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Complex networks interactions between bioactive compounds and adipose tissue vis-à-vis insulin resistance.

作者信息

Barrera-Esparza María, Carreón-Torres Elizabeth, Jiménez-Osorio Angélica Saraí, Angel-García Julieta, Jiménez-Garza Octavio, Flores-Chávez Olga Rocío, Mendoza-Catalán Geu S, Estrada-Luna Diego

机构信息

Coordinación de Unidades de Segundo Nivel, Oficina Central, Servicios de Salud del Instituto Mexicano del Seguro Social para el Bienestar (IMSS-BIENESTAR), Mexico City, Mexico.

Physics Institute, Universidad Nacional Autónoma de México (UNAM), Mexico City, Mexico.

出版信息

Front Endocrinol (Lausanne). 2025 May 13;16:1578552. doi: 10.3389/fendo.2025.1578552. eCollection 2025.


DOI:10.3389/fendo.2025.1578552
PMID:40433407
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12106009/
Abstract

Fatty acids disorders may lead to insulin resistance, resulting in long-term oxidative stress and inflammatory processes, both mediated by adipose tissue. Either in normal condition or obesogenic status, adipose cells components play an important role in several physiological and metabolic conditions. It has been shown that bioactive compounds can influence the development of obesity and its pathological complications such as insulin resistance. In this study, we performed a network between bioactive compounds and adipose tissue vis-a-vis insulin resistance. We constructed a regulatory network of 62 adipocyte cell components that incorporates current evidence of cellular and molecular interactions involved in healthy and obesity states. The network incorporated information about inflammation pathways and inhibition of insulin signaling; insulin signaling and GLUT 4 translocation; triglycerides production; ATP production; M2 macrophages recruitment; adipogenesis and lipolysis as well as mitochondrial biogenesis. Our mathematical model showed a discernment between the impact of various bioactive substances on the transitions from health to obesity and vice versa. We found that anthocyanins, punicalagin, oleanolic acid, and NRG4 proved to be critical nodes in the transition from obesity to the healthy state, due to their switch-on potential to up-regulate the complex network resulting in a beneficial transition.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6d/12106009/acd96255df73/fendo-16-1578552-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6d/12106009/b3f47c84416e/fendo-16-1578552-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6d/12106009/de27f58922e3/fendo-16-1578552-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6d/12106009/b840e071a6a1/fendo-16-1578552-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6d/12106009/2deffc6e30b1/fendo-16-1578552-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6d/12106009/1060cec17cbb/fendo-16-1578552-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6d/12106009/b70fcd39e491/fendo-16-1578552-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6d/12106009/acd96255df73/fendo-16-1578552-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6d/12106009/b3f47c84416e/fendo-16-1578552-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6d/12106009/de27f58922e3/fendo-16-1578552-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6d/12106009/b840e071a6a1/fendo-16-1578552-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6d/12106009/2deffc6e30b1/fendo-16-1578552-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6d/12106009/1060cec17cbb/fendo-16-1578552-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6d/12106009/b70fcd39e491/fendo-16-1578552-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6d/12106009/acd96255df73/fendo-16-1578552-g007.jpg

相似文献

[1]
Complex networks interactions between bioactive compounds and adipose tissue vis-à-vis insulin resistance.

Front Endocrinol (Lausanne). 2025-5-13

[2]
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[3]
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[4]
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[5]
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[6]
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J Clin Invest. 2021-12-1

[7]
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Nutr Metab Cardiovasc Dis. 2009-2

[8]
Adipocyte integrin-linked kinase plays a key role in the development of diet-induced adipose insulin resistance in male mice.

Mol Metab. 2021-7

[9]
Targetted inhibition of CD74 attenuates adipose COX-2-MIF-mediated M1 macrophage polarization and retards obesity-related adipose tissue inflammation and insulin resistance.

Clin Sci (Lond). 2018-7-31

[10]
Adipocyte-specific deletion of Depdc5 exacerbates insulin resistance and adipose tissue inflammation in mice.

Biochem Biophys Res Commun. 2021-9-10

本文引用的文献

[1]
Adipose endothelin signaling-An unusual suspect linking obesity to insulin resistance.

Acta Physiol (Oxf). 2024-12

[2]
Adiponectin Resistance in Obesity: Adiponectin Leptin/Insulin Interaction.

Adv Exp Med Biol. 2024

[3]
Picalm, a novel regulator of GLUT4-trafficking in adipose tissue.

Mol Metab. 2024-10

[4]
M2 macrophage-polarized anti-inflammatory microneedle patch for accelerating biofilm-infected diabetic wound healing via modulating the insulin pathway.

J Nanobiotechnology. 2024-8-14

[5]
Advancing cancer drug development with mechanistic mathematical modeling: bridging the gap between theory and practice.

J Pharmacokinet Pharmacodyn. 2024-12

[6]
Structure and dynamics of enterovirus genotype networks.

Sci Adv. 2024-6-21

[7]
Marine Compounds and Age-Related Diseases: The Path from Pre-Clinical Research to Approved Drugs for the Treatment of Cardiovascular Diseases and Diabetes.

Mar Drugs. 2024-5-3

[8]
Influence of glucagon-like peptide-1 receptor agonists on fat accumulation in patients with diabetes mellitus and non-alcoholic fatty liver disease or obesity: A systematic review and meta-analysis of randomized control trials.

J Diabetes Complications. 2024-6

[9]
Mathematical modeling of viral infection and the immune response controlled by the circadian clock.

J Biol Phys. 2024-6

[10]
Capsaicin induces ATP-dependent thermogenesis via the activation of TRPV1/β3-AR/α1-AR in 3T3-L1 adipocytes and mouse model.

Arch Biochem Biophys. 2024-5

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