Effect of Sucrose Overfeeding on Na,K-ATPase-Mediated 86Rb Uptake in Normal and ob/ob Mice

Abstract

When normal mice have their usual chow diets supplemented by free access to a solution of 10% sucrose, their caloric intake increases by about 30%. We have used this model to explore the effects of sucrose overfeeding on Na,K-ATPase-mediated cation transport. After 5 days of sucrose supplementation, Na,K-ATPase mediated K uptake is increased by 88% in liver slices and 26% in intact soleus muscles of these animals. Ob/ob mice are hyperphagic on an ad libitum chow diet, and they display even greater increments in caloric intake than do thin controls when similarly allowed access to sucrose. Despite hyperphagia while on a chow diet, Na,K-ATPase-mediated K uptake by liver slices of ob/ob mice is not significantly different from that of their thin littermates. In addition, Na,K-ATPase-mediated K uptake into liver slices of ob/ob mice does not significantly increase while on sucrose supplements. These findings demonstrate the influence of dietary factors on Na,K-ATPase-mediated ion transport in liver and muscle of normal mice, and suggest that ob/ob mice may have an impairment in such dietary control. These observations suggest an important role for nutritional factors in the overall regulation of monovalent cation transport, and may also have relevance for our understanding of the cellular mechanisms of dietary thermogenesis.

Animal and human tissue Na,K‐ATPase in normal and insulin‐resistant states: regulation, behaviour and interpretative hypothesis on NEFA effects

“…A high energy intake, in the form of sucrose supplement, increased Na,K‐ATPase‐mediated ion transport in liver and muscle of lean ob/ob control mice whereas ob/ob obese mice seemed to have an impairment in such dietary control (132).…”

Adenosine Triphosphatase Activity in Sciatic Nerve Tissue of Streptozocin-Induced Diabetic Rats with and without High Dietary Sucrose: Effect of Aldose Reductase Inhibitors

“…The rise in Na+,K+-ATPase activity was presumably due to hormonal mediators or activation of the sympathetic nervous system (36,37). Thus, with all the potential confounding metabolic and hormonal effects of high dietary sucrose, there may be unanticipated direct or indirect effects on the sciatic nerve which could affect the pathogenesis and treatment of diabetic neuropathy.…”

“…Administration of high dietary sucrose or fructose to diabetic rats is known to exacerbate tissue glucose levels, which in turn enhances polyol pathway activity (27)(28)(29), increases microangiopathy (28,(30)(31)(32), and accelerates the development of diabetic complications (29)(30)(31)(32). Additionally, high dietary sucrose induces systemic hormonal (33,34) and metabolic (33,35) alterations, which have been shown to either directly or indirectly affect Na+,K+-ATPase activity in a variety of tissues (36,37).…”

“…In addition to histopathologic changes (30-32), administration of high dietary sucrose to rodents induces hormonal and metabolic changes that are common to diabetic humans, including hyperinsulinemia (33,34), alterations in thyroid hormone metabolism (34), abnormal glucose and lipid metabolism (33,35), and elevated Na+,K+-ATPase activity in tissues such as liver and muscle (36). The rise in Na+,K+-ATPase activity was presumably due to hormonal mediators or activation of the sympathetic nervous system (36,37).…”

[Na++ K+]ATP-ase in Liver and Brain of Obese Mice

“…Both the reduced basal [Na + + K + ]ATP-ase activity and the response to thyroid hormones were restored by adrenalectomy (Shimomura, Bray and York 1981) although the mechanism of the inhibitory effect of adrenal steroids is unknown. In addition, the stimulation of hepatic [Na + + K^ATP-ase in response to dietary sucrose supplements which is observed in lean mice is absent in ob/ob mice (Flier, Usher and Deluise 1981).…”