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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Adipocyte hypertrophy parallels alterations of mitochondrial status in a cell model for adipose tissue dysfunction in obesity.
Life Sci. 265:118812 (2021)
Aims: Adipocyte hypertrophy is the main cause of obesity. A deeper understanding of the molecular mechanisms regulating adipocyte dysfunction may help to plan strategies to treat/prevent obesity and its metabolic complications. Here, we investigated in vitro the molecular alterations associated with early adipocyte hypertrophy, focusing on mitochondrial dysfunction. Main methods: As model of adipocyte hypertrophy, we employed 3T3-L1 preadipocytes firstly differentiated into mature adipocytes, then cultured with long-chain fatty acids. As a function of differentiation and hypertrophy, we assessed triglyceride content, lipid droplet size, radical homeostasis by spectrophotometry and microscopy, as well as the expression of PPARγ, adiponectin and metallothioneins. Mitochondrial status was investigated by electron microscopy, oxygraph 2 k (O2K) high-resolution respirometry, fluorimetry and western blot. Key findings: Compared to mature adipocytes, hypertrophic adipocytes showed increased triglyceride accumulation and lipid peroxidation, larger or unique lipid droplet, up-regulated expression of PPARγ, adiponectin and metallothioneins. At mitochondrial level, early-hypertrophic adipocytes exhibited: (i) impaired mitochondrial oxygen consumption with parallel reduction in the mitochondrial complexes; (ii) no changes in citrate synthase and HSP60 expression, and in the inner mitochondrial membrane polarization; (iii) no stimulation of mitochondrial fatty acid oxidation. Our findings indicate that the content, integrity, and catabolic activity of mitochondria were rather unchanged in early hypertrophic adipocytes, while oxygen consumption and oxidant production were altered. Significance: In the model of early adipocyte hypertrophy exacerbated oxidative stress and impaired mitochondrial respiration were observed, likely depending on reduction in the mitochondrial complexes, without changes in mitochondrial mass and integrity.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Adipocyte Hypertrophy ; Mitochondria ; Mitochondrial Respiration ; Obesity ; Oxidative Stress; Circulating Adiponectin Levels; Oxidative Stress; Ppar-gamma; Oxygen; Differentiation; Inflammation; Disease; Line
ISSN (print) / ISBN
0024-3205
e-ISSN
1879-0631
Zeitschrift
Life Sciences
Quellenangaben
Band: 265,
Artikelnummer: 118812
Verlag
Elsevier
Verlagsort
The Boulevard, Langford Lane, Kidlington, Oxford Ox5 1gb, England
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed
Förderungen
University of Genova