Evidence map›Paper›PMID 21228110›Full record

ArticleAmerican journal of physiology. Renal physiology2011

Chronic sodium-retaining action of insulin in diabetic dogs.

M Marlina Manhiani, Michael T Cormican, Michael W Brands

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.5field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Review
  3. The damaging duo: Obesity and excess dietary salt contribute to hypertension and cardiovascular disease.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2023
    Review
  4. Insulin: Trigger and Target of Renal Functions.Frontiers in cell and developmental biology · 2020
    Review
  5. Postprandial effects on electrolyte homeostasis in the kidney.American journal of physiology. Renal physiology · 2019
    Review
  6. Observational
  7. Article
  8. Article
  9. Review
  10. Physiological hyperinsulinemia caused by acute hyperglycemia minimizes renal sodium loss by direct action on kidneys.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Article
  11. Article
  12. Insights from direct renal insulin infusion: a new hammer for an age-old nail.American journal of physiology. Renal physiology · 2018
    Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. The normal increase in insulin after a meal may be required to prevent postprandial renal sodium and volume losses.American journal of physiology. Regulatory, integrative and comparative physiology · 2017
    Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

M Marlina ManhianiDepartment of Physiology, Medical College of Georgia, Augusta, Georgia, USA.
Michael T Cormican
Michael W Brands
Augusta University · US

Funding

Mechanisms for Cardiovascular Control Early in DiabetesR01HL056259 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI BRANDS, MICHAEL W. · 2003 to 2016
$4.4M
CARDIOVASCULAR AND RENAL DYSFUNCTION IN EARLY DIABETESR29HL056259 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI BRANDS, MICHAEL W · 1997 to 2000
$100k
NHLBI NIH HHS HL56259NHLBI NIH HHS R01 HL056259
6 · The paper itself

Abstract

Insulin-mediated sodium retention is implicated as a mechanism for hypertension in metabolic syndrome and type II diabetes. However, there is no direct experimental evidence for a sustained antinatriuretic effect of insulin outside of rodents, and all previous studies in dogs have been negative. This study used a novel approach to test for a chronic sodium-retaining action of insulin in dogs, by testing the hypothesis that natriuresis in type I diabetes is dependent on the decrease in insulin, rather than being due solely to osmotic actions of hyperglycemia. Dogs were chronically instrumented and housed in metabolic cages. Fasting blood glucose in alloxan-treated dogs was maintained at ~65 mg/dl by continuous intravenous insulin infusion. Then, a 6-day diabetic period was induced by either 1) decreasing the insulin infusion to induce type I diabetes (D; blood glucose = 449 ± 40 mg/dl) or 2) clamping the insulin infusion and infusing glucose continuously (DG; blood glucose = 470 ± 56 mg/dl). Control urinary sodium excretion (UnaV) averaged 70 ± 5 (D) and 69 ± 5 (DG) meq/day and increased on day 1 in both groups. UnaV remained elevated in the D group (115 ± 15 meq/day days 2-6), but it returned to control in the DG group (69 ± 11 meq/day days 2-6) and was accompanied by decreased lithium clearance. Thus, insulin had a sustained antinatriuretic action that was triggered by increased glucose, and it was powerful enough to completely block the natriuresis caused by hyperglycemia. These data may reveal an unrecognized physiologic function of insulin as a protector against hyperglycemia-induced salt wasting in diabetes.

Indexed as

Analysis of VarianceAnimalsBlood GlucoseBlood PressureDiabetes Mellitus, ExperimentalDogsHyperglycemiaImmunoenzyme TechniquesInsulinMaleNatriuresisRandom AllocationSodiumBlood GlucoseInsulinSodium

Identifiers

PMID21228110
PMCPMC3075000
OpenAlexW2009879091

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.