Glucose metabolism in fat cells stimulated by insulin and dependent on sodium.

Abstract

SPECIFIC transport of organic and inorganic substances through biological membranes has been well established1. Transport of organic substances, such as amino-acids and sugars, may be active and is, as a rule, linked to the transport of cations2, most frequently those of sodium and potassium3. Other transport mechanisms may agree rather with the definition of facilitated diffusion which seems to be independent of cations4. It is usually thought that in insulin tissues such as muscle and adipose tissue which respond to insulin, this hormone somehow favours the facilitated diffusion of glucose and of certain other sugars5,6. Insulin also facilitates, however, the entry of some substrates which pass through by active transport7, and, furthermore, it has been shown to increase the resting electrical potential of muscle8 and of adipose tissue9, while stimulating decreasing retention of potassium and sodium ions respectively in these tissues10,11. While Hagen12 has reported that insulin has less effect on glucose metabolism by adipose tissue in the absence of sodium or potassium ions, Rodbell13 has observed normal responsiveness to insulin of isolated fat cells in the absence of sodium ions. These conflicting views have encouraged us to investigate the effects of changing the concentration of cations in the medium glucose transport and metabolism by isolated fat cells, both in the presence and absence of insulin. A marked sodium dependency of insulin-stimulated glucose metabolism in fat cells on sodium has been found.