A high-fat diet has a tissue-specific effect on adiponectin and related enzyme expression.
OBJECTIVE
This study was designed to test whether adiponectin plays a role in diet-induced obesity and insulin resistance and acts as a mediator to induce or inhibit specific metabolic pathways involved in lipid metabolism


METHODS
Forty C57BL/6J male mice were fed either a high-fat (HF) or control diet for 4 months, and adiponectin, its receptors, and enzyme expression in liver and muscle tissue were measured.


RESULTS
Mice fed the HF diet exhibited significantly greater weight gain, abnormal oral glucose tolerance test curves, and elevated homeostasis model assessment of insulin resistance (5.3 +/- 0.89 vs. 2.8 +/- 0.39). A significant reduction of adiponectin RNA expression (51%) and protein levels (15%) was observed in the adipose tissue of HF animals; however, serum adiponectin levels did not differ between groups (7.12 +/- 0.34 mug/mL vs. 6.44 +/- 0.38 microg/mL). Expression of hepatic mRNA of AdipoR1 and AdipoR2 was reduced by 15% and 25%, respectively, in animals fed the HF diet. In contrast, receptor mRNA expression of AdipoR1 and AdipoR2 increased by 25% and 30%, respectively, in muscle tissue. No effect was found on hepatic adenosine monophosphate-activated protein kinase expression; however, a significant reduction of phosphoadenosine monophosphate kinase levels in muscles was observed. Hepatic acetyl-coenzyme A carboxylase was similar between groups, but in muscles, the inactive form phosphoacetyl-coenzyme A carboxylase was significantly reduced (p < 0.05).


CONCLUSIONS
The HF diet led to decreased insulin sensitivity accompanied by impaired activity of adiponectin-related enzymes in skeletal muscles but not in the liver. These results suggest that the HF diet has a tissue-specific effect on adiponectin and associated enzyme expression.
Barnea
Maayan
M
The Hebrew University of Jerusalem, Faculty of Agricultural, Food and Environmental Quality Sciences, Institute of Biochemistry, Food Science and Nutrition, P.O. Box 12, Rehovot, 76100 Israel.
Shamay
Avi
A
Stark
Aliza H
AH
Madar
Zecharia
Z
D000103:Acetyl-CoA Carboxylase / Q000378:metabolism; D052242:Adiponectin / Q000097:blood / Q000378:metabolism*; D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D015153:Blotting, Western; D004041:Dietary Fats / Q000008:administration & dosage*; D005786:Gene Expression Regulation; D007333:Insulin Resistance; D050356:Lipid Metabolism; D008099:Liver / Q000201:enzymology / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018482:Muscle, Skeletal / Q000201:enzymology* / Q000378:metabolism; D009765:Obesity / Q000097:blood / Q000201:enzymology / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D011863:Radioimmunoassay; D011897:Random Allocation; D054419:Receptors, Adiponectin; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism; D014018:Tissue Distribution
D052242:Adiponectin; D004041:Dietary Fats; D012333:RNA, Messenger; D054419:Receptors, Adiponectin; D011956:Receptors, Cell Surface; C475419:adiponectin receptor 1, mouse; C475421:adiponectin receptor 2, mouse; D000103:Acetyl-CoA Carboxylase