Nutrition Alters the Stiffness of Adipose Tissue and Cell Signaling

Adipose tissue is a complex organ composed of various cell types and an extracellular matrix (ECM). The visceral adipose tissue (VAT) is dynamically altered in response to nutritional regimens that lead to local cues affecting the cells and ECM. The adipocytes are in conjunction with the surrounding...

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Main Authors: Alex Naftaly, Nadav Kislev, Roza Izgilov, Raizel Adler, Michal Silber, Ruth Shalgi, Dafna Benayahu
Format: Article
Language:English
Published: MDPI AG 2022-12-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/23/23/15237
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author Alex Naftaly
Nadav Kislev
Roza Izgilov
Raizel Adler
Michal Silber
Ruth Shalgi
Dafna Benayahu
author_facet Alex Naftaly
Nadav Kislev
Roza Izgilov
Raizel Adler
Michal Silber
Ruth Shalgi
Dafna Benayahu
author_sort Alex Naftaly
collection DOAJ
description Adipose tissue is a complex organ composed of various cell types and an extracellular matrix (ECM). The visceral adipose tissue (VAT) is dynamically altered in response to nutritional regimens that lead to local cues affecting the cells and ECM. The adipocytes are in conjunction with the surrounding ECM that maintains the tissue’s niche, provides a scaffold for cells and modulates their signaling. In this study, we provide a better understanding of the crosstalk between nutritional regimens and the ECM’s stiffness. Histological analyses showed that the adipocytes in mice fed a high-fat diet (HFD) were increased in size, while the ECM was also altered with changes in mass and composition. HFD-fed mice exhibited a decrease in elastin and an increase in collagenous proteins. Rheometer measurements revealed a stiffer ECM in whole tissue (nECM) and decellularized (deECM) in HFD-fed animals. These alterations in the ECM regulate cellular activity and influence their metabolic function. HFD-fed mice expressed high levels of the receptor for advanced-glycation-end-products (RAGE), indicating that AGEs might play a role in these processes. The cells also exhibited an increase in phosphoserine<sup>332</sup> of IRS-1, a decrease in the GLUT4 transporter levels at the cells’ membrane, and a consequent reduction in insulin sensitivity. These results show how alterations in the stiffness of ECM proteins can affect the mechanical cues transferred to adipocytes and, thereby, influence the adipocytes’ functionality, leading to metabolic disorders.
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spelling doaj.art-e8b1cf8690c5419ea7ebd8c5085c0cfd2023-11-24T11:15:40ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-12-0123231523710.3390/ijms232315237Nutrition Alters the Stiffness of Adipose Tissue and Cell SignalingAlex Naftaly0Nadav Kislev1Roza Izgilov2Raizel Adler3Michal Silber4Ruth Shalgi5Dafna Benayahu6Department of Cell and Developmental Biology, Sackler School of Medicine, Tel Aviv University, Tel Aviv 6997801, IsraelDepartment of Cell and Developmental Biology, Sackler School of Medicine, Tel Aviv University, Tel Aviv 6997801, IsraelDepartment of Cell and Developmental Biology, Sackler School of Medicine, Tel Aviv University, Tel Aviv 6997801, IsraelDepartment of Cell and Developmental Biology, Sackler School of Medicine, Tel Aviv University, Tel Aviv 6997801, IsraelDepartment of Cell and Developmental Biology, Sackler School of Medicine, Tel Aviv University, Tel Aviv 6997801, IsraelDepartment of Cell and Developmental Biology, Sackler School of Medicine, Tel Aviv University, Tel Aviv 6997801, IsraelDepartment of Cell and Developmental Biology, Sackler School of Medicine, Tel Aviv University, Tel Aviv 6997801, IsraelAdipose tissue is a complex organ composed of various cell types and an extracellular matrix (ECM). The visceral adipose tissue (VAT) is dynamically altered in response to nutritional regimens that lead to local cues affecting the cells and ECM. The adipocytes are in conjunction with the surrounding ECM that maintains the tissue’s niche, provides a scaffold for cells and modulates their signaling. In this study, we provide a better understanding of the crosstalk between nutritional regimens and the ECM’s stiffness. Histological analyses showed that the adipocytes in mice fed a high-fat diet (HFD) were increased in size, while the ECM was also altered with changes in mass and composition. HFD-fed mice exhibited a decrease in elastin and an increase in collagenous proteins. Rheometer measurements revealed a stiffer ECM in whole tissue (nECM) and decellularized (deECM) in HFD-fed animals. These alterations in the ECM regulate cellular activity and influence their metabolic function. HFD-fed mice expressed high levels of the receptor for advanced-glycation-end-products (RAGE), indicating that AGEs might play a role in these processes. The cells also exhibited an increase in phosphoserine<sup>332</sup> of IRS-1, a decrease in the GLUT4 transporter levels at the cells’ membrane, and a consequent reduction in insulin sensitivity. These results show how alterations in the stiffness of ECM proteins can affect the mechanical cues transferred to adipocytes and, thereby, influence the adipocytes’ functionality, leading to metabolic disorders.https://www.mdpi.com/1422-0067/23/23/15237adipose tissuehigh-fat dietniche stiffnessAGE–RAGE
spellingShingle Alex Naftaly
Nadav Kislev
Roza Izgilov
Raizel Adler
Michal Silber
Ruth Shalgi
Dafna Benayahu
Nutrition Alters the Stiffness of Adipose Tissue and Cell Signaling
International Journal of Molecular Sciences
adipose tissue
high-fat diet
niche stiffness
AGE–RAGE
title Nutrition Alters the Stiffness of Adipose Tissue and Cell Signaling
title_full Nutrition Alters the Stiffness of Adipose Tissue and Cell Signaling
title_fullStr Nutrition Alters the Stiffness of Adipose Tissue and Cell Signaling
title_full_unstemmed Nutrition Alters the Stiffness of Adipose Tissue and Cell Signaling
title_short Nutrition Alters the Stiffness of Adipose Tissue and Cell Signaling
title_sort nutrition alters the stiffness of adipose tissue and cell signaling
topic adipose tissue
high-fat diet
niche stiffness
AGE–RAGE
url https://www.mdpi.com/1422-0067/23/23/15237
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