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

    Research output: Contribution to journalArticlepeer-review

    32 Downloads (Pure)

    Abstract

    Objective: Obesity 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. Methods: This 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. Results: Increased 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). Conclusions: The 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.

    Original languageEnglish
    Article number237
    Number of pages12
    JournalBMC Endocrine Disorders
    Volume22
    Issue number1
    Early online date23 Sept 2022
    DOIs
    Publication statusPublished - Dec 2022

    Bibliographical note

    © The Author(s) 2022. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which
    permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the
    original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or
    other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativeco
    mmons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data

    Funder

    Funding Information: This study is funded by grants from the Tehran University of Medical Sciences (TUMS). (Grant ID: 97-03-161-41017). Publisher Copyright: © 2022, The Author(s).

    Keywords

    • Research
    • Leptin
    • Leptin resistance
    • Galectin 3
    • Caveolin-1
    • Dietary inflammatory index
    • Interaction

    Fingerprint

    Dive into the research topics of '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'. Together they form a unique fingerprint.

    Cite this