Increased erythrocyte sodium efflux during overfeeding without evidence of mediation by circulating catecholamines or thyroid hormone

Fagerberg, Björn; Herlitz, Hans; Jonsson, Olof; Nauclér, J.; Nilsson, Ulla; Hedner, Thomas; Lindstedt, Göran; Andersson, Ove

doi:10.1016/0026-0495(84)90226-9

Cited by 7 publications

(7 citation statements)

References 24 publications

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“…Furthermore, Fagerberg et nl. [40] observed a decrease in intracellular sodium and an increase in the sodium efflux rate constant after overfeeding of obese patients, and the results of the present study are in agreement with that observation.…”

Section: Discussionsupporting

confidence: 93%

Normotensive young men with family histories of hypertension gain weight and decrease their intraerythrocyte sodium content during a 5‐year follow‐up

Widgren

Herlitz

Jonsson

et al. 1991

Journal of Internal Medicine

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Young normotensive men matched for age and body mass index with (n = 16) and without (n = 13) family histories of hypertension were investigated at baseline and after 5 years of follow-up with respect to blood pressure, body weight and intracellular sodium content. Subjects with positive family histories of hypertension increased significantly in body weight (from 81.9 +/- 11.5 kg to 89.5 +/- 11.4 kg, P less than 0.001) compared to subjects with negative family histories of hypertension (from 79.9 +/- 10.8 kg to 80.7 +/- 12.2 kg, NS). Their blood pressure did not differ initially (137 +/- 12/75 +/- 11 mmHg vs. 135 +/- 8/72 +/- 9 mmHg), but was reduced in subjects without family histories of hypertension (to 125 +/- 3/68 +/- 13 mmHg) in the follow-up examination. At follow-up, body mass index showed a positive correlation with blood pressure among subjects with positive family histories of hypertension (r = 0.77, P less than 0.001). At baseline, subjects with hypertensive fathers had significantly higher intraerythrocyte sodium levels than subjects with normotensive parents. At re-examination 5 years later, this difference was no longer present. We conclude that normotensive subjects with positive family histories of hypertension are predisposed to gain weight rather than to show an increase in blood pressure at this age. Normalization of intracellular sodium content, as found in the present study, could be a consequence of this weight gain and the ensuing metabolic adaption.

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Section: Discussionsupporting

confidence: 93%

Normotensive young men with family histories of hypertension gain weight and decrease their intraerythrocyte sodium content during a 5‐year follow‐up

Widgren

Herlitz

Jonsson

et al. 1991

Journal of Internal Medicine

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“…In rats, diet‐induced obesity alters BAT and Na,K‐pump activities (139). An increased erythrocyte Na efflux during overfeeding was reported in obese men, without measurable changes in thyroid hormone or catecholamine levels (140). On the other hand, an increase in erythrocyte Na‐pump (60 min after a meal) was reported in human obesity, although a great interindividual variability was noted (141).…”

Section: Literature Review and Discussionmentioning

confidence: 99%

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

2007

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The sodium(Na)- and potassium(K)-activated adenosine-triphosphatase (Na,K-ATPase) is a membrane enzyme that energizes the Na-pump by hydrolysing adenosine triphosphate and wasting energy as heat, so playing a role in thermogenesis and energy balance. Na,K-ATPase regulation by insulin is controversial; in tissue of hyperglycemic-hyperinsulinemic ob/ob mice, we reported a reduction, whereas in streptozotocin-treated hypoinsulinemic-diabetic Swiss and ob/ob mice we found an increased activity, which is against a genetic defect and suggests a regulation by hyperinsulinemia. In human adipose tissue from obese patients, Na,K-ATPase activity was reduced and negatively correlated with body mass index, oral glucose tolerance test-insulinemic area and blood pressure. We hypothesized that obesity is associated with tissue Na,K-ATPase reduction, apparently linked to hyperinsulinemia, which may repress or inactivate the enzyme, thus opposing thyroid hormones and influencing thermogenesis and obesity development. Insulin action on Na,K-ATPase, in vivo, might be mediated by the high level of non-esterified fatty acids, which are circulating enzyme inhibitors and increase in obesity, diabetes and hypertension. In this paper, we analyse animal and human tissue Na,K-ATPase, its level, and its regulation and behaviour in some hyperinsulinemic and insulin-resistant states; moreover, we discuss the link of the enzyme with non-esterified fatty acids and attempt to interpret and organize in a coherent view the whole body of the exhaustive literature on this complicated topic.

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“…Others have failed to demonstrate this (Beutler et al, 1983;De Luise et al, 1983). Long-term energy excess has been found to increase sodium pump activity both in rats (Flier et al, 1981), and in man (Fagerberg et al, 1984). In this latter study in humans (Fagerberg et al, 1984), the increase in erythrocyte sodium ERCs occurred within a week of overfeeding, and was unassociated with any increase in thyroxine or catecholamines.…”

Section: Discussionmentioning

confidence: 54%

“…Long-term energy excess has been found to increase sodium pump activity both in rats (Flier et al, 1981), and in man (Fagerberg et al, 1984). In this latter study in humans (Fagerberg et al, 1984), the increase in erythrocyte sodium ERCs occurred within a week of overfeeding, and was unassociated with any increase in thyroxine or catecholamines. Our results showed that oral glucose could increase the leucocyte ouabain-sensitive ERC in normal subjects, agreeing with some of the work on erythrocytes (Davis et al, 1985).…”

Section: Discussionmentioning

confidence: 54%

The Effect of Oral Glucose on the Leucocyte Sodium Pump in Normal and Obese Subjects

Hockaday

1987

Clinical Endocrinology

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The effect of oral glucose (40 g/m2 body surface area) on the leucocyte 22Na efflux rate constants (ERC) was studied in 13 normal weight and 10 obese subjects. The ouabain-sensitive 22Na ERC was higher in leucocytes isolated from fasting obese subjects (median [range] for obese 2.77 [2.33-3.11] vs normals 1.91 [1.57-2.77] h-1, P less than 0.001). There was no difference in the ouabain-resistant 22Na ERC. Oral glucose raised the ouabain-sensitive 22Na ERC after 2 h in normal subjects (1.91 [1.57-2.77] to 2.41 [2.11-3.02] h-1, P less than 0.001). The ouabain-resistant 22Na ERC fell from 0.71 [0.32-1.10] to 0.46 [0.35-0.68] h-1, P less than 0.008. Conversely, in obese subjects, the ouabain-sensitive ERC fell (2.77 [2.33-3.11] to 2.59 [2.11-2.92] h-1, P less than 0.06). There was no significant change in ouabain-resistant 22Na ERC 2 h after oral glucose. The fasting leucocyte 22Na ouabain-sensitive ERC correlated with fasting plasma insulin levels and insulin resistance (rs = 0.48, P less than 0.01 for both). The change in this ERC with oral glucose correlated with the incremental insulin response over 2 h (rs = -0.53, P less than 0.006) and to the insulin resistance (rs = -0.56, P less than 0.003). The failure of oral glucose to stimulate the leucocyte sodium pump in obesity could partially account for the defect in dietary thermogenesis in obesity. This defect in stimulation of the sodium pump is related to insulin resistance.

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Increased erythrocyte sodium efflux during overfeeding without evidence of mediation by circulating catecholamines or thyroid hormone

Cited by 7 publications

References 24 publications

Normotensive young men with family histories of hypertension gain weight and decrease their intraerythrocyte sodium content during a 5‐year follow‐up

Normotensive young men with family histories of hypertension gain weight and decrease their intraerythrocyte sodium content during a 5‐year follow‐up

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

The Effect of Oral Glucose on the Leucocyte Sodium Pump in Normal and Obese Subjects

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