1.Association Study of the Peroxisome Proliferators-Activated Receptor gamma2 Pro12Ala Polymorphism with Diabetic Nephropathy.
Min Jeong KWON ; Jeong Hyun PARK
Korean Diabetes Journal 2008;32(5):399-401
No abstract available.
Peroxisomes
2.Current Understanding of Peroxisome Proliferator-Activated Receptor delta.
Jungyeob HAM ; Dong Hwan WON ; Heonjoong KANG
Journal of Korean Society of Endocrinology 2003;18(3):239-249
No abstract available.
Peroxisomes*
;
PPAR delta*
3.Role of Peroxisome Proloferator-activated Receptor in the Lipid Metabolism.
Journal of Korean Society of Endocrinology 1998;13(3):303-307
No abstract available.
Lipid Metabolism*
;
Peroxisomes*
4.Colorectal Cancer Expression of Peroxisome Proliferator-Activated Receptor gamma Is Associated with Good Prognosis.
Intestinal Research 2009;7(1):71-72
No abstract available.
Colorectal Neoplasms
;
Peroxisomes
;
PPAR gamma
;
Prognosis
5.Peroxisomal disorders.
Hanyang Medical Reviews 2005;25(3):42-48
Peroxisomes are subcellular organells catalyzing a number of important functions in cellular metabolism. Their functions are mostly related to lipid metabolism. Genetic disorders of peroxisomes are divided into 2 categories: peroxisomal biogenesis disorders and single peroxisomal enzyme deficiencies. This paper describes an overview of the peroxisomal disorders, including metabolic basis, and clinical and laboratory findings.
Lipid Metabolism
;
Metabolism
;
Peroxisomal Disorders*
;
Peroxisomes
;
Organelle Biogenesis
6.New and emerging drugs in type 2 diabetes.
Korean Journal of Medicine 2007;72(5):446-450
Recent advances in understanding insulin secretion, action and signaling have led to the development of new pharmacological agents. Several new emerging drugs and drug classes for the management of diabetes are under development, including the incretin mimetic agents (exenatide, dipeptidyl peptidase 4 inhibitors, and glucagon-like peptide 1 analogues), the amylin analogue pramlintide, the cannabinoid-1 receptor antagonist rimonabant, the mixed peroxisome proliferator-activated receptor agonists muraglitazar and the inhaled insulin preparation Exubera. New drugs and technologic advances being made available will help achieve the goals of treating patients with diabetes to all the appropriate metabolic targets. Longer term studies will help providers weigh the benefits, adverse effects, cost, and unknown long-term risks of these medications.
Dipeptidyl-Peptidase IV Inhibitors
;
Glucagon-Like Peptide 1
;
Humans
;
Incretins
;
Insulin
;
Islet Amyloid Polypeptide
;
Peroxisomes
7.The association between PGC-1a and Alzheimer's disease.
Anatomy & Cell Biology 2016;49(1):1-6
Alzheimer's disease (AD) is a neurodegenerative disorder and its reported pathophysiological features in the brain include the deposition of amyloid beta peptide, chronic inflammation, and cognitive impairment. The incidence of AD is increasing worldwide and researchers have studied various aspects of AD pathophysiology in order to improve our understanding of the disease. Thus far, the onset mechanisms and means of preventing AD are completely unknown. Peroxisome proliferator-activated receptor-γ coactivator (PGC-1α) is a protein related to various cellular mechanisms that lead to the alteration of downstream gene regulation. It has been reported that PGC-1α could protect cells against oxidative stress and reduce mitochondrial dysfunction. Moreover, it has been demonstrated to have a regulatory role in inflammatory signaling and insulin sensitivity related to cognitive function. Here, we present further evidence of the involvement of PGC-1α in AD pathogenesis. Clarifying the relationship between PGC-1α and AD pathology might highlight PGC-1α as a possible target for therapeutic intervention in AD.
Alzheimer Disease*
;
Amyloid beta-Peptides
;
Brain
;
Incidence
;
Inflammation
;
Insulin Resistance
;
Neurodegenerative Diseases
;
Oxidative Stress
;
Pathology
;
Peroxisomes
8.PPARgamma Ligand-Induced Decrease of in vivo Tumor Growth Accompanied by Increased Cytolytic Activity of Splenocytes.
Kyu Yun JANG ; Ki Hoon YU ; Hak Yong LEE ; Kyung Ryoul KIM ; Ha Na CHOI ; Eun Jung CHA ; Ho Sung PARK ; Woo Sung MOON ; Myoung Jae KANG ; Dong Geun LEE
Korean Journal of Pathology 2007;41(1):7-14
BACKGROUND: Recent studies have proposed the use of peroxisome proliferator activated receptor-gamma (PPARgamma) ligands as new chemotherapeutic agents for human malignant tumors. However the in vivo mechanism of PPARgamma ligands on cellular toxicity is not clear. Therefore we examined the anti-tumor effects of the PPARgamma ligand, rosiglitazone (ROS), in animal models. METHODS: To evaluate the effect of RSO on splenocytes, an in vitro and in vivo study was performed. Cytolytic activity was measured by use of a 51Cr release assay. The splenic natural killer (NK) cell population and effector-target conjugation were measured by flow cytometric analysis. RESULTS: In 9L glioma bearing rats, 30 mg/kg/d of ROS treatment induced a significant decrease of subcutaneous tumor growth accompanied by an increased cytolytic activity of splenocytes and of the splenic NKR-P1bright/CD3- NK cell population. In normal rats, systemic administration of ROS also increased the cytolytic activity of splenocytes, the splenic NK cell population, and effector-target conjugation. Moreover, we found that a concentration of 20micrometer ROS caused an increase in the cytolytic activity of splenocytes, and a concentration of 50micrometer ROS increased effector-target conjugation in vitro. CONCLUSIONS: These results suggest that increased splenic cytolytic activity and NK cell population may contribute to the anti-tumor effects of PPARgamma ligands in vivo. However, the roles of NK cells in the PPARgamma ligand-induced anti-tumor activity should be further investigated.
Animals
;
Glioma
;
Humans
;
Killer Cells, Natural
;
Ligands
;
Models, Animal
;
Peroxisomes
;
PPAR gamma*
;
Rats
;
Spleen
9.An Incidentally Identified Sporadic Case with Adrenoleukodystrophy with the ABCD1 Mutation.
Soon Jung SHIN ; Ja Hye KIM ; Yoo Mi KIM ; Gu Hwan KIM ; Beom Hee LEE ; Han Wook YOO
Journal of Genetic Medicine 2013;10(1):43-46
Adrenoleukodystrophy (ALD) is an X-linked disorder which has diverse constellation of clinical pictures, ranging from the severe childhood cerebral form to adrenocortical insufficiency without neurological manifestations. This disorder is caused by the mutations in the ABCD1 gene encoding the adrenoleukodystrophy protein (ALDP), a transporter in the peroxisome membrane. ALD in most cases is inherited from one parent. Here, we report an incidentally identified sporadic case with ALD after traffic accident. He had adrenocortical insufficiency as well as abnormal findings in brain image. Genetic testing of ABCD1 gene revealed a previously reported mutation. With the description of clinical features of ALD in this patient, we discussed the difficulty in determining an appropriate therapeutic option for ALD patients with minimal neurological manifestation.
Accidents, Traffic
;
Adrenoleukodystrophy
;
Brain
;
Genetic Testing
;
Humans
;
Membranes
;
Neurologic Manifestations
;
Parents
;
Peroxisomes
10.Catalase and PPAR-gamma Polymorphisms of Rheumatoid Arthritis in Korean.
Chan Bum CHOI ; Ahmed El SOHEMY ; Sang Seokg SEONG ; Yong Wook PARK ; Hye Soon LEE ; Wan Sik UHM ; Tae Hwan KIM ; Jae Bum JUN ; Dae Hyun YOO ; Sang Cheol BAE
The Journal of the Korean Rheumatism Association 2004;11(3):217-226
OBJECTIVE: To investigate the association between a single nucleotide polymorphism in the catalase and peroxisome proliferator activated receptor- gamma (PPAR-gamma) genes with risk and severity of rheumatoid arthritis (RA) in Korea. METHODS: DNA was isolated from blood samples collected from 473 Korean patients with RA and 400 Korean controls. Genotyping for the C-262T polymorphism of catalase and the Pro12Ala polymorphism of PPAR-gamma was performed by PCR-RFLP (restriction fragment length polymorphism) analysis. Subjects were classified according to ACR criteria for RA, KHAQ, and radiological severity classification by Steinbroker. RESULTS: In patient group, catalase C/T and T/T polymorphism was seen in 23 (4.9%) and 0 patients while Pro/Ala and Ala/Ala PPAR-gamma polymorphism was seen in 42 (8.9%) and 1 (0.2%) patients. In control group, catalase C/T and T/T polymorphism was seen in 25 (6.3%) and 1 (0.2%) controls while Pro/Ala and Ala/Ala PPAR-gamma polymorphism was seen in 34 (8.5%) and 4 (1%) controls. Catalase and PPAR-gamma polymorphism showed no association with the susceptibility to RA individually but, when combined association was found although it had no statistical significance, which was possibly due to its low frequency. Catalase and HLA-DRB1 polymorphism showed significant interaction on development of RA but, no interaction was found between PPAR-gamma and HLA-DRB1. Catalase and PPAR-gamma polymorphism showed no association with the severity or functional status of RA. CONCLUSION: Our results show that genetic polymorphisms of catalase and PPAR-gamma has no association with the susceptibility to RA. Catalase and HLA-DRB1 polymorphism showed significant interaction on development of RA.
Arthritis, Rheumatoid*
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Catalase*
;
Classification
;
DNA
;
HLA-DRB1 Chains
;
Humans
;
Korea
;
Peroxisomes
;
Polymorphism, Genetic
;
Polymorphism, Single Nucleotide