• Proceedings of the Korean Society of Toxicology Conference
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• 2001.10a
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• pp.199-199
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• 2001

Both hypoxia and insulin induce same target genes including vascular endothelial growth factor (VEGF), glycolitic enzymes and glucose transporters. However these two signals eventually trigger quite different metabolic pathways. Hypoxia induces glycolysis for anaerobic ATP production, while insulin increase glycolysis for lipogenesis and energy storage. Hypoxia-induced gene expression is mediated by Hypoxia-inducible Factorl (HIF-1) that consists of HIF-1 $\alpha$ and $\beta$ subunit.(omitted)

• 대한생식의학회:학술대회논문집
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• 2004.11a
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• pp.69-70
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• 2004

• Preventive Nutrition and Food Science
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• v.2 no.3
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• pp.246-249
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• 1997

The maximum 30-fold level of fatty acid synthase (FAS) mRNA was achieved by 6hr after intraperitoneal injection of insulin. The kinetics and maximum effect of insulin were most evident on he 7.2 kb mRNA. In six hors after insulin administration there was about 100-fold increase in stead-state mRNA level. We observed a sharp decrease in 7.2kb mRNA by 8hr after insulin administation while there was no change in FAS mRNA content between the 6hr and 8hr-sampling periods. In contrast, a maximum induction of 4-fold was shown in the level of 5.1kb mRNA after insulin injection in streptozotocin-diabetic mice.

• Preventive Nutrition and Food Science
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• v.22 no.3
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• pp.172-183
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• 2017

Vitamin A and its metabolites modulate insulin resistance and regulate stearoyl-CoA desaturase 1 (SCD1), which are also known to affect insulin resistance. Here, we tested, whether vitamin A-mediated changes in insulin resistance markers are associated with SCD1 regulation or not. For this purpose, 30-week old male lean and glucose-intolerant obese rats of WNIN/GR-Ob strain were given either a stock or vitamin A-enriched diet, i.e. 2.6 mg or 129 mg vitamin A/kg diet, for 14 weeks. Compared to the stock diet, vitamin A-enriched diet feeding improved hyperglycemia and glucose-clearance rate in obese rats and no such changes were seen in lean rats receiving identical diets. These changes were corroborated with concomitant increase in circulatory insulin and glycogen levels of liver and muscle (whose insulin signaling pathway genes were up-regulated) in obese rats. Further, the observed increase in muscle glycogen content in these obese rats could be explained by increased levels of the active form of glycogen synthase, the key regulator of glycogen synthesis pathway, possibly inactivated through increased phosphorylation of its upstream inhibitor, glycogen synthase kinase. However, the unaltered hepatic SCD1 protein expression (despite decreased mRNA level) and increased muscle-SCD1 expression (both at gene and protein levels) suggest that vitamin A-mediated changes on glucose metabolism are not associated with SCD1 regulation. Chronic consumption of vitamin A-enriched diet improved hyperglycemia and glucose-intolerance, possibly, through the regulation of intracellular signaling and glycogen synthesis pathways of muscle and liver, but not associated with SCD1.

• The Journal of Internal Korean Medicine
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• v.39 no.4
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• pp.751-763
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• 2018

Objective: This study was undertaken to investigate how magnolia bark extract affects ob/ob mouse in terms of metabolic inflammation and insulin resistance. Methods: Leptin-deficient ob/ob mice were divided into 2 groups (n=5): a normal saline treatment (=control) and magnolia bark treatment. Wild type mice were the lean group (n=5). After 5 weeks, we measured fasting blood sugar (FBS) and conducted oral glucose tolerance tests (OGTTs) in each group. After 6 weeks, we measured body weight, epididymal fat pad weight, liver weight, serum glucose, serum insulin, and gene expression of tumor necrosis factor-${\alpha}$, interferon-${\gamma}$, and interleukin-6. We characterized the phenotype of adipose tissue macrophages (ATMs) and analyzed fractions of the phenotype in each group by flow cytometry. Results: In the magnolia bark group, fasting blood sugar, oral glucose tolerance levels, and insulin resistance (HOMA-IR) were significantly decreased. The population and proportion of ATMs among leukocytes in adipose tissue were significantly decreased in the magnolia bark group. The population and proportion of M1 type ATMs among ATMs were significantly decreased in the magnolia bark group. Gene expression of tumor necrosis factor-${\alpha}$ was significantly decreased in the magnolia bark group. Conclusions: These results support a positive effect of magnolia bark on metabolic diseases such as insulin resistance and metabolic inflammation in leptin-deficient ob/ob mice.

• Asian-Australasian Journal of Animal Sciences
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• v.28 no.1
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• pp.20-24
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• 2015

Insulin-like growth factor-1 (IGF-1) and insulin-like growth factor binding protein-1 (IGFBP-1) play a pivotal role in regulating cellular hypoxic response. In this study, we cloned and characterized the genes encoding IGF-1 and IGFBP-1 to improve the current knowledge on their roles in highland Bos grunniens (Yak). We also compared their expression levels in the liver and kidney tissues between yaks and lowland cattle. We obtained full-length 465 bp IGF-1 and 792 bp IGFBP-1, encoding 154 amino acids (AA) IGF-1, and 263 AA IGFBP-1 protein, respectively using reverse transcriptase-polyerase chain reaction (RT-PCR) technology. Analysis of their corresponding amino acid sequences showed a high identity between B. grunniens and lowland mammals. Moreover, the two genes were proved to be widely distributed in the examined tissues through expression pattern analysis. Real-time PCR results revealed that IGF-1 expression was higher in the liver and kidney tissues in B. grunniens than in Bos taurus (p<0.05). The IGFBP-1 gene was expressed at a higher level in the liver (p<0.05) of B. taurus than B. grunniens, but it has a similar expression level in the kidneys of the two species. These results indicated that upregulated IGF-1 and downregulated IGFBP-1 are associated with hypoxia adaptive response in B. grunniens.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.6 no.1
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• pp.52-57
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• 2006

Permanent neonatal diabetes(PND) is a rare form of diabetes characterized by insulin-requiring hyperglycemia that is diagnosed within the first 3 months of life. In most cases, the causes are not known. Recently, mutations in the gene KCNJ11 encoding the Kir6.2 subunit of the ATP-sensitive K+ charmel have been described in patients with PND. We report a child with PND due to a lysine-to-arginine substitution at position 170(K170R) of gene encoding Kir6.2 Our patient was diagnosed at 7 weeks of age and had been treated with subcutaneous insulin for 6.5 years. Recently, our patient has been changed from subcutaneous insulin to oral glibenclamide therapy at a daily dose of 7.5 mg 3 times a day(0.9 mg/kg/day) at the age of 6.5 years. Before glibenclamide therapy, c-peptide level was 0.1 ng/ml(normal 1.0-3.5 ng/ml) and hemoglobin HbA1c level was 7.8%(normal <6%). After 6 days of treatment, her c-peptide and insulin levels were 2.3 ng/ml and $9.6{\mu}U/ml$(normal $5-25{\mu}U/ml$), respectively. After 1 month later, the insulin and c-peptide levels were in the nonnal range without any episodes of hyper- or hypoglycemia. This case demonstrated that oral sulfonylurea may be the treatment of choice in PND patients with KCNJ11 mutation even at a young age.

• Animal cells and systems
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• v.7 no.3
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• pp.249-253
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• 2003

Abnormalities in fibrinolysis system is associated with risk of hypertension. In this report, the Alu repeat insertion/deletion (I/D) polymorphism of tissue plasminogen activator (t-PA) and the Hind III RFLP of plasminogen activator inhibitor-1 (PAI-1) genes were investigated in 115 normotensives and 83 patients with hypertension, and their association with anthropometrical data and plasma biochemical parameters were analyzed. There were no significant differences in the gene frequencies of the two candidate genes between normotensives and hypertensives, respectively. Our results indicate lack of associations between the two polymorph isms in t-PA and PAI-1 genes and risk of hypertension in the population under study. However, the Hind III RFLP of PAI-1 gene was significantly associated with plasma glucose level, suggesting its role in glucose metabolism. It needs to be tested whether this RFLP of PAI-1 gene is associated with insulin resistance syndrome or non-insulin dependent diabetes mellitus (NIDDM) in the Korean population.

• Reproductive and Developmental Biology
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• v.35 no.3
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• pp.239-245
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• 2011

The overexpression of Phosphoprotein Enriched in Astrocytes (PEA15) gene is commonly found in human diabetic patients. The overexpression of this gene in skeletal muscle and fat tissues have been reported to cause insulin resistance, thereby impairing insulin stimulated glucose uptake. We introduced a gene of mouse PEA15 (mPEA15) and enhanced green fluorescent protein (EGFP) into fertilized one cell pig zygotes using microinjection, and produced a piglet that showed overexpression of mPEA15 in the muscle tissues and expression of EGFP in the ear tissues and hooves. RT-PCR RFLP, southern blot and FISH analysis showed that the tissues carried the transgene. Real-time RT-PCR and western blots demonstrated that PEA15 gene was overexpressed in the various tissues and muscle tissues, respectively. These fads suggest that expression vector system is normally expressed in the transgenic (TG) pigs. To use as animal diseases model for type 2 diabetes, further study is necessary to confirm whether diabetes occur in these TG pigs, especially insulin resistance.

• Animal cells and systems
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• v.13 no.2
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• pp.127-132
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• 2009

We have examined the hypothesis that the Gly972Arg variant of the insulin receptor substrate 1 (IRS1) gene is associated with the components contributing to overweight (obesity) and metabolic syndrome. We describe IRS1 genotype frequencies in 274 Korean men. The frequencies of Gly972Gly (GIG) and Gly972Arg (G/A variant) of the IRS1 gene were 88.3% and 11.7%, respectively, and the differences in frequencies between the overweight (BMI$\geq$25kg/m$^2$) group and non-overweight (BMI<25kg/m$^2$) group were statistically significant. The subjects with G/A variant of IRS1 gene in non-overweight had significantly higher level of visceral fat thickness and adiponectin/leptin ratio than those with GIG alleles. In overweight group, the subjects with G/A variant of IRS1 gene also showed significantly higher level of insulin than those with GIG alleles. These results suggest that the IRS1 genetic polymorphism is involved in the occurrence of overweight, as well as metabolic syndrome.