Korea University · Medicine
Professor Dae Ryong's research lab specializes in molecular mechanisms underlying diabetic complications, with a primary focus on diabetic nephropathy, insulin resistance, and metabolic inflammation. The lab investigates key signaling pathways such as NF-κB, endocannabinoid system, VEGF, PPARs, and aldosterone in type 2 diabetic animal models, particularly db/db mice and OLETF rats. Current research directions include identifying therapeutic targets through pharmacological modulation of these pathways to ameliorate renal, cardiac, and metabolic dysfunctions in diabetes. The lab also explores genetic polymorphisms, such as the VEGF 936 C/T variant, in relation to diabetic microvascular complications.
Figures are computed from collected data and may differ slightly.
The NF-κB pathway plays an important role in chronic inflammatory and autoimmune diseases. Recently, NF-κB has also been suggested as an important mechanism linking obesity, inflammation, and metabolic disorders. However, there is no current evidence regarding the mechanism of action of NF-κB inhibition in insulin resistance and diabetic nephropathy in type 2 diabetic animal models. We investigated the effects of the NF-κB inhibitor celastrol in db/db mice. The treatment with celastrol for 2 mon
The endocannabinoid system is important in the pathogenesis of obesity-related metabolic disorders. However, the effect of inhibiting the endocannabinoid system in type 2 diabetic nephropathy is unclear. Therefore, we examined the effect of the cannabinoid (CB)1 receptor antagonist, SR141716, on insulin resistance and diabetic nephropathy in db/db mice. Six-week-old db/db mice were treated with the CB1-specific antagonist SR141716 (10 mg/kg · d) for 3 months. Treatment with SR141716 significantl
Vascular endothelial growth factor (VEGF) has been implicated in the pathogenesis of diabetic nephropathy. We investigated serial changes of VEGF in the kidney and assessed whether glomerular and urinary VEGF levels are related to the severity of diabetic nephropathy. Furthermore, we examined the relationship between urinary VEGF levels and the urinary albumin excretion (UAE) rate in Otsuka-Long-Evans-Tokushima-Fatty (OLETF) rats. Glomerular VEGF mRNA expression and protein synthesis were evalua
Peroxisome proliferator-activated receptors (PPARs) are nuclear transcription factors and play a central role in insulin sensitivity, lipid metabolism, and inflammation. Both PPARalpha and -gamma are expressed in the kidney, and their agonists exhibit renoprotective effects in type 2 diabetes. In the present studies, we investigated the effect of the PPARalpha/gamma dual agonist tesaglitazar on diabetic nephropathy in type 2 diabetic db/db mice. Treatment of db/db mice with tesaglitazar for 3 mo
In the last 10 years, many studies have focused on the non-classical action of aldosterone. One of the most important new aspects of aldosterone is its pathogenic role as proinflammatory and profibrotic molecules. It has been reported that aldosterone induces myocardial fibrosis and vascular inflammation through up-regulation of various proinflammatory and profibrotic cytokines. We investigated the effect of aldosterone and spironolactone, which is a non-selective mineralocorticoid receptor anta
Our study suggests that the 936 C/T polymorphism of the VEGF gene may be an important factor determining plasma VEGF levels and that its polymorphism is related with diabetic retinopathy. Urinary levels of VEGF are not associated with plasma VEGF levels and associated with the stage of diabetic nephropathy.
A 12-week treatment with gemigliptin improved glycaemic control and provided UACR reduction in T2DM patients with moderate to severe RI. Gemigliptin was well tolerated, with no additional risk of hypoglycaemia and change in body weight.
These data suggest that PPARalpha gene deficiency may protect aged mice from developing insulin resistance and albuminuria induced by a HFD.
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