Regulation of fatty acid oxidation in the mammalian heart in health and disease.

A method using 3-O-methyl-D-glucose and phloretin for the determination of intracellular water space of cells in monolayer culture.

Glucose improvement of memory: a review.

Transport of nucleosides, nucleic acid bases, choline and glucose by animal cells in culture.

The rates of utilization of glycogen and exogenous glucose by hearts perfused at low coronary flows and high perfusate oxygen tension (ischemia) and by hearts perfused at high coronary flows and low perfusate oxygen tension (anoxia) were studied in the isolated, working rat heart. Ischemic tissue had a glycolytic rate that was 25% of the anoxic rate and 50% of the control rate. Inhibition of carbohydrate utilization during ischemia was due to a lower flux through the glycolytic pathway and not to a lower rate of glucose transport or substrate availability. Insulin and elevated perfusate glucose increased glucose transport and caused accumulation of free intracellular glucose, but ischemia still inhibited glucose utilization. Insulin failed to maintain tissue levels of high-energy phosphates or to prevent mechanical failure in ischemic hearts. In the absence of insulin, tissue lactate increased tenfold during 20 minutes of ischemia, although it increased only threefold in anoxic tissue. The increased tissue lactate in ischemic hearts corresponded to the inhibition of glycolysis and to the failure of mechanical performance. Insulin caused a further increase in tissue lactate during ischemia. These findings illustrate several important differences between anoxia and ischemia and suggest that insulin may be more harmful than it is beneficial in severely ischemic tissue.

Comparison of the effects of anoxia and whole heart ischemia on carbohydrate utilization in isolated working rat hearts.

Mediated (nonactive) transport of glucose in mammalian cells is characterized by saturation kinetics, stereospecificity, sensitivity to inhibition by phlorizin and certain sulfhydryl-blocking agents, a temperature coefficient of about 2, an inability to utilize metabolic energy, and countertransport. Countertransport can be explained by the development of carrier gradients in the cell membrane and provides the best evidence for carrier mobility. Efforts to identify and isolate chemical components of the transport system, have not been successful. Transport among different types of mammalian cells shows a wide range of activities (Vmax values differ by three or more orders of magnitude) and different sensitivities to hormones. Glucose enters the liver cell by mediated transport, as shown by a difference in the penetration rates of D- and L-glucose and sensitivity to phlorizin. The activity of the system is one of the highest known. Transport in muscle is the most important rate-controlling step for glucose utilization and is strongly accelerated by hypoxia, work, and insulin. The effect of work or insulin is strongly inhibited by metabolism, of fatty acids. Insulin also stimulates glucose transport in adipose tissue. Using isolated fat cells, it could be shown that insulin is rapidly bound to sites on the cell surface. The effect is lost within a few minutes after the exogenous hormone is removed. The bound insulin is not released as such, but is metabolized to unknown products. Binding is prevented by preexposure of cells to maleimide, which presumably blocks certain sulfhydryl groups at or near the insulin-binding site. Pretreatment with insulin protects against maleimide. Digestion of the cell with trypsin eliminates the acceleration of glucose transport and the inhibition of lipolysis by insulin. The glucose transport and adenyl cyclase systems are not grossly affected by trypsin, indicating that the insulin effector system is a separate entity.

https://rupress.org/jgp/article-pdf/52/1/296/1244395/296.pdf

Mediated (nonactive) transport of glucose in Mammalian cells and its regulation.

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Mediated (nonactive) transport of glucose in Mammalian cells and its regulation.