1.A Family of Benign Familial Hematuria.
Ran NAMKUNG ; Jun Hee SUL ; Pyung Kil KIM ; In Joon CHOI
Journal of the Korean Pediatric Society 1981;24(4):358-366
No abstract available.
Hematuria*
;
Humans
3.Double Kidneys, Double Ureters and Ureterocele in Identical Female Twins.
Ran NAMKUNG ; Do Kwang YUN ; Jun Hee SUL ; Jae Seung LEE ; Pyung Kil KIM ; Jin Moo LEE
Journal of the Korean Pediatric Society 1981;24(2):145-152
No abstract available.
Female*
;
Humans
;
Kidney*
;
Ureter*
;
Ureterocele*
4.Are Podoplanin Gene Polymorphisms Associated with Atopic Dermatitis in Koreans?.
Jung Hyun NAMKUNG ; Eugene KIM ; Yong Doo PARK ; Geontae PARK ; Jun Mo YANG
Annals of Dermatology 2015;27(3):275-282
BACKGROUND: The histologic characteristics of atopic dermatitis (AD) include perivascular edema and dilated tortuous vessels in the papillary dermis. A single nucleotide polymorphism (SNP) of the fms-related tyrosine kinase 4 (FLT4) gene is associated with AD. OBJECTIVE: To investigate the associations between podoplanin (PDPN) gene SNPs and AD. METHODS: We genotyped 9 SNPs from 5 genes of 1,119 subjects (646 AD patients and 473 controls). We determined the promoter activity of 1 SNP (rs355022) by luciferase assay; this SNP was further investigated using 1,133 independent samples (441 AD patients and 692 controls). RESULTS: The rs355022 and rs425187 SNPs and the C-A haplotype in the PDPN gene were significantly associated with intrinsic AD in the initial experiment. The rs355022 SNP significantly affected promoter activity in the luciferase assay. However, these results were not replicated in the replication study. CONCLUSION: Two SNPs and the C-A haplotype in the PDPN gene are significantly associated with intrinsic AD; although, the results were confirmed by luciferase assay, they could not be replicated with independent samples. Nevertheless, further replication experiments should be performed in future studies.
Dermatitis, Atopic*
;
Dermis
;
Edema
;
Haplotypes
;
Humans
;
Luciferases
;
Polymorphism, Genetic
;
Polymorphism, Single Nucleotide
;
Protein-Tyrosine Kinases
5.Serotonin Regulates De Novo Lipogenesis in Adipose Tissues through Serotonin Receptor 2A
Ko Eun SHONG ; Chang-Myung OH ; Jun NAMKUNG ; Sangkyu PARK ; Hail KIM
Endocrinology and Metabolism 2020;35(2):470-479
Background:
Obesity is defined as excessive fat mass and is a major cause of many chronic diseases such as diabetes, cardiovascular disease, and cancer. Increasing energy expenditure and regulating adipose tissue metabolism are important targets for the treatment of obesity. Serotonin (5-hydroxytryptophan [5-HT]) is a monoamine metabolite of the essential amino acid tryptophan. Here, we demonstrated that 5-HT in mature adipocytes regulated energy expenditure and lipid metabolism.
Methods:
Tryptophan hydroxylase 1 (TPH1) is the rate-limiting enzyme during 5-HT synthesis in non-neural peripheral tissues. We generated adipose tissue-specific Tph1 knockout (Tph1 FKO) mice and adipose tissue-specific serotonin receptor 2A KO (Htr2a FKO) mice and analyzed their phenotypes during high-fat diet (HFD) induced obesity.
Results:
Tph1 FKO mice fed HFD exhibited reduced lipid accumulation, increased thermogenesis, and resistance to obesity. In addition, Htr2a FKO mice fed HFD showed reduced lipid accumulation in white adipose tissue and resistance to obesity.
Conclusion
These data suggest that the inhibition of serotonin signaling might be an effective strategy in obesity.
7.Inhibition of Serotonin Synthesis Induces Negative Hepatic Lipid Balance.
Jun NAMKUNG ; Ko Eun SHONG ; Hyeongseok KIM ; Chang Myung OH ; Sangkyu PARK ; Hail KIM
Diabetes & Metabolism Journal 2018;42(3):233-243
BACKGROUND: Hepatic steatosis is caused by metabolic stress associated with a positive lipid balance, such as insulin resistance and obesity. Previously we have shown the anti-obesity effects of inhibiting serotonin synthesis, which eventually improved insulin sensitivity and hepatic steatosis. However, it is not clear whether serotonin has direct effect on hepatic lipid accumulation. Here, we showed the possibility of direct action of serotonin on hepatic steatosis. METHODS: Mice were treated with para-chlorophenylalanine (PCPA) or LP-533401 to inhibit serotonin synthesis and fed with high fat diet (HFD) or high carbohydrate diet (HCD) to induce hepatic steatosis. Hepatic triglyceride content and gene expression profiles were analyzed. RESULTS: Pharmacological and genetic inhibition of serotonin synthesis reduced HFD-induced hepatic lipid accumulation. Furthermore, short-term PCPA treatment prevented HCD-induced hepatic steatosis without affecting glucose tolerance and browning of subcutaneous adipose tissue. Gene expression analysis revealed that the expressions of genes involved in de novo lipogenesis and triacylglycerol synthesis were downregulated by short-term PCPA treatment as well as long-term PCPA treatment. CONCLUSION: Short-term inhibition of serotonin synthesis prevented hepatic lipid accumulation without affecting systemic insulin sensitivity and energy expenditure, suggesting the direct steatogenic effect of serotonin in liver.
Animals
;
Diabetes Mellitus
;
Diet
;
Diet, High-Fat
;
Energy Metabolism
;
Fatty Liver
;
Fenclonine
;
Gene Expression
;
Glucose
;
Insulin Resistance
;
Lipogenesis
;
Liver
;
Mice
;
Obesity
;
Serotonin*
;
Stress, Physiological
;
Subcutaneous Fat
;
Transcriptome
;
Triglycerides
8.Increased Serum Angiopoietin-Like 6 Ahead of Metabolic Syndrome in a Prospective Cohort Study
Jun NAMKUNG ; Joon Hyung SOHN ; Jae Seung CHANG ; Sang Wook PARK ; Jang Young KIM ; Sang Baek KOH ; In Deok KONG ; Kyu Sang PARK
Diabetes & Metabolism Journal 2019;43(4):521-529
BACKGROUND: Despite being an anti-obesity hepatokine, the levels of serum angiopoietin-like 6 (ANGPTL6) are elevated in various metabolic diseases. Thus, ANGPTL6 expression may reflect metabolic burden and may have compensatory roles. This study investigated the association between serum ANGPTL6 levels and new-onset metabolic syndrome. METHODS: In total, 221 participants without metabolic syndrome were randomly selected from a rural cohort in Korea. Baseline serum ANGPTL6 levels were measured using an enzyme-linked immunosorbent assay. Anthropometric and biochemical markers were analyzed before and after follow-up examinations. RESULTS: During an average follow-up period of 2.75 (interquartile range, 0.76) years, 82 participants (37.1%) presented new-onset metabolic syndrome and had higher ANGPTL6 levels before onset than those without metabolic syndrome (48.03±18.84 ng/mL vs. 64.75±43.35 ng/mL, P=0.001). In the multivariable adjusted models, the odds ratio for the development of metabolic syndrome in the highest quartile of ANGPTL6 levels was 3.61 (95% confidence interval, 1.27 to 10.26). The use of ANGPTL6 levels in addition to the conventional components improved the prediction of new-onset metabolic syndrome (area under the receiver operating characteristic curve: 0.775 vs. 0.807, P=0.036). CONCLUSION: Increased serum ANGPTL6 levels precede the development of metabolic syndrome and its components, including low high density lipoprotein, high triglyceride, and high glucose levels, which have an independent predictive value for metabolic syndrome.
Biomarkers
;
Cohort Studies
;
Enzyme-Linked Immunosorbent Assay
;
Follow-Up Studies
;
Glucose
;
Korea
;
Lipoproteins
;
Metabolic Diseases
;
Odds Ratio
;
Prospective Studies
;
ROC Curve
;
Triglycerides
9.Inhibition of biofilm formation of periodontal pathogens by D-Arabinose
Sun-Jin AN ; Jong-Uk NAMKUNG ; Kyung-Won HA ; Hye-Kyoung JUN ; Hyun Young KIM ; Bong-Kyu CHOI
International Journal of Oral Biology 2021;46(3):111-118
Periodontitis and periimplantitis are caused as a result of dental biofilm formation. This biofilm is composed of multiple species of pathogens. Therefore, controlling biofilm formation is critical for disease prevention. To inhibit biofilm formation, sugars can be used to interrupt lectin-involving interactions between bacteria or between bacteria and a host. In this study, we evaluated the effect of D-Arabinose on biofilm formation of putative periodontal pathogens as well as the quorum sensing activity and whole protein profiles of the pathogens. Crystal violet staining, confocal laser scanning microscopy, and scanning electron microscopy revealed that D-Arabinose inhibited biofilm formation of Porphyromonas gingivalis, Fusobacterium nucleatum, and Tannerella forsythia. D-Arabinose also significantly inhibited the activity of autoinducer 2 of F. nucleatum and the expression of representative bacterial virulence genes.Furthermore, D-Arabinose treatment altered the expression of some bacterial proteins. These results demonstrate that D-Arabinose can be used as an antibiofilm agent for the prevention of periodontal infections.
10.Inhibition of biofilm formation of periodontal pathogens by D-Arabinose
Sun-Jin AN ; Jong-Uk NAMKUNG ; Kyung-Won HA ; Hye-Kyoung JUN ; Hyun Young KIM ; Bong-Kyu CHOI
International Journal of Oral Biology 2021;46(3):111-118
Periodontitis and periimplantitis are caused as a result of dental biofilm formation. This biofilm is composed of multiple species of pathogens. Therefore, controlling biofilm formation is critical for disease prevention. To inhibit biofilm formation, sugars can be used to interrupt lectin-involving interactions between bacteria or between bacteria and a host. In this study, we evaluated the effect of D-Arabinose on biofilm formation of putative periodontal pathogens as well as the quorum sensing activity and whole protein profiles of the pathogens. Crystal violet staining, confocal laser scanning microscopy, and scanning electron microscopy revealed that D-Arabinose inhibited biofilm formation of Porphyromonas gingivalis, Fusobacterium nucleatum, and Tannerella forsythia. D-Arabinose also significantly inhibited the activity of autoinducer 2 of F. nucleatum and the expression of representative bacterial virulence genes.Furthermore, D-Arabinose treatment altered the expression of some bacterial proteins. These results demonstrate that D-Arabinose can be used as an antibiofilm agent for the prevention of periodontal infections.