Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2006-5-4
pubmed:abstractText
Peroxisome proliferator-activated receptor alpha (PPARalpha) is a member of the ligand-activated nuclear receptor superfamily, and plays an important role in lipid metabolism and glucose homeostasis. The purpose of this study is to determine whether the activation of PPARalpha by fenofbrate would improve diabetes and its renal complications in type II diabetes mellitus. Male C57 BLKS db/db mice and db/m controls at 8 weeks of age were divided to receive either a regular diet chow (db/db, n=8; db/m, n=6) or a diet containing fenofibrate (db/db, n=8; db/m, n=7). Mice were followed for 8 weeks. Fenofibrate treatment dramatically reduced fasting blood glucose (P<0.001) and HbA1c levels (P<0.001), and was associated with decreased food intake (P<0.01) and slightly reduced body weight. Fenofibrate also ameliorated insulin resistance (P<0.001) and reduced plasma insulin levels (P<0.05) in db/db mice. Hypertrophy of pancreatic islets was decreased and insulin content markedly increased (P<0.05) in fenofibrate-treated diabetic animals. In addition, fenofibrate treatment significantly reduced urinary albumin excretion (P<0.001). This was accompanied by dramatically reduced glomerular hypertrophy and mesangial matrix expansion. Furthermore, the addition of fenofibrate to cultured mesangial cells, which possess functional active PPARalpha, decreased type I collagen production. Taken together, the PPARalpha agonist fenofibrate dramatically improves hyperglycemia, insulin resistance, albuminuria, and glomerular lesions in db/db mice. The activation of PPARalpha by fenofibrate in mesangial cells may partially contribute to its renal protection. Thus, fenofibrate may serve as a therapeutic agent for type II diabetes and diabetic nephropathy.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0085-2538
pubmed:author
pubmed:issnType
Print
pubmed:volume
69
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1511-7
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:16672921-Albuminuria, pubmed-meshheading:16672921-Animals, pubmed-meshheading:16672921-Blood Glucose, pubmed-meshheading:16672921-Body Weight, pubmed-meshheading:16672921-Cells, Cultured, pubmed-meshheading:16672921-Collagen Type I, pubmed-meshheading:16672921-Diabetes Mellitus, Type 2, pubmed-meshheading:16672921-Diabetic Nephropathies, pubmed-meshheading:16672921-Fenofibrate, pubmed-meshheading:16672921-Hemoglobin A, Glycosylated, pubmed-meshheading:16672921-Hyperglycemia, pubmed-meshheading:16672921-Hypolipidemic Agents, pubmed-meshheading:16672921-Insulin, pubmed-meshheading:16672921-Insulin Resistance, pubmed-meshheading:16672921-Islets of Langerhans, pubmed-meshheading:16672921-Kidney Glomerulus, pubmed-meshheading:16672921-Male, pubmed-meshheading:16672921-Mesangial Cells, pubmed-meshheading:16672921-Mice, pubmed-meshheading:16672921-Mice, Mutant Strains, pubmed-meshheading:16672921-PPAR alpha, pubmed-meshheading:16672921-Treatment Outcome
pubmed:year
2006
pubmed:articleTitle
PPARalpha agonist fenofibrate improves diabetic nephropathy in db/db mice.
pubmed:affiliation
Division of Nephrology and Hypertension, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural