A saturated fatty acid-rich diet induces an obesity-linked proinflammatory gene expression profile in adipose tissue of subjects at risk of metabolic syndrome.
BACKGROUND
Changes in dietary fat composition could lower the risk of developing metabolic syndrome. Adipose tissue is an interesting tissue in this respect because of its role in lipid metabolism and inflammation.


OBJECTIVE
Our objective was to investigate the effect of a saturated fatty acid (SFA)- and a monounsaturated fatty acid (MUFA)-rich diet on insulin sensitivity, serum lipids, and gene expression profiles of adipose tissue in subjects at risk of metabolic syndrome.


METHODS
A parallel controlled-feeding trial was conducted in 20 abdominally overweight subjects. Subjects received an SFA diet or a MUFA diet for 8 wk. Plasma and subcutaneous adipose tissue samples were obtained, and insulin sensitivity was measured by using a hyperinsulinemic-euglycemic clamp. Adipose tissue samples underwent whole-genome microarray and histologic analysis. Plasma and adipose tissue fatty acid composition and concentrations of serum cholesterol and plasma cytokine were determined.


RESULTS
Consumption of the SFA diet resulted in increased expression of genes involved in inflammation processes in adipose tissue, without changes in morphology or insulin sensitivity. The MUFA diet led to a more antiinflammatory gene expression profile, which was accompanied by a decrease in serum LDL-cholesterol concentrations and an increase in plasma and adipose tissue oleic acid content.


CONCLUSIONS
Consumption of an SFA diet resulted in a proinflammatory "obesity-linked" gene expression profile, whereas consumption of a MUFA diet caused a more antiinflammatory profile. This suggests that replacement of dietary SFA with MUFA could prevent adipose tissue inflammation and may reduce the risk of inflammation-related diseases such as metabolic syndrome. This trial was registered at clinicaltrials.gov as NCT00405197.
van Dijk
Susan J
SJ
The Division of Human Nutrition, Wageningen University, Wageningen, Netherlands.
Feskens
Edith J M
EJ
Bos
Marieke B
MB
Hoelen
Dianne W M
DW
Heijligenberg
Rik
R
Bromhaar
Mechteld Grootte
MG
de Groot
Lisette C P G M
LC
de Vries
Jeanne H M
JH
Müller
Michael
M
Afman
Lydia A
LA
D052242:Adiponectin / Q000097:blood / Q000235:genetics; D000273:Adipose Tissue / Q000378:metabolism*; D000328:Adult; D000368:Aged; D018946:Chemokine CCL5 / Q000097:blood; D003176:Complement C3 / Q000032:analysis; D005227:Fatty Acids / Q000008:administration & dosage*; D005260:Female; D020869:Gene Expression Profiling; D006801:Humans; D007150:Immunohistochemistry; D007333:Insulin Resistance; D008055:Lipids / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome / Q000378:metabolism*; D008875:Middle Aged; D020411:Oligonucleotide Array Sequence Analysis; D047495:PPAR gamma / Q000235:genetics
D052242:Adiponectin; C483024:CCL5 protein, human; D018946:Chemokine CCL5; D003176:Complement C3; D005227:Fatty Acids; D008055:Lipids; D047495:PPAR gamma