Linked Life Data

16838191

Source:http://linkedlifedata.com/resource/pubmed/id/16838191

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2006-9-7
pubmed:abstractText
FAT/CD36 is a long-chain fatty acid transporter and scavenger receptor for oxidized LDL. Defects in FAT/CD36 have been linked to the hypertriglyceridemia and insulin resistance. Expression of FAT/CD36 was reported increase in type 1 diabetes; however, it remains unclear whether serum glucose or insulin plays an important role in this regulation. To elucidate the individual contribution of plasma glucose and insulin in the regulation of FAT/CD36 mRNA expression, we induced type 1 diabetes in male Sprague-Dawley rats using streptozotocin (STZ) and compared traditional insulin treatment with administration of the orally absorbed chemical agent vanadate, which reduces blood glucose levels via mechanisms that bypass insulin receptor action. STZ-exposed animals showed significant decreases in body weight (285.5 +/- 2.8 vs. 233.1 +/- 3.5 g, P < 0.001) and serum insulin levels (9.7 +/- 0.7 vs. 2.8 +/- 0.6 microU/ml, P < 0.05), accompanied by significant increases in blood glucose (71 +/- 3 vs. 433 +/- 11 mg/dl, P < 0.001), water intake (38.9 +/- 0.9 vs. 205.9 +/- 3.3 ml/day, P < 0.001) and food intake (22.0 +/- 0.4 vs. 36.9 +/- 1.0 g/day, P < 0.001). Diabetic animals demonstrated significant increases in FAT/CD36 mRNA levels in duodenum (2.2-fold), jejunum (1.8-fold), ileum (1.5-fold), adipose tissue (1.7-fold), and heart (2.5-fold) (P < 0.05). Insulin treatment reversed body weight loss and corrected hyperglycemia at diabetic rats as expected. Insulin treatment also corrected increased FAT/CD36 mRNA expression at diabetic rats. Vanadate significantly reduced serum glucose levels without increasing serum insulin or affecting body weight but reversed increased FAT/CD36 mRNA expression in diabetic rats. These data suggest that plasma glucose levels play more important role in the regulation of FAT/CD36 expression than concurrent changes in plasma insulin.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0179-0358
pubmed:author
pubmed:issnType
Print
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
647-54
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:16838191-Adipose Tissue, pubmed-meshheading:16838191-Animals, pubmed-meshheading:16838191-Antigens, CD36, pubmed-meshheading:16838191-Blood Glucose, pubmed-meshheading:16838191-Blotting, Northern, pubmed-meshheading:16838191-Blotting, Western, pubmed-meshheading:16838191-Body Weight, pubmed-meshheading:16838191-Diabetes Mellitus, Experimental, pubmed-meshheading:16838191-Enzyme Inhibitors, pubmed-meshheading:16838191-Gene Expression Regulation, pubmed-meshheading:16838191-Hyperglycemia, pubmed-meshheading:16838191-Insulin, pubmed-meshheading:16838191-Intestine, Small, pubmed-meshheading:16838191-Male, pubmed-meshheading:16838191-PPAR gamma, pubmed-meshheading:16838191-RNA, Messenger, pubmed-meshheading:16838191-Radioimmunoassay, pubmed-meshheading:16838191-Rats, pubmed-meshheading:16838191-Rats, Sprague-Dawley, pubmed-meshheading:16838191-Streptozocin, pubmed-meshheading:16838191-Vanadates
pubmed:year
2006
pubmed:articleTitle
The role of hyperglycemia in FAT/CD36 expression and function.
pubmed:affiliation
Department of Surgery, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
pubmed:publicationType
Journal Article