No abstract available.
Peroxisomes

No abstract available.
Lipid Metabolism* ; Peroxisomes*

No abstract available.
Peroxisomes* ; PPAR delta*

No abstract available.
Colorectal Neoplasms ; Peroxisomes ; PPAR gamma ; Prognosis

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

Phthalates are commonly used as plasticizers and vehicles for cosmetic ingredients. Phthalate metabolites have documented biochemical activity including activating peroxisome proliferator-activated receptor and antiandrogenic effects, which may contribute to the development of obesity. In vitro and in vivo studies suggest that phthalates have significant effects on the development of obesity, especially after prenatal exposure at low doses. Although few studies have examined the effects of phthalate on obesity development in humans, some work has shown that phthalates affect humans and animals similarly. In this paper, we review the possible mechanisms of phthalate-induced obesity, and discuss evidence supporting the role of phthalates in the development of obesity in humans.
Animals ; Child ; Diethylhexyl Phthalate ; Endocrine Disruptors ; Humans ; Obesity ; Pediatric Obesity* ; Peroxisomes ; Plasticizers ; Plastics

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

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

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

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