Lee 2017 MiPschool Obergurgl
Lee HK (2017)
Event: MiPschool Obergurgl 2017
• Bioblast editor: Kandolf G
Labels: MiParea: Comparative MiP;environmental MiP, mt-Medicine, mt-Awareness Pathology: Diabetes, Obesity
Event: E2, Review
- Dept Internal Medicine, Eulji Univ College Medicine.- email@example.com
Table and figures
Table 1. Environmental chemicals associated with T2DM and obesity Abbreviations used: BFR, brominated flame retardant; BPA, bisphenol A; DBP, dibutyl phthalate; DDT, dichlorodiphenyltrichloroethane; DDE, dichlorodiphenyldichloroethylene; DEHP, diethylhexyl phthalate; DEP, diethyl phthalate; HCB, hexachlorobenzene; MEHP, Bis(2-ethylhexyl) phthalate; OCPs, organochlorine pesticides; PBDE, polybrominated diphenyl ether; PCB, polychlorinated biphenyl; PCDD, polychlorinated dibenzo-p-dioxins; PCDF, polychlorinated dibenzofurans; PFC, polyfluoroalkyl compound; PFOA, perfluorooctanoate; PFOS, perfluorooctane sulfonate; TBT, tributyltin chloride; TCDD, 2,3,7,8-tetrachlorodibenzo-p-dioxin; TPTO, bis(triphenyltin) oxide; AhR, aryl hydrocarbon receptor; AR, androgen receptor; CAR, constitutive androstane receptor; ER, estrogen receptor; GR, glucocorticoid receptor; PPAR, peroxisome proliferator–activated receptor; PXR, pregnane X receptor; RXR, retinoid X receptor; TR, thyroid hormone receptor; MetS, metabolic syndrome; T2DM, type 2 diabetes; OCR, oxygen consumption rate
Figure 1. Role of mitochondria on insulin secretion in pancreatic β-cells. Environmental chemical-induced mitochondrial damages decreased ATP production, leading to closure of KATP channel and depolarization of membrane potential. Consequently, insulin vesicles do not undergo exocytosis because there is no calcium ions influx into cytoplasm through voltage-dependent calcium channel (VDCC). Incretins activating G-coupled receptor enhance cAMP for insulin secretion.
Figure 2. Role of mitochondria on insulin signaling pathway in insulin responding cells, such as liver, muscle, fat and brain cells. Environmental chemical-induced mitochondrial damages decreased Akt phosphorylation leading to failure on insulin responses. Insulin-stimulated Akt activation stimulates activities of glucose transporter (Glut), glycogen synthase (GS), sterol response element binding protein (SREBP), acyl CoA carboxylase (ACC) and mTOR. Insulin also represses activities of lipase, phosphoenolpyruvate carboxykinase (PEPCK) and glucose 6-phosphatase (G6Pase).