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Applications of Pluripotent Stem Cells in the Therapy and Modeling of Diabetes and Metabolic Diseases
Published in Deepak A. Lamba, Patient-Specific Stem Cells, 2017
Suranjit Mukherjee, Shuibing Chen
In the pathogenesis of obesity-linked T2DM, the adipose tissue becomes increasingly insulin resistant, resulting in less glucose uptake and increased hydrolysis of stored lipids. These free fatty acids then enter circulation and deposit in the muscle and the liver, leading to steatosis and tissue dysfunction. Attempts to elucidate the mechanism underlying adipose tissue expansion and insulin resistance have revealed that in mouse models of obesity, the expansion of adipocytes in response to increasing triacylglyceride content leads to a lipotoxicity that recruits macrophages and other inflammatory cell types, setting off a series of cytokine events that are linked to insulin resistance (2). GWASs have also helped shed light on some of the genetic components behind predispositions to obesity, with the identification of SNPs in PPARγ and polymorphisms in the FTO gene, being highly correlated to obesity and T2DM (28,29).
Ameliorative effect of quercetin on pancreatic damage in rodent: a meta-analysis
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Tri Wiyono, Khoirun Nisa, Sri Handayani, Anjar Windarsih, Septi Nur Hayati, Martha Purnami Wulanjati, Eti Nurwening Sholikhah, Woro Rukmi Pratiwi
Pancreatic damage, both acute and chronic, is mediated by reactive oxygen species (ROS) toxicity [30,50–52]. Streptozotocin (STZ) triggers ROS production by activating xanthine oxidase and DNA alkylation [52]. High fat diet induces pancreatic damage through lipotoxicity mechanisms, de novo ceramide synthesis which triggers endoplasmic reticulum stress and mitochondrial dysfunction [30,51]. Fructose and glucose promote ROS production by increasing NADPH, an electron donor, on the outer mitochondrial wall. Meanwhile, cerulein triggers ROS production by activating NADPH oxidase [50].