Body Composition and Glucose Metabolism in Hypertensive Middle‐aged Males

Berglund, Göran; Larsson, Bo; Ok, Andersson; Larsson, O; Svärdsudd, Kurt; Björntorp, Per; Wilhelmsen, Lars

doi:10.1111/j.0954-6820.1976.tb08215.x

Cited by 111 publications

(5 citation statements)

References 16 publications

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“…DeFronzo hypothesized in 1981 (28) that this sodium-retaining action of insulin caused, or at least contributed to, obesity hypertension via expansion of the extracellular fluid volume and increased cardiac output (28). Obesity already was known to be linked to hypertension (26,86) and also to be associated with insulin resistance and hyperinsulinemia (8,54,84). Thus, in obesity, hyperinsulinemia was hypothesized to cause volume-loading hypertension (28).…”

Section: Insulin Is a Sodium Retainer: Early Evidencementioning

confidence: 99%

“…Although this was the appropriate approach to test the question about effects of insulin, we wondered whether it was appropriate in the context of the human subjects in which the insulin-hypertension question was most relevant. Hypertensive subjects with obesity and metabolic syndrome are hyperglycemic and hyperinsulinemic (8,35,56,63,88). Therefore, we questioned whether euglycemic, hyperinsulinemia was the appropriate model.…”

Section: Neither Conclusion Has Been Supported Adequatelymentioning

confidence: 99%

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Sodium-retaining effect of insulin in diabetes

Brands¹,

Manhiani²

2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Brands MW, Manhiani MM. Sodium-retaining effect of insulin in diabetes. Am J Physiol Regul Integr Comp Physiol 303: R1101-R1109, 2012. First published October 3, 2012 doi:10.1152/ajpregu.00390.2012.-Insulin has long been hypothesized to cause sodium retention, potentially of enough magnitude to contribute to hypertension in obesity, metabolic syndrome, and Type II diabetes. There is an abundance of supportive evidence from correlational analyses in humans, acute insulin infusion studies in humans and animals, and chronic insulin infusion studies in rats. However, the absence of hypertension in human insulinoma patients, and negative results for sodium-retaining or blood pressure effects of chronic insulin infusion in a whole series of dog studies, strongly refute the insulin hypothesis. We recently questioned whether the euglycemic, hyperinsulinemia model used for most insulin infusion studies, including the previous chronic dog studies, was the most appropriate model to test the renal actions of insulin in obesity, metabolic syndrome, and Type II diabetes. In those circumstances, hyperinsulinemia coexists with hyperglycemia. Therefore, we tested the sodium-retaining effect of insulin in chronically instrumented, alloxan-treated diabetic dogs. We used 24 h/day intravenous insulin infusion to regulate plasma insulin concentration. Induction of diabetes (ϳ400 mg/dl) caused sustained natriuresis and diuresis. However, if we clamped insulin at baseline, control levels, i.e., prevented it from decreasing, then the sustained natriuresis and diuresis were completely reversed, despite the same level of hyperglycemia. We also found that 24 h/day intrarenal insulin infusion had the same effect in diabetic dogs but had no sodium-retaining action in normal dogs. This new evidence that insulin has a sodium-retaining effect during hyperglycemia may have implications for maintaining sodium balance in uncontrolled Type II diabetes.diabetes; insulin; diuresis; natriuresis; sodium balance RAISING THE QUESTION of whether insulin causes renal sodium retention, either in a scientific presentation or in the literature, immediately evokes one of two responses from the audience: 1) "I already know that insulin causes sodium retention", or 2) "Insulin does not cause sodium retention." Those maintaining the latter essentially have closed the book on the subject, and those holding to the former are interested in mechanisms but not the overarching question of whether insulin causes renal sodium retention. There is a wealth of literature to support both positions. However, nuances in many early studies raised issues that never were resolved. Inertia in the literature left many of those issues fading in the distance, all but erased from current thinking. We recently revisited the question about insulin and sodium retention, and our results were so striking that both positions on the subject warrant reconsideration. This review will chronologically present the literature supporting each position and show how our recent reports add new insigh...

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Section: Insulin Is a Sodium Retainer: Early Evidencementioning

confidence: 99%

Section: Neither Conclusion Has Been Supported Adequatelymentioning

confidence: 99%

Sodium-retaining effect of insulin in diabetes

Brands¹,

Manhiani²

2012

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Linkage of hyperinsulinism and insulin resistance to obesity was thoroughly investigated as early as the 1950s and 1960s [7][8][9]. The connections among insulin response/impaired glucose tolerance and dyslipidemia [10,11] and BP [12] with obesity/body habitus became further established during this time. In short, the inter-relationships among these variables have been the subject of study for many decades [13][14][15].…”

Section: Introductionmentioning

confidence: 99%

Update on the metabolic syndrome in children

Saland

2007

Current Opinion in Pediatrics

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Purpose of reviewProvides an update on the metabolic syndrome in childhood. Recent findingsThe metabolic syndrome is increasingly recognized among children. It is nearly exclusively encountered in overweight and obese individuals and is associated with atherosclerosis. Development and clustering of cardiovascular risk factors is influenced by many characteristics including heritable traits, prenatal and infantile influences, diet, physical activity, and socioeconomic status. Summary Epidemiological data have become mature in this area. Efforts to design and implement systems to prevent and treat the metabolic syndrome are required.

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“…Aux deux âges étudiés, si l'HTA n'est pas encore décelable, les glycémies élevées, associées à de faibles poids corporels des SHR, apparaissent cependant comme autant de signes attestant l'installation de cette pathologie. Cette tendance, déjà observée chez des patients et des modèles animaux hypertendus [54][55][56][57], s'explique par une sensibilité tissulaire à l'insuline réduite, du fait de récepteurs hormonaux défaillants [58].…”

Section: Discussionunclassified

Composition en acides gras des hémisphères cérébraux de rats spontanément hypertendus allaités par des femelles Wistar

Savelli

Narce

Fustier

et al. 2003

Comptes Rendus. Biologies

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Nous avons comparé les compositions en acides gras des lipides totaux des hémisphères cérébraux de rats spontanément hypertendus (SHR) mâles à celles de leurs témoins normotendus Wistar Kyoto (WKY). Tous les animaux ont été allaités par des mères adoptives Wistar, puis nourris par un régime standard. Nous n'observons aucune différence entre les deux hémisphères cérébraux des WKY âgés de 10 et 30 jours. Les hémisphères cérébraux des SHR sacrifiés à 10 jours présentent des différences, l'hémisphère gauche des SHR étant plus exposé à des modifications que celui des WKY, phénomènes qui s'estompent à 30 jours. Les très jeunes SHR ont donc des compositions en acides gras des hémisphères cérébraux différentes des WKY, et ce malgré une alimentation identique pour les deux souches. L'hypertension artérielle génétiquement programmée apparaît impliquée dans ces modifications, directement ou indirectement.

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Body Composition and Glucose Metabolism in Hypertensive Middle‐aged Males

Cited by 111 publications

References 16 publications

Sodium-retaining effect of insulin in diabetes

Sodium-retaining effect of insulin in diabetes

Update on the metabolic syndrome in children

Composition en acides gras des hémisphères cérébraux de rats spontanément hypertendus allaités par des femelles Wistar

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