Diet fat composition alters membrane phospholipid composition, insulin binding, and glucose metabolism in adipocytes from control and diabetic animals.
The present study was designed to determine if diet fat-induced alteration in the fatty acid composition of the adipocyte plasma membrane alters insulin binding and the insulin responsiveness of glucose metabolism in control and diabetic states. Normal (control) and diabetic (streptozotocin-induced) rats were fed high fat semipurified diets providing a high or low polyunsaturated to saturated fatty acid (P/S) ratio. Feeding a high P/S diet increased the polyunsaturated fatty acid content of major membrane phospholipids of the adipocyte plasma membrane from both normal and diabetic animals. The diabetic state was associated with an elevated content of linoleic acid and a reduced level of arachidonic acid consistent with reduced delta 6-desaturation. Feeding the high P/S diet to diabetic animals increased membrane linoleic acid content and prevented the decrease observed in the arachidonic acid of membrane phospholipids. The high P/S diet was associated with increased insulin binding in nondiabetic animals but did not change the amount of insulin bound by cells from diabetic animals. Significantly (p less than 0.05) increased rates of insulin-stimulated glucose transport and lipogenesis (glucose incorporation into lipids) were observed in control animals fed the high as compared to the low P/S diet. The rates of insulin-stimulated glucose transport, oxidation, and lipogenesis were lower (p less than 0.05) for cells from diabetic as compared to control animals. However, feeding a high P/S diet significantly improved rates for all three of these functions (p less than 0.05). It is concluded that diet-induced alterations in membrane composition may provide a mechanism for improving the cellular response to insulin in cells from diabetic animals.
Field
C J
CJ
Nutrition and Metabolism Research Group, Faculty of Medicine, University of Alberta, Edmonton, Canada.
Ryan
E A
EA
Thomson
A B
AB
Clandinin
M T
MT
D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism; D001692:Biological Transport / Q000187:drug effects; D001786:Blood Glucose / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D004041:Dietary Fats / Q000008:administration & dosage / Q000494:pharmacology*; D005227:Fatty Acids / Q000008:administration & dosage / Q000378:metabolism; D005231:Fatty Acids, Unsaturated / Q000008:administration & dosage; D005947:Glucose / Q000378:metabolism*; D007328:Insulin / Q000097:blood / Q000378:metabolism* / Q000494:pharmacology; D019787:Linoleic Acid; D008041:Linoleic Acids / Q000378:metabolism; D008297:Male; D008563:Membrane Lipids / Q000378:metabolism*; D010084:Oxidation-Reduction; D010713:Phosphatidylcholines / Q000378:metabolism; D010714:Phosphatidylethanolamines / Q000378:metabolism; D010716:Phosphatidylinositols / Q000378:metabolism; D010743:Phospholipids / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D001095:Arachidonic Acids; D001786:Blood Glucose; D004041:Dietary Fats; D005227:Fatty Acids; D005231:Fatty Acids, Unsaturated; D007328:Insulin; D008041:Linoleic Acids; D008563:Membrane Lipids; D010713:Phosphatidylcholines; D010714:Phosphatidylethanolamines; D010716:Phosphatidylinositols; D010743:Phospholipids; D016718:Arachidonic Acid; D019787:Linoleic Acid; D005947:Glucose