Functional correlates of Na+,K+-ATPase in lean and obese () mice

Lin, Ming Huey; Romsos, Dale R.; Akera, Tai; Leveille, Gilbert A.

doi:10.1016/0026-0495(81)90176-1

Cited by 18 publications

(6 citation statements)

References 39 publications

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“…Despite this exaggerated hyperphagia in response to sucrose, pumpmediated K uptake by liver slices did not increase significantly ( Figure 3). It should be noted that our finding of normal pump mediated 86 Rb uptake in ob/ob liver slices during chow feeding contrasts with earlier reports showing that obese mice have reduced ATPase enzymatic activity (assessed by ATP hydrolysis) 11 as well as reduced number of enzyme units (assessed by 3 H ouabain binding) 12 when these measurements were made in homogenates of liver and muscle. To assess this discrepancy, we measured both enzyme-mediated 86 Rb uptake into liver pieces and enzyme-mediated ATP hydrolysis 11 liver homogenates of ob/ob mice had Na,K-ATPase activity reduced by a mean of 34 ± 10%.…”

Section: Effects Of Sucrose Overfeeding On Nak-pump-mediated 86contrasting

confidence: 99%

“…Thyroid hormone, 7 insulin, 8 beta adrenergic agonists, 9 and aldosterone 10 have each been shown to have specific effects on either the number of pump units or their activity in various organs, but the integrated physiologic role of these or other factors in regulation of the enzyme in health and disease has not been defined. Interest in this question has been increased by recent observations that the activity 11 and number 12 of Na.K-ATPase units is diminished in liver and muscle of obese mice (ob/ob) and in red blood cells of some obese humans, 13 -14 and that Na.K-ATPase activity is increased in liver homogenates of obese humans. 15 To probe the dietary and hormonal regulation of Na,Kpump activity in normal and disease states, we have employed the model of voluntary sucrose overfeeding.…”

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confidence: 99%

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

Flier¹,

Usher²,

Deluise³

1981

Diabetes

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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.

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Section: Effects Of Sucrose Overfeeding On Nak-pump-mediated 86contrasting

confidence: 99%

mentioning

confidence: 99%

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

Flier¹,

Usher²,

Deluise³

1981

Diabetes

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“…Bray and Yukimura reported decreased Na C /K C -ATPase activity in the liver of animals with experimental obesity (Bray & Yukimura 1978). Furthermore, Lin et al (1978Lin et al ( , 1981 have shown that the protein levels of Na C /K C -ATPase subunits are lower in the skeletal muscle and liver of adult obese (ob/ob) mice than in those of their lean counterparts, probably due to the decrease in the number of enzyme units. This, of course, cannot be due to an inhibitory effect, but could be the result of a repressing effect (Iannello et al 2007a).…”

Section: And Obesitymentioning

confidence: 99%

Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular diseases

Obradović¹,

Bjelogrlić²,

Rizzo³

et al. 2013

Journal of Endocrinology

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“…[ [22][23]. Despite observations which included reduced Na + -K + -ATPase activity in several tissues (liver, kidney and skeletal muscle) of ob/ob mice [24][25], these mechanisms were considered to have two key disadvantages. First, there was little evidence that they would make more than a minor contribution to thermogenesis, and in the case of protein turnover, could be rapidly switched on and off without wider implications for metabolic regulation.…”

Section: A Link Between Brown Adipose Tissue Diet-induced Thermogenementioning

confidence: 99%

Origins and early development of the concept that brown adipose tissue thermogenesis is linked to energy balance and obesity

Trayhurn

2017

Biochimie

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Brown adipose tissue (BAT) was identified as a thermogenic organ in 1961, and in 1978 shown to be the major site of thermoregulatory non-shivering thermogenesis in rats acclimated to the cold. Investigations in the mid-late 1970s established the uncoupling of oxidative phosphorylation through a proton conductance pathway across the mitochondrial inner membrane as the mechanism for heat production in BAT, this being regulated by UCP1 which was first discovered as a 32,000 M cold-inducible protein. These developments came when those concerned with nutritional energetics were proposing that thermogenesis is a significant factor in energy balance and the aetiology of obesity. A link with BAT was first demonstrated in obese ob/ob mice, which were shown to have decreased thermogenic activity in the tissue, and in rats exhibiting diet-induced thermogenesis (DIT) during overfeeding on a cafeteria diet where an activation of brown fat was evident. These pioneering observations led to extensive studies on BAT in different animal models of obesity, both genetic (particularly ob/ob and db/db mice, fa/fa rats) and experimentally-induced. In each case, indices of BAT activity and capacity (mitochondrial content, GDP binding, amount of UCP1) indicated that the tissue plays a role in DIT and that obesity is characterised by reduced thermogenesis. Links between BAT and whole-body energetics were also made in physiological situations such as lactation and fasting. Studies in the 1980s also provided clear evidence for the presence of BAT in adult humans, particularly through the detection of UCP1, and its activation in patients with phaeochromocytoma. Interest in BAT in energetics and obesity waned by the 1990s; the current major renewal of interest has undoubtedly been contingent on the pioneering developments that emerged some 40 years ago.

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Functional correlates of Na+,K+-ATPase in lean and obese () mice

Cited by 18 publications

References 39 publications

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

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

Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular diseases

Origins and early development of the concept that brown adipose tissue thermogenesis is linked to energy balance and obesity

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