A novel peroxisome proliferator-activated receptor (PPAR)gamma agonist, NIP-222, reduces urinary albumin excretion in streptozotocin-diabetic mice independent of PPARgamma activation.

Abstract	NIP-222 is a novel peroxisome proliferator-activated receptor (PPAR)gamma agonist. This study provides evidence that NIP-222 decreases urinary albumin excretion (UAE) in diabetic mice independent of its PPARgamma activation. We compared the effect of NIP-222 and another PPARgamma agonist, troglitazone, on UAE, plasma glucose level, blood pressure, and creatinine clearance (C(cr)) in streptozotocin (STZ)-induced diabetic mice. Treatment for 3 weeks with NIP-222 (30 mg/kg) was associated with a significant decrease in UAE without any change in blood pressure, creatinine clearance, or plasma glucose level. In contrast, UAE did not decrease in mice treated with troglitazone (300 mg/kg). These results indicate that NIP-222 has PPARgamma independent effects on UAE in diabetic mice and suggest that this agent may have potential to minimize the development and progression of diabetic nephropathy.
Authors	Takashi Yotsumoto, Takeshi Naitoh, Tatsuro Kanaki, Maho Matsuda, Nobutomo Tsuruzoe
Journal	Metabolism: clinical and experimental (Metabolism) Vol. 52 Issue 12 Pg. 1633-7 (Dec 2003) ISSN: 0026-0495 [Print] United States
PMID	14669169 (Publication Type: Journal Article)
Chemical References	Angiotensin-Converting Enzyme Inhibitors Blood Glucose Chromans Hypoglycemic Agents NIP-222 Receptors, Cytoplasmic and Nuclear Thiazolidinediones Transcription Factors Captopril Luciferases Troglitazone
Topics	Albuminuria (complications, drug therapy) Angiotensin-Converting Enzyme Inhibitors (pharmacology) Animals Blood Glucose (metabolism) Blood Pressure (drug effects) Body Weight (drug effects) Captopril (pharmacology) Chromans (pharmacology) Diabetes Mellitus, Experimental (complications, urine) Diabetes Mellitus, Type 2 (genetics, metabolism) Diabetic Nephropathies (metabolism, pathology) Genes, Reporter (genetics) Hypoglycemic Agents (pharmacology) Kidney (drug effects, pathology) Luciferases (genetics) Male Mice Organ Size (drug effects) Plasmids (genetics) Receptors, Cytoplasmic and Nuclear (agonists, metabolism) Thiazolidinediones (pharmacology) Transcription Factors (agonists, metabolism) Troglitazone Urodynamics (drug effects)

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