The Effects of Dietary Carbohydrate Content on Insulin Binding and Glucose Metabolism by Isolated Rat Adipocytes*

Abstract

The effects of changes in the amount of dietary carbohydrate (CHO) on cellular insulin and glucose metabolism have been assessed in rat adipocytes. Feeding animals a 67% CHO (fat-free) diet resulted in decreased insulin binding but enhanced activity of both the glucose transport system and intracellular pathways of glucose metabolism. Feeding rats a 67% fat (CHO-free) diet resulted in decreased insulin receptors as well as decreased activity of the glucose transport system and intracellular glucose metabolism. Therefore, the in vivo insulin resistance caused by a high fat, low CHO diet seems to be adequately explained, since all aspects of insulin's cellular action were depressed. On the other hand, at first approximation, the increased in vivo insulin response caused by a high CHO diet appears contradictory to the observed decrease in insulin binding. However, a probable explanation for this apparent paradox is provided by the enhanced activity of the cellular insulin effector systems distal to the insulin receptor. Therefore, the increased in vivo insulin responsiveness after high CHO feedings is most likely due to post receptor increases in various aspects of glucose metabolism.

Physiologic evaluation of factors controlling glucose tolerance in man: measurement of insulin sensitivity and beta-cell glucose sensitivity from the response to intravenous glucose.

“…Nonetheless, we believe that a more complete study of the range of doses over which the model is applicable would be worthwhile. is independent of acute changes in insulin it may be related to the influence of basal insulin concentration on the levels of those enzymes that are dependent upon a constant insulin environment for their activities, such as glucokinase and glycogen synthase in the liver (29,30) and glucose transport units in tissues for which glucose transport is insulin dependent (31). Thus, the diminished glucose effectiveness may be related to insulin resistance in that it could be a secondary manifestation of the resistance of tissues to the "permissive" rather than acute effects of the hormone.…”

The effect of diet on fat cell metabolism. A review

“…A higher carbohydrate content in the diet of rats may, after a longer time, reduce insulin binding by cells of this tissue and intensify intracellular degradation of the hormone. Despite this, the uptake of glucose by fat cells may by elevated (Olefsky and Seakow, 1978). Glucose is then converted to a greater degree to triglycerides (Olefsky and Seakow, 1978).…”

“…Despite this, the uptake of glucose by fat cells may by elevated (Olefsky and Seakow, 1978). Glucose is then converted to a greater degree to triglycerides (Olefsky and Seakow, 1978). In experiments using fat cells from young pigs, it was shown that feeding these animals feeds with the addition of maize starch caused a distinct rise in lipogenesis stimulated by insulin (Smith et al, 1996).…”

“…Increasing the fat level of a diet distinctly inhibits the de novo synthesis of fatty acids in fat cells obtained from growing pigs (Allee et al, 1971;Mersmann et al, 1984;Benmansour et al, 1991) and rats (Smith et al, 1974;Lavau at al., 1979). This seems to result from the fact that a high dietary fat content markedly restricts the uptake of glucose by fat cells (Ip et al, 1977;Olefsky and Seakow 1978;Pedersen et al, 1991;Sevilla et al, 1997). The maximum transportation speed of this sugar is, as a result, reduced (Olefsky and Seakow 1978).…”

“…This seems to result from the fact that a high dietary fat content markedly restricts the uptake of glucose by fat cells (Ip et al, 1977;Olefsky and Seakow 1978;Pedersen et al, 1991;Sevilla et al, 1997). The maximum transportation speed of this sugar is, as a result, reduced (Olefsky and Seakow 1978). Deterioration of the transport of glucose into cells appears as the result of a drastic reduction of the number of glucose transporters in cell membranes.…”