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Metformin Induces Lipogenesis and Apoptosis in H4IIE Hepatocellular Carcinoma Cells
박덕배,이수경,부혜진 한국발생생물학회 2023 발생과 생식 Vol.27 No.2
Metformin is the most widely used anti-diabetic drug that helps maintain normal blood glucose levels primarily by suppressing hepatic gluconeogenesis in type II diabetic patients. We previously found that metformin induces apoptotic death in H4IIE rat hepatocellular carcinoma cells. Despite its anti-diabetic roles, the effect of metformin on hepatic de novo lipogenesis (DNL) remains unclear. We investigated the effect of metformin on hepatic DNL and apoptotic cell death in H4IIE cells. Metformin treatment stimulated glucose consumption, lactate production, intracellular fat accumulation, and the expressions of lipogenic proteins. It also stimulated apoptosis but reduced autophagic responses. These metformin-induced changes were clearly reversed by compound C, an inhibitor of AMP-activated protein kinase (AMPK). Interestingly, metformin massively increased the production of reactive oxygen species (ROS), which was completely blocked by compound C. Metformin also stimulated the phosphorylation of p38 mitogen-activated protein kinase (p38MAPK). Finally, inhibition of p38MAPK mimicked the effects of compound C, and suppressed the metformininduced fat accumulation and apoptosis. Taken together, metformin stimulates dysregulated glucose metabolism, intracellular fat accumulation, and apoptosis. Our findings suggest that metformin induces excessive glucose-induced DNL, oxidative stress by ROS generation, activation of AMPK and p38MAPK, suppression of autophagy, and ultimately apoptosis.
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박덕배 대한소아내분비학회 2010 Annals of Pediatirc Endocrinology & Metabolism Vol.15 No.2
Non-alcoholic fatty liver disease (NAFLD), the most common liver disease, represents a spectrum of disease including steatohepatitis, fibrosis, and irreversible cirrhosis. Although a "benign" condition, NAFLD is a risk factor eventually leading to fibrosis and to non-alcoholic steatohepatitis (NASH). A number of evidences support an association between NAFLD/NASH and metabolic syndrome. The pathogenesis of NAFLD/NASH and metabolic syndrome seems to have common pathophysiological mechanisms, with focus on insulin resistance as a key factor. This review discusses the new aspects of NAFLD/NASH pathogenesis, and anticipate that such knowledge will eventually serve to the deveolpment of novel treatment strategies for this disease.
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바울형 미분기 베인휠에서의 유속 불균일 개선에 관한 연구
박덕배,허진혁,문승재,Park, Deok-Bae,Hur, Jin-Huek,Moon, Seung-Jae 한국플랜트학회 2010 플랜트 저널 Vol.6 No.2
The stability of coal pulverizer in the 800 MW coal-fired plants is vital to maintain their performance. Thus, this study analyzed the uneven abrasion of the deflector and coal spillage due to the air velocity maldistribution in the vane wheel of a bowl-type pulverizer as it is a possible cause for problems of facility using pulverized coal. In addition, air flow in the underbowl of a bowl-type pulverizer was studied to check air velocity maldistribution in the vane wheel using numerical method. In an attempt to correct the maldistribution of air velocity, air flow of the modified duct vane was studied as enlarging the length of the duct vanes installed at the air inlet duct of the pulverizer and increasing the angle of inclination. It was found that modified duct vane make the velocity distribution at the vane wheel uniform. formed by the duct vanes installed at the air inlet duct of the pulverizer and swirling flow is the major factor in making the velocity distribution of vane wheel exit uniform. This can prevent the uneven abrasion of the deflector, which is one of the components inside the pulverizer and coal spillage.
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박덕배 대한당뇨병학회 2015 Diabetes and Metabolism Journal Vol.39 No.6
Background: Metformin, a well-known anti-diabetic drug, has gained interest due to its association with the reduction of the prevalence of cancer in patients with type 2 diabetes and the anti-proliferative effect of metformin in several cancer cells. Here, we investigated the anti-proliferative effect of metformin with respect to apoptosis and autophagy in H4IIE hepatocellular carcinoma cells. Methods: H4IIE rat cells were treated with metformin in glucose-free medium for 24 hours and were then subjected to experiments examining the onset of apoptosis and/or autophagy as well as the related signaling pathways. Results: When H4IIE cells were incubated in glucose-free media for 24 hours, metformin and 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) reduced the viability of cells. Inhibition of AMP-activated protein kinase (AMPK) by compound C significantly blocked cell death induced by metformin or AICAR. Pro-apoptotic events (nuclear condensation, hydrolysis of intact poly ADP ribose polymerase and caspase-3) were stimulated by metformin and then suppressed by compound C. Interestingly, the formation of acidic intracellular vesicles, a marker of autophagy, was stimulated by compound C. Although the deprivation of amino acids in culture media also induced apoptosis, neither metformin nor compound C affected cell viability. The expression levels of all of the autophagy-related proteins examined decreased with metformin, and two proteins (light chain 3 and beclin-1) were sensitive to compound C. Among the tested inhibitors against MAP kinases and phosphatidylinositol-3-kinase/mammalian target of rapamycin, SB202190 (against p38MAP kinase) significantly interrupted the effects of metformin. Conclusion: Our data suggest that metformin induces apoptosis, but suppresses autophagy, in hepatocellular carcinoma cells via signaling pathways, including AMPK and p38 mitogen-activated protein kinase.
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Biphasic Activity of Chloroquine in Human Colorectal Cancer Cells
박덕배,이영기 한국발생생물학회 2014 발생과 생식 Vol.18 No.4
Autophagy is a homeostatic degradation process that is involved in tumor development and normaldevelopment. Autophagy is induced in cancer cells in response to chemotherapeutic agents, and inhibition of autophagyresults in enhanced cancer cell death or survival. Chloroquine (CQ), an anti-malarial drug, is a lysosomotropic agent and iscurrently used as a potential anticancer agent as well as an autophagy inhibitor. Here, we evaluate the characteristics of thesedual activities of CQ using human colorectal cancer cell line HCT15. The results show that CQ inhibited cell viability in doseandtime-dependent manner in the range between 20 to 80 uM, while CQ did not show any antiproliferative activity at 5 and10 uM. Cotreatment of CQ with antitumor agent NVP-BEZ235, a dual inhibitor of PI3K/mTOR, rescued the cell viability atlow concentrations meaning that CQ acted as an autophagy inhibitor, but CQ induced the lethal effect at high concentrations. Acridine orange staining revealed that CQ at high doses induced lysosomal membrane permeabilization (LMP). High doses ofCQ produced cellular reactive oxygen species (ROS) and cotreatment of antioxidants, such as NAC and trolox, with highdoses of CQ rescued the cell viability. These results suggest that CQ may exert its dual activities, as autophagy inhibitor orLMP inducer, in concentration-dependent manner.
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