Effects of the Type of Dietary Fatty Acid on the Insulin Receptor Function in Rat Epididymal Fat Cells

Abstract

Feeding young rats diets containing sunflowerseed oil (SSO) or palm oil (PO) induced several differences in the properties of the isolated epididymal fat cells: (1) insulin stimulated deoxyglucose uptake 127% over the basal value in cells of the SSO group but only 47 % in those of the PO group; the insulin concentration giving half maximal stimulation differing only slightly; (2) insulin binding to the cells was higher in the SSO group; Scatchard analysis revealed that this was due to a significantly higher number of low-affinity binding sites, and (3) the epididymal fat pad showed a concomitant change in the fatty acid pattern of the phospholipids, reflecting to a limited extent the differences in the composition of the diets. Neither the average diameters of the isolated fat cells, nor the serum insulin level at the time of sacrifice of the rats differed for the two types of dietary fat. These results indicate that a diet high in linoleic acid (SSO) induces a better response of fat cells to insulin than a diet high in saturated fatty acids (PO).

A High Fat Diet Impairs Stimulation of Glucose Transport in Muscle

“…In rats fed the high fat diet used in the present study, total visceral fat weight (retroperitoneal, mesenteric, and epididymal fat depots) is already ϳ50% greater than in chow-fed controls after 8 weeks (6). In this context, it seemed possible that the insulin resistance induced by a high fat diet could be mediated either by a membrane composition-related change in receptor function (38,39,49) or as a consequence of decreased receptor number and/or activity associated with the obesity (7-9, 50). The initial steps in the stimulation of system A amino acid transport by insulin are the same as those involved in the stimulation of glucose transport (35).…”

“…36), and two of the key proteins involved in the regulation of glucose transport, the glucose transporter and the insulin receptor, are constituents of the plasma membrane. There is considerable evidence that the catalytic activities of the glucose transporters (20,21) and the binding properties of the insulin receptor (37)(38)(39) are markedly sensitive to changes in the properties of the membrane lipid bilayer.…”

Effect of saturated fatty acid-rich dietary vegetable oils on lipid profile, antioxidant enzymes and glucose tolerance in diabetic rats

“…have also reported that PO feeding resulted in a lower rate of insulin-stimulated glucose uptake and insulin binding to the cells (lower number of low-affinity binding sites) than feeding sunflower oil. [22] Therefore, based on our results, we can state that the insulin insensitivity due to the higher intake of saturated fat may be relevant to palmitic acid-rich oil but may not be due to lauric acid-rich CO.…”

Saturated fat intake and insulin resistance in men with coronary artery disease. The Stanford Coronary Risk Intervention Project Investigators and Staff.

“…The best models contained saturated fatty acids '35 Fat cells from rats fed a high saturated fatty acid diet bind less insulin compared with cells from rats fed a high glucose diet36 or high polyunsaturated fatty acid diet.37 Insulin-stimulated glucose uptake is lower in adipocytes from rats fed a high saturated fatty acid diet versus a high polyunsaturated fatty acid diet. 37 In healthy men, glucosestimulated insulin secretion is increased after ingestion of saturated fatty acids, and this may be due to a rise in plasma gastric inhibitory polypeptide.38 Healthy volunteers exhibit decreased binding to monocyte insulin receptors when fed a high calorie diet rich in saturated fatty acids.19 Feeding a diet with a high ratio of polyunsaturated to saturated fatty acids to diabetics is associated with higher insulin binding compared with that on a low ratio diet. 39 In vitro enrichment of cells with monounsaturated and polyunsaturated fatty acids increases cell membrane fluidity and is associated with an increase in the number of insulin receptors, albeit with some decrease in receptor affinity.40 Changes in the phospholipid milieu of the cell membrane in which the insulin receptor is embedded may cause alterations in receptor structure,40 which could affect receptor function.…”