- Insulin-dependent Stimulation of a Subtype of p38Map Kinases and Its Role in Insulin's Antiapoptotic Activity.
-
Shin Hae Kang, Ji Hoon Kang, Hee Kyoung Kang, Dae Ho Lee, Young Ki Lee, Deok Bae Park
-
J Korean Endocr Soc. 2004;19(4):358-368. Published online August 1, 2004
-
-
-
 Abstract
 PDF
- BACKGROUND
The p38 mitogen-activated protein kinases (p38Map kinases) are a family of prolinedirected serine/threonine kinases. At least four isoforms of p38Map kinases have been identified; however, their physiological significances remain to be understood. Recently, the role of p38Map kinase in insulin-stimulated glucose uptake has been suggested. The present study aimed to investigate which isoform(s) were responsive to insulin stimulation. In addition, the activities of p38 Map kinase isoforms that may participate in the insulin's antiapoptotic function in CHO-IR cells were also determined. METHODS: Chinese hamster ovary cells, expressing wild- or mutated human insulin receptors (CHO-IR cells), were used to investigate whether insulin can stimulate any of the isoform(s) of the p38Map kinases. The p38Map kinase activity was determined by measuring the degree of 32P-labelling of ATF-2 protein, a specific substrate of p38Map kinase. A DNA laddering assay was performed to examine the degree of apoptosis and a RT-PCR analysis to determine which isoform(s) of the p38Map kinases were expressed in response to insulin. RESULTS: p38Map kinase activation by insulin was sharply suppressed in only the CHO-IR/A1018K cells, which lack the intrinsic tyrosine kinase activity of insulin receptors. Insulin stimulation of p38Map kinase was insensitive to SB203580, an inhibitor of the alpha(alpha)-and beta(beta)-isoforms of p38Map kinases. Moreover, orthovanadate, known as a specific stimulator of the gamma(gamma)-and delta(delta-) isoforms, stimulated the p38Map kinase activity in CHO-IR cells. Insulin increased the degree of mRNA expression of the delta-isoform, but not that of the alpha-isoform p38Map kinase. Interestingly, PD98059, an inhibitor of ERK, suppressed p38Map kinase stimulation, as well as the antiapoptotic protection of cells by insulin. As insulin was found to still protect ERK-lacking cells (CHO-IR/ SOS) from apoptosis, any substantial role(s) of ERK might be excluded. CONCLUSION: Our data suggest that insulin may stimulate the activity and expression of the-isoform of p38Map kinase in a MEK1/2-dependent manner. The involvement of the delta-isoform of p38Map kinase in insulin's antiapoptotic protection was also suggested, but remains to be investigated further to clarify the nature of its mechanism of action
- Regulation of FSH Gene Expression and Release in Cultured Rat Anterior Pituitary Cells.
-
Min Seok Cheon, Deok Bae Park, Yong Bin Park, Kyung Yoon Kam, Kyung Za Ryu
-
J Korean Endocr Soc. 2000;15(2):179-189. Published online January 1, 2001
-
-
-
Abstract
PDF
- BACKGROUND
FSH is a heterodimeric glycoprotein and is composed of alpha and beta subunits. alpha subunit is common to FSH and LH, while an unique beta subunit determines the biological specificity of each hormone. The synthesis of beta subunit is the primary rate-limiting step in the synthesis of each hormone. Although FSH plays a pivotal role in folliculogenesis and ovulation, very little studies have been performed on the regulation of FSH beta gene expression. Therefore, the present study attempted to examine the effect of GnRH or activin on the expression of FSH beta mRNA as well as FSH release and signaling pathway involved in their actions. METHODS: The primary cultures of rat anterior pituitary were used for this study. To determine FSH beta mRNA levels, northern blotting method was used. The concentration of FSH in the culture medium was evaluated by using a specific radioimmunoassay for rat FSH. RESULTS: PMA, an activator of PKC, increased FSH beta mRNA levels and FSH release, whereas forskolin, an activator of adenylate cyclase, showed no effect. The application of GnRH augmented FSH release, but not FSH beta mRNA levels. However, the administration of activin increased FSH beta mRNA levels as well as FSH release. Staurosporine, an inhibitor of PKC, suppressed activin-induced increment of FSH beta mRNA levels and FSH release. CONCLUSION: The present study demonstrated that activin rather than GnRH is a major regulator for FSH beta mRNA expression, and suggest that PKC-dependent pathway is also involved in the action of activin on the expression of FSH beta mRNA and FSH release.
- The Effects of Growth Hormone Tretment on Body Composition and Glucose Metabolism in Adult Hypophysectomized Rats.
-
Kwan Woo Lee, Hyun Chul Lee, Kap Bum Huh, Yoon Sok Chung, Deok Bae Park, Yup Kang, Hyeon Man Kim, Seoung Oh Yang
-
J Korean Endocr Soc. 1997;12(1):53-60. Published online January 1, 2001
-
-
-
Abstract
PDF
- BACKGROUND
It is well known that growth hormone (GH) stimulates animal growth, but studies on metabolic effects of growth hormone have recently been increasing. The purpose of this study was to clarify the effects of growth hormone treatment on body composition and glucose metabolism in hypophysectomized growth hormone-deficient rats. METHODS: The 20-week-old rnale Sprague-Dawley rats were hypophysectomized and replaced with cortisol and thyroxine for 8 weeks, then administered with recombinant human growth hormone for 2 weeks. Group 1 consisted of intact controls (n 15), while group 2 consisted of hypophysectomized controls (n 12), and group three consisted of those with GH treatment (n 13). The body weights, body composition, blood glucose levels, plasma insulin-like growth factor-I (IGF-I) levels, euglycemic hyperinsulinemic clamp test, and glycogen synthase activities in gastrocnemius muscle were measured before and after growth hormone treatment. RESULTS: Plasma IGF-I levels in GH-treated group increased to intact control group levels after 2 weeks of GH treatment. There were significant changes in body composition after the treatment (fat mass significantly decreased and lean body mass significantly increased). There were no changes in glucose metabolism in peripheral tissue after 2 weeks of GH treatment. CONCLUSION: Human GH treatment (4 IU/kg/day) in adult hypophysectomized GH-deficient rats changed the body composition, but did not alter the glucose metabolism in peripheral tissue.
- A Case of Propylthiouracil - Induced Hepatitis; Showed Chronic Active Hepatitis by Pathologic Finding.
-
Yoon Sok Chung, Hyeon Man Kim, Deok Bae Park, Kwang Hwa Park, Chull Sim, Min Kyung Song, Heui Chul Chung
-
J Korean Endocr Soc. 1994;10(3):289-294. Published online November 6, 2019
-
-
-
Abstract
PDF
- A 15-year old girl developed propylthiouracil-induced hepatitis documented as chronic active hepatitis by liver biopsy, who had suffered from Graves' disease for 1 year and treated with propylthiouracil. The result of lymphocyte transformation test was negative which was performed after 3 months of onset of hepatitis.
- Two Cases of Hypothyroidism Associated with Chromosomal Abnormality.
-
Yoon Sok Chung, Hyeon Man Kim, Min Kyung Song, Deok Bae Park, Si Hoon Han, Hyun Ju Kim, Hee Sun Jeon
-
J Korean Endocr Soc. 1994;10(2):170-174. Published online November 6, 2019
-
-
-
Abstract
PDF
- No abstract available.
- A Case of Propylthiouracil - Induced Hepatitis ; showed chronic active hepatitis by pathologic finding.
-
Yoon Sok Chung, Hyeon Man Kim, Min Kyung Song, Deok Bae Park, Kwang Hwa Park, Chull Sim
-
J Korean Endocr Soc. 1994;10(2):165-167. Published online November 6, 2019
-
-
-
Abstract
PDF
- No abstract available.
|
KES
