Evidence map›Paper›PMID 26334732›Full record

ArticlePloS one2015

Irisin and the Metabolic Phenotype of Adults with Prader-Willi Syndrome.

Harry J Hirsch, Itai Gross, Yehuda Pollak, Talia Eldar-Geva, Varda Gross-Tsur

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Salivary and serum irisin in healthy adults before and after exercise.European journal of translational myology · 2023
    Article
  5. Review
  6. Review
  7. Article
  8. Irisin and Secondary Osteoporosis in Humans.International journal of molecular sciences · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
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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

5 authors at 2 institutions in 1 country.

Harry J HirschIsrael Multidisciplinary Prader-Willi Syndrome Clinic, Neuropediatric Unit, Department of Pediatrics, Shaare Zedek Medical Center, Jerusalem, Israel.
Itai GrossDepartment of Pediatrics, Hadassah Hospital, Ein Kerem, Jerusalem, Israel.
Yehuda PollakIsrael Multidisciplinary Prader-Willi Syndrome Clinic, Neuropediatric Unit, Department of Pediatrics, Shaare Zedek Medical Center, Jerusalem, Israel; The School of Education, The Hebrew University, Jerusalem, Israel.
Talia Eldar-GevaThe Hebrew University Faculty of Medicine, Jerusalem, Israel; Reproductive Endocrinology and Genetics Unit, Department of Obstetrics and Gynecology, Shaare Zedek Medical Center, Jerusalem, Israel.
Varda Gross-TsurIsrael Multidisciplinary Prader-Willi Syndrome Clinic, Neuropediatric Unit, Department of Pediatrics, Shaare Zedek Medical Center, Jerusalem, Israel; The Hebrew University Faculty of Medicine, Jerusalem, Israel.
Shaare Zedek Medical Center · ILHebrew University of Jerusalem · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

contextHyperphagia, low resting energy expenditure, and abnormal body composition contribute to severe obesity in Prader Willi syndrome (PWS). Irisin, a circulating myokine, stimulates "browning" of white adipose tissue resulting in increased energy expenditure and improved insulin sensitivity. Irisin has not been previously studied in PWS.

objectivesCompare plasma and salivary irisin in PWS adults and normal controls. Examine the relationship of irisin to insulin sensitivity and plasma lipids. DESIGN AND STUDY

participantsA fasting blood sample for glucose, lipids, insulin, leptin, adinopectin, and irisin was obtained from 22 PWS adults and 54 healthy BMI-matched volunteers. Saliva was collected for irisin assay in PWS and controls.

resultsFasting glucose (77 ± 9 vs 83 ± 7 mg/dl, p = 0.004), insulin (4.1 ± 2.0 vs 7.9 ± 4.7 μU/ml, p<0.001), and triglycerides (74 ± 34 vs 109 ± 71 mg/dl, p = 0.007) were lower in PWS than in controls. Insulin resistance (HOMA-IR) was lower (0.79 ± 0.041 vs 1.63 ± 1.02, p<0.001) and insulin sensitivity (QUICKI) was higher (0.41 ± 0.04 vs 0.36 ± 0.03, p<0.001) in PWS. Plasma irisin was similar in both groups, but salivary irisin (64.5 ± 52.0 vs 33.0 ± 12.1ng/ml), plasma leptin (33.5 ± 24.2 vs 19.7 ± 19.3 ng/ml) and plasma adinopectin (13.0 ± 10.8 vs 7.6 ± 4.5μg/ml) were significantly greater in PWS (p<0.001). In PWS, plasma irisin showed positive Pearson correlations with total cholesterol (r = 0.58, p = 0.005), LDL-cholesterol (r = 0.59, p = 0.004), and leptin (r = 0.43, p = 0.045). Salivary irisin correlated negatively with HDL-cholesterol (r = -0.50, p = 0.043) and positively with LDL-cholesterol (r = 0.51, p = 0.037) and triglycerides (r = 0.50, p = 0.041).

conclusionsSalivary irisin was markedly elevated in PWS although plasma irisin was similar to levels in controls. Significant associations with plasma lipids suggest that irisin may contribute to the metabolic phenotype of PWS.

Indexed as

AdolescentAdultBlood GlucoseCase-Control StudiesFemaleFibronectinsHumansInsulinInsulin ResistanceLeptinLipidsMalePhenotypePrader-Willi SyndromeSalivaYoung AdultBlood GlucoseFibronectinsFNDC5 protein, humanInsulinLeptinLipids

Identifiers

PMID26334732
PMCPMC4559418
OpenAlexW1818635750

What OpenQuestion holds

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LicenceCC BY
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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.