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1.
Diabetes & Metabolism Journal ; : 248-254, 2011.
Article in English | WPRIM | ID: wpr-42483

ABSTRACT

BACKGROUND: Chemerin is a novel adipokine that is associated with inflammation and adipogenesis. However, it remains unclear whether chemerin is involved in patients with cardiovascular disease. We investigated whether the serum chemerin levels of Korean patients with coronary artery disease correlated with specific cardiometabolic parameters. METHODS: In total, 131 patients, all of whom had coronary artery stenosis exceeding 50%, participated in this study. Their serum chemerin levels and cardiometabolic parameters were measured. The serum chemerin levels of two groups of patients were compared; those with one stenotic vessel (n=68) and those with multiple stenotic vessels, including left main coronary artery disease (n=63). RESULTS: Serum chemerin levels correlated positively with the degree of coronary artery stenosis and fasting glucose, triglyceride, total cholesterol, low density lipoprotein cholesterol, and high sensitive C-reactive protein levels. The group with multiple stenotic vessels, including left main disease, had higher chemerin levels than the group with one stenotic vessel (t=-2.129, P=0.035). Multiple binary logistic regression showed chemerin was not an independent risk factor of multiple vessel disease (odds ratio, 1.018; confidence interval, 0.997 to 1.040; P=0.091). CONCLUSION: Serum chemerin levels have a significant correlation with several cardiometabolic risk factors and the degree of coronary artery stenosis in Korean patients with coronary artery disease. However, multiple binary logistic regression showed chemerin was not an independent risk factor of multiple vessel disease. Additional investigations are necessary to fully elucidate the role of chemerin in cardiovascular disease.


Subject(s)
Humans , Adipogenesis , Adipokines , C-Reactive Protein , Cardiovascular Diseases , Cholesterol , Cholesterol, LDL , Coronary Artery Disease , Coronary Stenosis , Coronary Vessels , Fasting , Glucose , Glycosaminoglycans , Inflammation , Lipoproteins , Logistic Models , Risk Factors
2.
Korean Journal of Medicine ; : 503-506, 2010.
Article in Korean | WPRIM | ID: wpr-227574

ABSTRACT

Sunitinib is a tyrosine-kinase inhibitor used to treat metastatic renal cell carcinoma and imatinib-resistant gastrointestinal stromal tumors. Hypothyroidism is a common side effect of sunitinib therapy. Nevertheless, overt thyrotoxicosis induced by destructive thyroiditis after sunitinib treatment is very rare. Here, we report a patient with overt thyrotoxicosis related to sunitinib therapy.


Subject(s)
Humans , Carcinoma, Renal Cell , Hypothyroidism , Indoles , Pyrroles , Thyrotoxicosis
3.
Endocrinology and Metabolism ; : 378-381, 2010.
Article in Korean | WPRIM | ID: wpr-186896

ABSTRACT

Growth hormone (GH) and thyroid stimulating hormone (TSH)-secreting pituitary adenomas are very rare and they account for only 0.5% for all pituitary adenomas. These adenomas are usually treated with surgery, but this surgery is not easy because the tumor is usually huge and invasive. We reported here on a case of a GH-TSH-secreting adenoma in a 23-year-old male patient who was initially treated with octreotide LAR. He presented with symptoms of headache, palpitation and a visual defect that he had for the 3 months. He had hypertrophy of the frontal bone and enlargement of both the hands and feet. The visual field test showed bitemporal hemianopsia. The laboratory examinations showed high serum levels of free T4, TSH and free alpha-subunit. Additionally, the serum levels of GH and insulin-like growth factor-I (IGF-I) were increased. GH was not suppressed below 1microg/L by an oral 75g glucose loading test, and TSH was not stimulated by thyrotropin-releasing hormone (TRH). Because sellar MRI showed invasive macroadenoma encasing the vessels, we initially tried octreotide LAR for treatment. A year later, the IGF-I and thyroid function tests were normalized and the size of the tumor was reduced with cystic change. The symptoms of palpitation and headache were improved without a change of the visual field defect.


Subject(s)
Humans , Male , Young Adult , Acromegaly , Adenoma , Foot , Frontal Bone , Glucose , Growth Hormone , Hand , Headache , Hemianopsia , Hypertrophy , Insulin-Like Growth Factor I , Octreotide , Pituitary Neoplasms , Thyroid Function Tests , Thyrotropin , Thyrotropin-Releasing Hormone , Visual Field Tests , Visual Fields
4.
Korean Diabetes Journal ; : 312-319, 2010.
Article in English | WPRIM | ID: wpr-23770

ABSTRACT

BACKGROUND: The highly developed endoplasmic reticulum (ER) structure in pancreatic beta cells is heavily involved in insulin biosynthesis. Thus, any perturbation in ER function inevitably impacts insulin biosynthesis. Recent studies showed that the expression of tribbles-related protein 3 (TRB3), a mammalian homolog of Drosophilia tribbles, in various cell types is induced by ER stress. Here, we examined whether ER stress induces TRB3 expression in INS-1 cells and found that TRB3 mediates ER stress-induced suppression of insulin gene expression. METHODS: The effects of tunicamycin and thapsigargin on insulin and TRB3 expression in INS-1 cells were measured by Northern and Western blot analysis, respectively. The effects of adenovirus-mediated overexpression of TRB3 on insulin, PDX-1 and MafA gene expression in INS-1 cells were measured by Northern blot analysis. The effect of TRB3 on insulin promoter was measured by transient transfection study with constructs of human insulin promoter. RESULTS: The treatment of INS-1 cells with tunicamycin and thapsigargin decreased insulin mRNA expression, but increased TRB3 protein expression. Adenovirus-mediated overexpression of TRB3 decreased insulin gene expression in a dose-dependent manner. A transient transfection study showed that TRB3 inhibited insulin promoter activity, suggesting that TRB3 inhibited insulin gene expression at transcriptional level. Adenovirus-mediated overexpression of TRB3 also decreased PDX-1 mRNA expression, but did not influence MafA mRNA expression. CONCLUSIONS: This study showed that ER stress induced TRB3 expression, but decreased both insulin and PDX-1 gene expression in INS-1 cells. Our data suggest that TRB3 plays an important role in ER stress-induced beta cell dysfunction.


Subject(s)
Humans , Blotting, Northern , Blotting, Western , Endoplasmic Reticulum , Endoplasmic Reticulum Stress , Gene Expression , Insulin , Insulin-Secreting Cells , RNA, Messenger , Thapsigargin , Transfection , Tunicamycin
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