Evidence map›Paper›PMID 28178338›Full record

ArticlePloS one2017

The impact of obesity and adiponectin signaling in patients with renal cell carcinoma: A potential mechanism for the "obesity paradox".

Ryuichi Ito, Shintaro Narita, Mingguo Huang, Taketoshi Nara, Kazuyuki Numakura, Koichiro Takayama, Hiroshi Tsuruta, Atsushi Maeno, Mitsuru Saito, Takamitsu Inoue and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. The Association Between Adiponectin Gene Polymorphism (rs1501299) and Metabolic Syndrome.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
    Article
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  4. Review
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  8. Renal Cell Cancer and Obesity.International journal of molecular sciences · 2022
    Review
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  10. Article
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  14. Article
  15. 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

13 authors at 3 institutions in 1 country.

Ryuichi ItoDepartment of Urology, Akita University Graduate School of Medicine, Akita, Japan.
Shintaro NaritaDepartment of Urology, Akita University Graduate School of Medicine, Akita, Japan.
Mingguo HuangDepartment of Urology, Akita University Graduate School of Medicine, Akita, Japan.
Taketoshi NaraDepartment of Urology, Yamagata University Graduate School of Medicine, Yamagata, Japan.
Kazuyuki NumakuraDepartment of Urology, Akita University Graduate School of Medicine, Akita, Japan.
Koichiro TakayamaDepartment of Urology, Akita University Graduate School of Medicine, Akita, Japan.
Hiroshi TsurutaDepartment of Urology, Akita University Graduate School of Medicine, Akita, Japan.
Atsushi MaenoDepartment of Urology, Akita University Graduate School of Medicine, Akita, Japan.
Mitsuru SaitoDepartment of Urology, Akita University Graduate School of Medicine, Akita, Japan.
Takamitsu InoueDepartment of Urology, Akita University Graduate School of Medicine, Akita, Japan.
Norihiko TsuchiyaDepartment of Urology, Yamagata University Graduate School of Medicine, Yamagata, Japan.
Shigeru SatohCenter for Kidney Disease and Transplantation, Akita University Hospital, Akita, Japan.
Tomonori HabuchiDepartment of Urology, Akita University Graduate School of Medicine, Akita, Japan.
Akita University · JPYamagata University · JPAkita University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although obesity increases the risk of renal cell carcinoma (RCC), obese patients with RCC experience longer survival than non-obese patients. However, the mechanism of this "obesity paradox" is unknown. We examined the impact of preoperative BMI, serum total adiponectin (sAd) level, total adiponectin secretion from perinephric adipose tissue, and intratumoral expression of adiponectin receptors on RCC aggressiveness and survival. We also investigated the mechanism underlying enhanced cancer aggressiveness in RCC cells stimulated with exogenous adiponectin. Overweight and obese patients had significantly lower grade cancers than normal patients in all patients and in those without metastasis (p = 0.003 and p = 0.027, respectively). Cancer-specific survival was significantly longer in overweight and obese patients than in normal patients in all patients (p = 0.035). There was a weak inverse correlation between sAd level and BMI in RCC patients (r = -0.344, p = 0.002). Tumor size was slightly correlated with sAd level, and high sAd was significantly associated with poor overall survival rates in patients with non-metastatic RCC (p = 0.035). Adiponectin levels in perinephric adipose tissue and intratumoral AdipoR1/R2 expression were not correlated with RCC aggressiveness or survival. Proliferation significantly increased in 786-O and Caki-2 cells exposed to exogenous adiponectin, whereas cell invasion and migration were unaffected. In addition, exogenous adiponectin significantly inhibited starvation- and metformin-induced apoptosis, and up-regulated p-AMPK and Bcl-xL levels. In summary, low BMI and high adiponectin levels are associated with aggressive cell behaviors and poor survival in surgically-treated RCC patients. The effects of adiponectin on proliferation and apoptosis might underlie the "obesity paradox" of RCC.

Indexed as

Signal TransductionAdiponectinAdultAgedAged, 80 and overApoptosisBiomarkersBody Mass IndexCarcinoma, Renal CellCell Line, TumorCell ProliferationDisease ProgressionFemaleHumansImmunohistochemistryMaleAdiponectinBiomarkers

Identifiers

PMID28178338
PMCPMC5298294
OpenAlexW2586530606

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LicenceCC BY
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Registered trials

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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.