) enhanced $CCl_4-induced$ hepatotoxicity by >5-fold, relative to $CCl_4$ treatment alone, concomitant treatment of animals with both propyl sulfide and YH439 at the doses of 100 and 200 mg/kg prevented propyl sulfide-potentiated $CCl_4$ hepatotoxicity by 35% and 90%, respectively. Allyl sulfide, a suppressant of hepatic P450 2E1 expression, completely blocked the propyl sulfide-enhanced hepatotoxicity, indicating that propyl sulfide potentiation of $CCl_4$ hepatotoxicity was highly associated with the expression of P450 2E1 and that YH439 blocked the propyl sulfide-enhanced hepatotoxicity through modulation of P450 2E1 levels. Propyl sulfide- and $CCl_4-induced$ stimulation of lipid peroxidation was also suppressed by YH439 in a dose-related manner, as supported by decreases in malonedialdehyde production. The role of P450 2E1 induction in the potentiation of $CCl_4$ toxicity and the effects of YH439 were further evaluated using pyridine as a P450 2E1 inducer. Pyridine pretreatment substantially enhanced the $CCl_4$ hepatotoicity by 23-fold, relative to $CCl_4$ alone. YH439, however, failed to reduce the pyridine-potentiated toxicity, suggesting that the other form(s) of cytochroms P450 inducible by pyridine, but not suppressible by YH439 treatment, may play a role in potentiating $CCl_4-induced$ hepatotoxicity. YH439 was capable of blocking cadmium chloride-induced liver toxicity in mice. These results demonstrated that YH439 efficiently blocks Vit-A-enhanced hepatotoxiciy through Kupffer cell inactivation and that the suppression of P450 2E1 expression by YH439 is highly associated with blocking of propyl sulfide-mediated hepatotoxicity.