Evidence map›Paper›PMID 36151575›Full record

ArticleBMC endocrine disorders2022

The interaction between rs 3,807,992 genotypes with the dietary inflammatory index on Leptin, Leptin resistance, and Galectin 3 in obese and overweight women.

Farideh Shiraseb, Mena Farazi, Niloufar Rasaei, Cain C T Clark, Shahin Jamili, Khadijeh Mirzaei

Open access · goldAbstract read
In one paragraph

Article in BMC endocrine disorders, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 45% 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

4 citing papers in PubMed, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.

  1. Pooled it
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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

6 authors at 3 institutions in 2 countries.

Farideh ShirasebDepartment of Community Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences (TUMS), P.O.Box: 14155-6117, Tehran, Iran.
Mena FaraziDepartment of Community Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences (TUMS), P.O.Box: 14155-6117, Tehran, Iran.
Niloufar RasaeiDepartment of Community Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences (TUMS), P.O.Box: 14155-6117, Tehran, Iran.
Cain C T ClarkCentre for Intelligent Healthcare, Coventry University, Coventry, CV1 5FB, UK.
Shahin JamiliGeneral Surgeon (Fellowship of Minimally Invasive Surgery), Department of Surgery, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Khadijeh MirzaeiDepartment of Community Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences (TUMS), P.O.Box: 14155-6117, Tehran, Iran. mirzaei_kh@tums.ac.ir.
Tehran University of Medical Sciences · IRIntelligent Health (United Kingdom) · GBShahid Beheshti University of Medical Sciences · IR

Funding

Tehran University of Medical Sciences and Health Services 97-03-161-41017
6 · The paper itself

Abstract

objectiveObesity is related to increasing leptin and some inflammatory factors that are associated with low-grade inflammation. Moreover, several studies have shown Caveolin-1 (CAV1) genetic variations may be associated with dietary intake. The current study aimed to evaluate the interaction of CAV1 rs3807992 with types of the energy-adjusted dietary inflammatory index (EDII) in leptin, leptin resistance, and Galectin 3, as inflammatory factors.

methodsThis cross-sectional study was carried out on 363 overweight and obese females. Dietary intake and DII were obtained from a 147-item food frequency questionnaire (FFQ). The CAV-1 genotype was measured using the PCR-RFLP method. Anthropometric values and serum levels of leptin and Galectin 3 were measured by standard methods.

resultsIncreased adherence to EDII in the interaction with CAV1 genotypes led to an increase in leptin level 79.15 (mg/l) (β = 79.15, CI = - 1.23,163.94, P = 0.04) in model 3, after controlling for further potential confounders. By contrast, adherence to EDII in the interaction with the genotype including risk alleles showed no significant interaction, even after adjustment in model 3 (β = 0.55, CI = - 0.99, 2.09, P = 0.48). Although, a marginal positive significant interaction was found between EDII and CAV1 genotypes on Galectin 3, after adjustment in model 3 (β = 31.35, CI = 0.13, 77.13, P = 0.05).

conclusionsThe present study indicates that a high adherence of EDII and CAV1 genotypes containing risk alleles may be a prognostic factor and increase both leptin and Galectin3. However, it seems that the presence of interaction was not on leptin resistance. Further functional studies are necessary to elucidate the exact mechanism.

Indexed as

Caveolin 1Galectin 3LeptinObesityOverweightCross-Sectional StudiesFemaleGenotypeHumansCAV1 protein, humanCaveolin 1Galectin 3LeptinCaveolin-1Dietary inflammatory indexGalectin 3InteractionLeptinLeptin resistance

Identifiers

PMID36151575
PMCPMC9508720
OpenAlexW4296896702

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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.