title: Dietary conjugated linoleic acid preserves pancreatic function and reduces inflammatory markers in obese, insulin-resistant rats.
abstract: Pancreatic preservation is an important part of diabetes management that may occur with improved peripheral insulin sensitivity and attenuated low-grade adipose tissue inflammation. The objective of the current study was to determine the response of obese, insulin-resistant fa/fa Zucker rats vs lean controls to dietary conjugated linoleic acid (CLA) supplementation with respect to pancreatic islet size, insulin resistance, and markers of inflammation and adipose glucose uptake. Six-week-old fa/fa and lean Zucker rats (n = 20 per genotype) were fed either a 1.5% CLA mixture or control diet for 8 weeks. Oral glucose tolerance testing was conducted at 7.5 weeks. Fasting serum haptoglobin, insulin, and C-peptide were assayed, and select messenger RNA (mRNA) and protein markers of inflammation and glucose metabolism were measured in adipose and liver tissues. CLA-fed fa/fa Zucker rats had smaller islet cell size, improved oral glucose tolerance and insulinemia, and attenuated serum haptoglobin levels compared with control-fed fa/fa Zucker rats, despite no differences in body weight and a slightly higher visceral adipose mass. CLA did not alter insulin sensitivity or islet size in lean Zucker rats. The CLA-fed fa/fa rats also had greater adipose glucose transporter-4 mRNA and less adipose tumor necrosis factor alpha mRNA and protein compared with control-fed fa/fa rats. In contrast, other markers of inflammation and glucose metabolism including adipose macrophage inflammatory factor, macrophage inflammatory protein-2, and liver pyruvate carboxylase and pyruvate dehydrogenase kinase 4 were not significantly changed. These results suggest that CLA supplementation preserved pancreatic function in conjunction with improved peripheral glucose use and reduced inflammation in fa/fa Zucker rats.
authors.affiliation: Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, MB, Canada R3T 2N2.
authors.forename: Amy
authors.initials: A
authors.lastname: Noto
authors.forename: Peter
authors.initials: P
authors.lastname: Zahradka
authors.forename: Natasha R
authors.initials: NR
authors.lastname: Ryz
authors.forename: Natalia
authors.initials: N
authors.lastname: Yurkova
authors.forename: Xueping
authors.initials: X
authors.lastname: Xie
authors.forename: Carla G
authors.initials: CG
authors.lastname: Taylor
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D015153:Blotting, Western; D002097:C-Reactive Protein / Q000378:metabolism; D004042:Dietary Fats, Unsaturated / Q000008:administration & dosage*; D005951:Glucose Tolerance Test; D006242:Haptoglobins / Q000378:metabolism; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology*; D050417:Insulin-Secreting Cells / Q000166:cytology / Q000378:metabolism*; D044243:Linoleic Acids, Conjugated / Q000008:administration & dosage*; D008099:Liver / Q000201:enzymology / Q000378:metabolism; D009929:Organ Size / Q000187:drug effects / Q000502:physiology; D010179:Pancreas / Q000033:anatomy & histology / Q000378:metabolism; D011494:Protein Kinases / Q000235:genetics / Q000378:metabolism; D017346:Protein Serine-Threonine Kinases; D011766:Pyruvate Carboxylase / Q000235:genetics / Q000378:metabolism; D000081382:Pyruvate Dehydrogenase Acetyl-Transferring Kinase; D051381:Rats; D011924:Rats, Zucker; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D004042:Dietary Fats, Unsaturated; D006242:Haptoglobins; D007328:Insulin; D044243:Linoleic Acids, Conjugated; D000081382:Pyruvate Dehydrogenase Acetyl-Transferring Kinase; D002097:C-Reactive Protein; D011494:Protein Kinases; D017346:Protein Serine-Threonine Kinases; D011766:Pyruvate Carboxylase