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An In Vitro Model to Probe the Regulation of Adipocyte Differentiation under Hyperglycemia
Kusampudi Shilpa, Thangaraj Dinesh, Baddireddi Subhadra Lakshmi
Diabetes Metab J. 2013;37(3):176-180.   Published online June 14, 2013
DOI: https://doi.org/10.4093/dmj.2013.37.3.176
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AbstractAbstract PDFPubReader   
Background

The aim of this study was an in vitro investigation of the effect of high glucose concentration on adipogenesis, as prolonged hyperglycemia alters adipocyte differentiation.

Methods

3T3-L1 preadipocytes differentiated in the presence of varying concentrations of glucose (25, 45, 65, 85, and 105 mM) were assessed for adipogenesis using AdipoRed (Lonza) assay. Cell viability and proliferation were measured using MTT reduction and [3H] thymidine incorporation assay. The extent of glucose uptake and glycogen synthesis were measured using radiolabelled 2-deoxy-D-[1-3H] glucose and [14C]-UDP-glucose. The gene level expression was evaluated using reverse transcription-polymerase chain reaction and protein expression was studied using Western blot analysis.

Results

Glucose at 105 mM concentration was observed to inhibit adipogenesis through inhibition of CCAAT-enhancer-binding proteins, sterol regulatory element-binding protein, peroxisome proliferator-activated receptor and adiponectin. High concentration of glucose induced stress by increasing levels of toll-like receptor 4, nuclear factor κB and tumor necrosis factor α thereby generating activated preadipocytes. These cells entered the state of hyperplasia through inhibition of p27 and proliferation was found to increase through activation of protein kinase B via phosphoinositide 3 kinase dependent pathway. This condition inhibited insulin signaling through decrease in insulin receptor β. Although the glucose transporter 4 (GLUT4) protein remained unaltered with the glycogen synthesis inhibited, the cells were found to exhibit an increase in glucose uptake via GLUT1.

Conclusion

Adipogenesis in the presence of 105 mM glucose leads to an uncontrolled proliferation of activated preadipocytes providing an insight towards understanding obesity.

Citations

Citations to this article as recorded by  
  • Adipogenesis-Related Metabolic Condition Affects Shear-Stressed Endothelial Cells Activity Responding to Titanium
    Thaís Silva Pinto, Anderson Moreira Gomes, Paula Bertin de Morais, Willian F. Zambuzzi
    Journal of Functional Biomaterials.2023; 14(3): 162.     CrossRef
  • Chronic and Transient Hyperglycemia Induces Changes in the Expression Patterns of IL6 and ADIPOQ Genes and Their Associated Epigenetic Modifications in Differentiating Human Visceral Adipocytes
    Adam Wróblewski, Justyna Strycharz, Ewa Świderska, Aneta Balcerczyk, Janusz Szemraj, Józef Drzewoski, Agnieszka Śliwińska
    International Journal of Molecular Sciences.2021; 22(13): 6964.     CrossRef
  • Effects of high glucose conditions on the expansion and differentiation capabilities of mesenchymal stromal cells derived from rat endosteal niche
    Ahmed Makki A. Al-Qarakhli, Norhayati Yusop, Rachel J. Waddington, Ryan Moseley
    BMC Molecular and Cell Biology.2019;[Epub]     CrossRef
  • Inhibition of WNT/β-catenin signaling under serum starvation and hypoxia induces adipocytic transdifferentiation in human leiomyoma cells
    Hiroshi Harada, Yojiro Tsuda, Kei Yabuki, Eisuke Shiba, Kazuyoshi Uchihashi, Atsuji Matsuyama, Yoshihisa Fujino, Toru Hachisuga, Masanori Hisaoka
    Laboratory Investigation.2018; 98(4): 439.     CrossRef
  • Effects of high glucose on caveolin-1 and insulin signaling in 3T3-L1 adipocytes
    Sara Palacios-Ortega, Maider Varela-Guruceaga, J. Alfredo Martínez, Carlos de Miguel, Fermín I. Milagro
    Adipocyte.2016; 5(1): 65.     CrossRef
  • Pathophysiological role of enhanced bone marrow adipogenesis in diabetic complications
    Meghan A Piccinin, Zia A Khan
    Adipocyte.2014; 3(4): 263.     CrossRef
  • Letter: AnIn VitroModel to Probe the Regulation of Adipocyte Differentiation under Hyperglycemia (Diabetes Metab J2013;37:176-80)
    In-Kyung Jeong
    Diabetes & Metabolism Journal.2013; 37(4): 296.     CrossRef
  • Response: AnIn VitroModel to Probe the Regulation of Adipocyte Differentiation under Hyperglycemia (Diabetes Metab J2013;37:176-80)
    Kusampudi Shilpa, Thangaraj Dinesh, Baddireddi Subhadra Lakshmi
    Diabetes & Metabolism Journal.2013; 37(4): 298.     CrossRef
Decreased Expression and Induced Nucleocytoplasmic Translocation of Pancreatic and Duodenal Homeobox 1 in INS-1 Cells Exposed to High Glucose and Palmitate
Gyeong Ryul Ryu, Jun Mo Yoo, Esder Lee, Seung-Hyun Ko, Yu-Bae Ahn, Ki-Ho Song
Diabetes Metab J. 2011;35(1):65-71.   Published online February 28, 2011
DOI: https://doi.org/10.4093/dmj.2011.35.1.65
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  • 4 Crossref
AbstractAbstract PDFPubReader   
Background

Type 2 diabetes mellitus (T2DM) is often accompanied by increased levels of circulating fatty acid. Elevations in fatty acids and glucose for prolonged periods of time have been suggested to cause progressive dysfunction or apoptosis of pancreatic beta cells in T2DM. However, the precise mechanism of this adverse effect is not well understood.

Methods

INS-1 rat-derived insulin-secreting cells were exposed to 30 mM glucose and 0.25 mM palmitate for 48 hours.

Results

The production of reactive oxygen species increased significantly. Pancreatic and duodenal homeobox 1 (Pdx1) expression was down-regulated, as assessed by reverse transcription-polymerase chain reaction and Western blot analyses. The promoter activities of insulin and Pdx1 were also diminished. Of note, there was nucleocytoplasmic translocation of Pdx1, which was partially prevented by treatment with an antioxidant, N-acetyl-L-cysteine.

Conclusion

Our data suggest that prolonged exposure of beta cells to elevated levels of glucose and palmitate negatively affects Pdx1 expression via oxidative stress.

Citations

Citations to this article as recorded by  
  • Nrf2 Activation Protects Mouse Beta Cells from Glucolipotoxicity by Restoring Mitochondrial Function and Physiological Redox Balance
    Johanna Schultheis, Dirk Beckmann, Dennis Mulac, Lena Müller, Melanie Esselen, Martina Düfer
    Oxidative Medicine and Cellular Longevity.2019; 2019: 1.     CrossRef
  • Early overnutrition reduces Pdx1 expression and induces β cell failure in Swiss Webster mice
    Maria M. Glavas, Queenie Hui, Eva Tudurí, Suheda Erener, Naomi L. Kasteel, James D. Johnson, Timothy J. Kieffer
    Scientific Reports.2019;[Epub]     CrossRef
  • Anti-diabetic effect of mulberry leaf polysaccharide by inhibiting pancreatic islet cell apoptosis and ameliorating insulin secretory capacity in diabetic rats
    Yao Zhang, Chunjiu Ren, Guobing Lu, Zhimei Mu, Weizheng Cui, Huiju Gao, Yanwen Wang
    International Immunopharmacology.2014; 22(1): 248.     CrossRef
  • The Furan Fatty Acid Metabolite CMPF Is Elevated in Diabetes and Induces β Cell Dysfunction
    Kacey J. Prentice, Lemieux Luu, Emma M. Allister, Ying Liu, Lucy S. Jun, Kyle W. Sloop, Alexandre B. Hardy, Li Wei, Weiping Jia, I. George Fantus, Douglas H. Sweet, Gary Sweeney, Ravi Retnakaran, Feihan F. Dai, Michael B. Wheeler
    Cell Metabolism.2014; 19(4): 653.     CrossRef
High Glucose Modulates Vascular Smooth Muscle Cell Proliferation Through Activation of PKC-sigma-dependent NAD(P)H oxidase.
Bo Hyun Kim, Chang Won Lee, Jung Lae Park, Yang Ho Kang, In Ju Kim, Yong Ki Kim, Seok Man Son
Korean Diabetes J. 2006;30(6):416-427.   Published online November 1, 2006
DOI: https://doi.org/10.4093/jkda.2006.30.6.416
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  • 1 Crossref
AbstractAbstract PDF
BACKGROUND
Oxidative stress is thought to be one of the causative factors contributing to macrovascular complications in diabetes. However, the mechanisms of development and progression of diabetic vascular complications are poorly understood. We hypothesized that PKC-sigma isozyme contributes to ROS generation and determined their roles in the critical intermediary signaling events in high glucose-induced proliferation of vascular smooth muscle (VSM) cells. METHODS: We treated primary cultured rat aortic smooth muscle cells for 72 hours with medium containing 5.5 mmol/L D-glucose (normal glucose), 30 mmol/L D-glucose (high glucose) or 5.5 mmol/L D-glucose plus 24.5 mmol/L mannitol (osmotic control). We then measured cell number, BrdU incorporation, cell cycle and superoxide production in VSM cells. Immunoblotting of PKC isozymes using phoshospecific antibodies was performed, and PKC activity was also measured. RESULTS: High glucose increased VSM cell number and BrdU incorporation and displayed significantly greater percentages of S and G2/M phases than compared to 5.5 mmol/L glucose and osmotic control. The nitroblue tetrazolium (NBT) staining in high glucose-treated VSM cell was more prominent compared with normal glucose-treated VSM cell, which was significantly inhibited by DPI (10 micrometer), but not by inhibitors for other oxidases. High glucose also markedly increased activity of PKC-sigma isozyme. When VSM cells were treated with rottlerin, a specific inhibitor of PKC-sigma or transfected with PKC-sigma siRNA, NBT staining and NAD(P)H oxidase activity were significantly attenuated in the high glucose-treated VSM cells. Furthermore, inhibition of PKC-sigma markedly decreased VSM cell number by high glucose. CONCLUSION: These results suggest that high glucose-induced VSM cell proliferation is dependent upon activation of PKC-sigma, which may responsible for elevated intracellular ROS production in VSM cells, and this is mediated by NAD(P)H oxidase.

Citations

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  • High Glucose and/or Free Fatty Acid Damage Vascular Endothelial Cells via Stimulating of NAD(P)H Oxidase-induced Superoxide Production from Neutrophils
    Sang Soo Kim, Sun Young Kim, Soo Hyung Lee, Yang Ho Kang, In Ju Kim, Yong Ki Kim, Seok Man Son
    Korean Diabetes Journal.2009; 33(2): 94.     CrossRef
Cell Cycle Progression of Vascular Smooth Muscle cell Through Modulation of p38 MAPK and GSK-3beta Activities Under High Glucose Condition.
Yang Ho Kang, In Ju Kim, Yong Ki Kim, Seok Man Son
Korean Diabetes J. 2005;29(5):418-431.   Published online September 1, 2005
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BACKGOUND: Macroangiopathy, with atherosclerosis, is the leading cause of mortality and morbidity in diabetic patients. Vascular smooth muscle cells play a crucial role in atherosclerosis, as they proliferate, migrate and express genes that encode inducible growth factors. However, the mechanisms induced by hyperglycemia that accelerate the proliferative change of vascular smooth muscle cells in diabetes remain unclear. This study was aimed at clarifying the respective roles of hyperglycemia in the acceleration of vascular complications in diabetes, examine the effects of hyperglycemia on vascular smooth muscle cell proliferation and the possible underlying mechanisms, including cell cycle progression. METHODS: Primary cultured rat aortic RASMs were exposed to normal glucose(5 mmol/L D-glucose), high glucose(30 mmol/L D-glucose) or an osmotic control (5mmol/L D-glucose plus 24.5 mmol/L mannitol) for 72 hours. The effect of high glucose on cell proliferation was determined by assessing the cell count and BrdU incorporation. Proteins involved in the cell proliferation pathway (PDK1, Akt/PKB, p42/44 MAPK, p38 MAPK, GSK-3beta) and those in cell cycle progression (cdk4, cyclin D, cdk2, cyclin E and ppRb phosphorylation) were determined by Western blot analysis. cdk4 kinase and PKC activity assays were also performed. RESULTS: A high level of glucose increased both the cell count(P<0.01) and BrdU incorporation(P<0.01). The PDK1, Akt/PKB and p42/44 MAPK activities were not significantly increased. A high level of glucose significantly increased the activities of p38 MAPK (P<0.01) and GSK-3beta(P<0.05) and the expressions of cdk4, cyclin D and ppRb phosphorylation. The cdk4 (P<0.01) and PKC (P<0.05) activities were also significantly increased. The inhibition of protein kinase C with GF109203X markedly reduced the phosphorylations of p38 MAPK and GSK-3betaand the expressions of cdk4 and cyclin D. In addition, pretreatment with GF109203X decreased the cell number in response to a high glucose level. CONCLUSION: These findings suggest that a high level of glucose increases vascular smooth muscle cell proliferation, with the possible mechanism further increases the G1 to S phase cell cycle progression via the activation of PKC, p38 MAPK and GSK-3beta.
The Effect of High Glucose on the Proliferation and Migration of Vascular Smooth Muscle Cells.
Mi Kyoung Kim, Yang Ho Kang, Seok Man Son, In Ju Kim, Yong Ki Kim
Korean Diabetes J. 2004;28(5):407-415.   Published online October 1, 2004
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AbstractAbstract PDF
BACKGROUND
Oxidative stress contributes to vascular diseases for patients with diabetes by promoting vascular smooth muscle cell (VSMC) proliferation, monocyte/macrophage infiltration, and vascular tone alteration. As the mechanism of development and progression of diabetic vascular complications is poorly understood, this study was aimed to assess the potential role of hyperglycemia-induced oxidative stress and to determine whether thise oxidative stress is a major factor in hyperglycemia-induced migration and proliferation of VSMCs. METHODS: Rat aortic VSMCs were incubated for 48 hours in either a normal glucose (NG, 5.5 mM) or a high glucose (HG, 30 mM) condition. We then measured the proliferation and migration of VSMCs and the superoxide production. RESULTS: The migration and proliferation of VSMCs incubated under a HG condition were markedly increased compared to the NG condition. Treatment with diphenyleneiodonium (DPI, 10 M) and superoxide dismutase (SOD, 500 U/mL) significantly suppressed the HG-induced migration and proliferation of VSMCs. Superoxide production was significantly increased in the HG condition, and it was markedly decreased after a treatment with DPI and SOD. CONCLUSION: These data suggest that HG-induced VSMC migration and proliferation are related to the production of superoxide anion that is derived from NAD(P)H oxidase.
Increased ROS Production by High Glucose in Cultured Mouse Insulinoma Cell Line.
Jin Hwa Kim, Jung In Kim, Dong Hyun Choi, Young Uk Seo, Young Dae Kim, Jong Chan Oh, Beom Ju Lee, Keo Woon Park, Sang Yong Kim, Hak Yoen Bae, Byoung Rai Lee
Korean Diabetes J. 2004;28(4):273-283.   Published online August 1, 2004
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BACKGROUND
To investigate the effects of high glucose on oxidative stress of islet beta cells, the effects of high glucose on antioxidant enzymes, the production of free reactive substances and paraquat-induced cytotoxicity were examined in cultured mouse insulinoma cells (MIN6N8a). METHODS: The MIN6N8a cell line (Obtained from Diabetic research center, Univer sity of Calgary, Canada) was maintained in RPMI1640 medium supplemented with 10% fetal bovine serum, at 37degrees C under an atmosphere of 5% CO2 and 100 % humidity. The MIN6N8a cells were cultured in high glucose (22.4 mM) and normogl-ucose (5.6 mM) containing RPMI1640 media, for 1-6 days, and the superoxide dismutase (SOD), catalase and glutathione peroxidase (GSHPx) activities in the MIN6N8a cells assayed. The levels of reactive oxygen species in the MIN6N8a cells was determined using dihydroethidium (DHE). Paraquatinduced cytotoxicity was determined using the 3-[4,5-dimethylthiazol-2-yl]-2, 5diphenyl tetraz olium bromide (MTT) method. RESULTS: No difference was observed catalase in the catalase and GSHPx activities in MIN6N8a cells between the high glucose (22.4 mM) and normoglucose (5.6 mM) groups. The CuZn-SOD activity of MIN6N8a cells was decreased by 32% in the high glucose (25.4 mM) medium compared to normoglucose (5.6 mM) medium, while the Mn-SOD activity was increased by 24% in high glucose group. The paraquat induced cytotoxicity of MIN6N8a cells was potentiated by high glucose. and the amount of DHE oxidation increased. CONCLUSION: The Oxidative stress in MIN6N8a cells was increased by high glucose as a resulted of the decreased CuZn-SOD activity and increased production of reactive oxygen species. Increased oxidative stress in MIN6N8a cells by high glucose may play some roles in the pathogenesis of diabetes.
Effect and Mechanism of High Glucose Level on the Expression of an Adhesion Protein, beta ig-h3, and Cellular Function in Endothelial Cells.
Sung Woo Ha, Hye Jin Yeo, Jong Sup Bae, Sung Chang Chung, Jung Guk Kim, In San Kim, In Kyu Lee, Bo Wan Kim
Korean Diabetes J. 2003;27(4):323-331.   Published online August 1, 2003
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BACKGROUND
Diabetes mellitus is a high risk condition for the development of atherosclerotic and thromboembolic macroangiopathy. There are many factors which are involved in development of these processes. Given the central pathogenic role of endotheliopathy in atherosclerosis, it is likely that this vascular monolayer is the ultimate target of injury in response to many cytokines and growth factors. A dysfunctional endothelium may contribute to the proatherogenic environment. Transforming growth factor (TGF-beta) is a key factor in the development of diabetic angiopathy and atherosclerosis because of its effect on the accumulation of extracellular matrix proteins and endothelial function. The adhesive molecule betaig-h3 is an extracellular matrix protein whose expression is induced by TGF-beta. Considering that TGF-beta plays an important role in diabetic complications and that betaig-h3 is a downstream target gene of TGF-beta, we hypothesized that betaig-h3 may also play a role in the development of diabetic angiopathy through its effect on the endothelial function. Therefore, we examined the effects of high glucose level on the expression of betaig-h3 and endothelial function in human umbilical vein endothelial cells (HUVECs). We also studied the mechanisms of this high glucose-induced betaig-h3 expression. METHODS: Endothelial cells were isolated from human umbilical cord and conditioned with different concentrations of TGF-beta or glucose. We measured TGF-beta and betaig-h3 protein presence/concentration/expression in cell supernatant by ELISA and examined whether TGF-beta is involved in high glucose-induced betaig-h3 expression. Finally, we investigated the biologic function of betaig-h3 in endothelial cells by using adhesion assay. RESULTS: Our study demonstrated that both high glucose level and TGF-beta induced betaig-h3 protein expression in HUVECs. High glucose level also induced TGF-beta protein expression in cells. Anti-TGF-beta antibody almost completely blocked high glucose-induced betaig-h3 expression. betaig-h3 was found to support the adhesion of endothelial cells. CONCLUSION: These results suggest that high glucose level upregulates betaig-h3 protein levels through the induction of TGF-beta and that betaig-h3 may play an important role in diabetic angiopathy by regulating adhesive function of endothelial cells.
Effect of Transforming Growth Factor-Induced Gene Product, beta ig-h3 on Proliferation, Migration, and Adhesion of Aortic Smooth Muscle Cells Cultured in High Glucose.
Sung Woo Ha, Gui Hwa Jung, He Jin Yeo, Jong Sup Bae, Soon Hee Lee, Jung Guk Kim, Rang Woon Park, In San Kim, Bo Wan Kim
Korean Diabetes J. 2002;26(4):286-295.   Published online August 1, 2002
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AbstractAbstract PDF
BACKGROUND
Diabetes mellitus is associated with a substantial increase in the prevalence of atherosclerotic disease. There are many factors which are involved in development of these processes. Transforming growth factor (TGF-beta) is known to be an important factor in the pathogenesis of diabetic vascular complications. TGF-beta-induced gene-h3 (beta ig-h3) is an adhesive molecule whose expression is induced by TGF-beta. Considering that TGF-beta plays an important role in diabetic complications and that beta ig-h3 is induced by TGF-beta, we hypothesized that beta ig-h3 may also play a role in the development of diabetic angiopathy. Then, we examined the effects of beta ig-h3 on biologic function of vascular smooth muscle cells (VSMCs) and potential roles of beta ig-h3 in the pathognesis of diabetic angiopathy. METHODS: VSMCs were isolated from rat thoracic aorta. We conditioned cells with different concentration of TGF-beta or glucose. We measured TGF-beta and beta ig-h3 protein in cell supernatant by ELISA. We also examined whether TGF-beta involves in high glucose-induced beta ig-h3 expression. Finally, we did proliferation, migration, and adhesion assay to investigate biologic function of beta ig-h3 in VSMCs. RESULTS: Our results demonstrated that TGF-beta induced beta ig-h3 expression in VSMCs in dose dependent manners. High glucose induced TGF expression as well as beta ig-h3 protein. Finally, beta ig-h3 was found to support the proliferation, migration, and adhesion of rat VSMCs. CONCLUSION: These results suggest that high glucose-and TGF-beta-induced beta ig-h3 may play an important role in diabetic angiopathy by regulating proliferation, migration, and adhesion of VSMCs.
Study on Role of Neutrophil in Endothelial Cell Injury under High Glucose Condition.
Seok Man Son, In Ju Kim, Yong Ki Kim
Korean Diabetes J. 2000;24(6):652-665.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
High glucose level plays a major role in the injury of endothelium during the early event in diabetic vascular complication. It was speculated that high glucose level may cause endothelial cell injury by neutrophil activation. METHODS: The human umbilical vein endothelial cells (HUVEC) were obtained from American Type Culture Collection. The cells were incubated as long as 24 hours to evaluate the expression of E-selectin on the cell surface using whole cell ELISA method. The adherence of neutrophils to human umbilical endothelial cell monolayers and transendothelial migration of 51Cr-labeled neutrophils were evaluated under the condition of different concentrations of D-glucose (5.5, 15, and 30 mmol/L). L-glucose (30 mmol/L) was used as an osmotic control after 24h incubation. We also measured neutrophil-mediated endothelial cell cytotoxicity using a 51Cr-release assay and release of activating markers (lactoferrin and myeloeroxidase) from neutrophils under the same conditions. RESULTS: The expression of E-selectin was increased on endothelium when incubated with medium containing high glucose (30 mmol/L) compared to control (5.5 mmol/L) preparation (1.36 OD vs. 0.79 OD, p<0.05). Increased adherence of neutrophils to HUVEC was observed with high glucose when compared to control (10.4% vs. 2.9%, p<0.01). Similarly, neutrophil migration across the cultured endothelial monolayers were also significantly increased by high glucose (49.8% vs. 27.3%, p<0.05). 51Cr-release from endothelial cells by neutrophils stimulated with high glucose was greater than that with control (27.5% vs. 10.6%, p<0.05). Release of activating markers from neutrophils incubated with high glucose was greater than that from neutrophils incubated with control. CONCLUSION: These results indicate that high glucose increases the adherence and transendothelial migration of neutrophils and cause endothelial cell injury through neutrophil activation. Thus, it is concluded that high glucose level maybe contribute to manifestation of the diabetic vascular disease, including the early step in the initiation of an acute inflammation of vascular endothelial cells.
Effect of Transforming Growth Factor-B1 and Platelet Derived Growth Factor on Synthesis and Gene Expression of Collagen and Non-Collagen Protein in Aortic Smooth Muscle Cells Cultured in Different Concentrations of Insulin and Glucose.
Kun Young Sohn, In San Kim, Bo Wan Kim, Jung Guk Kim, Sung Woo Ha, Jick Hwa Nam, Seong Mo Koo, Rang Woon Park, Sam Kweon
Korean Diabetes J. 1999;23(4):518-529.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
The mechanism for accelerated atberosclerosis in diabetes mellitus is unclear although diabetes mellitus is associated with substantial increase in prevalence of atherosclerotic disease. Extracellular matrix formation by vascular smooth muscle cells has been accepted as playing important roles during development of atherosclerosis. High glucose condition has been reported to increase the synthesis of extracellular matrix such as collagen and fibronectin in cultured mesangial cells. Insulin and some cytokines such as TGF-B and PGF have also been reported to stimulate the synthesis of collagen in mesangial cells. So we studied the effect of high glucose, insulin, TGF-Band PDGF on vascular smooth muscle cells. METHODS: To determine the effect of bigh glucose condition on collagen synthesis in vascular smooth muscle cells, cells were grown in the culture medium containing either normal (5.5 mM) or high (25 mM) glucose. And we used several concentrations of TGF-B1PDGF-BB and insulin in order to determine the synergistic effects of collagen synthesis and type I collagen mRNA expression. RESULTS: We observed that cells cultured in high glucose media synthesized more collagen and increased expression of type I collagen mRNA as compared to normoglycemic media. The amount of synthesized collagen and type I collagen mRNA expression increased proportionally to the increase in insulin concentration. There was no relationship of TGF-B1or PDGF-BB with the expression of type I collagen mRNA but these cytokines stimulated the synthesis of collagen and noncollagen protein. There was no synergistic effect of col)agen synthesis and type 1collagen mRNA expression by high glucose, insulin, and cytokines. CONCLUSION: These results suggest that TGF-Band PDGF may not influence type I collagen mRNA expression under hyperglycemia or hyperinsulinemia in vascular smooth muscle cells. Further studies about the other types of collagen expressions such as type IV, and V are needed because TGF-Band PDGF stimulated the synthesis of collagen and noncollagen protein.

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