| 논문분류 | 춘계학술대회 초록집 |
|---|---|
| 제목 | Renoprotective Effects of Dipeptidyl Peptidase-IV Inhibition in High Fat Diet-induced Obese Mice |
| 저자 | Hyunwook Kim1, Ji Eun Lee1, Mi Hwa Lee2, Jung Eun Kim2, Hye Kyoung Song2, Jin Joo Cha2, Hye Sook Min2, Mi Jin Lee2, Sang Yeob Han3, Geum Hyun Han3, Young Youl Hyun4, Jee Young Han5, Young Sun Kang2, Dae Ryong Cha2 |
| 출판정보 | 2013; 2013(1): |
| 키워드 | DPP-IV, 당뇨병성 신증, 비만/ DPP-IV, Diabetic nephropathy, Obesity |
| 초록 | Aims: dipeptidyl petidase-IV (DPP-IV) inhibition is currently being regarded as a promising strategy for diabetes management. However, its direct anti-enzymatic effect on kidney and its consequences are largely unknown. Therefore, in this study, we tested whether DPP-IV inhibition contributes to renoprotection and identified its mechanisms using high fat diet-induced obese mice model. Methods: normal chow-fed control mice, vehicle-treated high fat diet-induced obese mice, and DPP-IV inhibitor (LC15-0444)-treated high fat diet-induced obese mice were assessed by various metabolic parameters and by the changes in DPP-IV activity of target organs, including kidney. Results: after 3 months of treatment, the high fat-induced obese mice administered LC15-0444 at the dose of 3 mg/kg via gastric intubation showed no differences in the levels of blood glucose, blood pressure, insulin resistance and oxidative stress parameters, or pro-inflammatory and fibrotic mRNA expressions both in kidney and adipose tissue, compared with vehicle-treated high fat-induced obese mice. However, treatment with LC15-0444 significantly decreased levels of DPP-IV activity measured by fluorophotometric assay in serum, kidney, and liver of the experimental mice. Furthermore, the mice treated with LC15-0444 showed significantly reduced microalbuminuria excretion and the tendency to preserve renal function measured by creatinine clearance. In addition, the mice treated with LC15-0444 also showed significantly decreased left ventricular mass index. Conclusion: DPP-IV inhibition seems to contribute to target organ protection via modulation of DPP-IV activity, possibly independently of blood glucose control or modulation of metabolic parameters. Further investigations are warranted to elucidate these mechanisms. |
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