Autophagy in Adipose Tissue

Maixner, Nitzan; Kovsan, Julia; Harman-Boehm, Ilana; Blüher, Matthias; Bashan, Nava; Rudich, Assaf

doi:10.1159/000343983

Cited by 31 publications

(21 citation statements)

References 119 publications

(93 reference statements)

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“…Recent studies revealed that autophagy is up-regulated in human obesity [9] and it has been shown that autophagy is more pronounced in omental than in subcutaneous adipose tissue [17]. In this study we demonstrate that insulin resistant adipose tissue of WOKW rats display enhanced autophagy with increased expression of autophagy genes.…”

Section: Discussionsupporting

confidence: 62%

The polygenetically inherited metabolic syndrome of male WOKW rats is associated with enhanced autophagy in adipose tissue

Kosacka

Koch

Gericke

et al. 2013

Diabetol Metab Syndr

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BackgroundRecent studies revealed that autophagy is up-regulated in obese individuals, as evidenced by increased expression of autophagy related genes. As argued elsewhere, it is possible that initially insulin resistance functions as an adaptive mechanism to increase autophagy in order to protect cells against death. We have shown that Wistar Ottawa Karlsburg W (RT1u) rats (WOKW) develop a metabolic syndrome with insulin resistance in adipose tissue, closely resembling the human disease. Therefore, the aim of this study was to characterize the autophagy phenotype in WOKW rats to clarify the interrelation between insulin resistance and autophagy in adipose tissue.MethodsSubcutaneous and epidydimal adipose tissue samples of 5-months-old WOKW and healthy LEW.1 W male rats were investigated and protein levels (Western blot and immunhistochemistry) of key autophagy genes, including Atg5, Atg7, LC3-II/LC3-I and apoptosis marker cleaved caspase-3 were analyzed.ResultsWOKW rats displayed a significant increase of autophagy related proteins (Atg5, Atg7) in adipose tissue compared with LEW.1 W. This increase was predominantly found in epididymal adipose tissue. Furthermore, the LC3-II/LC3-I ratio as a marker of autophagosomes was significantly up-regulated in subcutaneous adipose tissue of WOKW rats. Cleaved caspase-3 was just slightly detectable in visceral adipose tissue and not detected in subcutaneous fat.ConclusionInsulin resistance in adipose tissue of obese WOKW rats is associated with up-regulation of differing autophagy markers in visceral and subcutaneous fat depots. This fact not only qualifies the WOKW rat for further detailed analysis of genetic determinants of metabolic syndrome but also highlights its suitability for autophagy research.

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Section: Discussionsupporting

confidence: 62%

The polygenetically inherited metabolic syndrome of male WOKW rats is associated with enhanced autophagy in adipose tissue

Kosacka

Koch

Gericke

et al. 2013

Diabetol Metab Syndr

Self Cite

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“…Expansion of AT during weight gain is frequently associated with increasingly “stressful conditions” including hypoxia [20], cellular stresses such as oxidative and endoplasmatic reticulum stress [10], autophagy [21], and apoptosis [22], which are reflected by increased macrophage infiltration into AT [23, 24]. AT dysfunction is associated with local inflammation and ROS accumulation subsequently leading to altered tissue crosstalk through adipokines and AT-derived metabolites [10, 25].…”

Section: Discussionmentioning

confidence: 99%

Effects of Weight Loss on Glutathione Peroxidase 3 Serum Concentrations and Adipose Tissue Expression in Human Obesity

et al. 2018

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Background/Aims: Altered expression and circulating levels of glutathione peroxidase 3 (GPX3) have been observed in obesity and type 2 diabetes (T2D) across species. Here, we investigate whether GPX3 serum concentrations and adipose tissue (AT) GPX3 mRNA expression are related to obesity and weight loss. Methods: GPX3 serum concentration was measured in 630 individuals, including a subgroup (n = 293) for which omental and subcutaneous (SC) GPX3 mRNA expression has been analyzed. GPX3 analyses include three interventions: 6 months after bariatric surgery (n = 80) or combined exercise/hypocaloric diet (n = 20) or two-step bariatric surgery (n = 24) studies. Results: Bariatric surgery-induced weight loss (–25.8 ± 8.4%), but not a moderate weight reduction of –8.8 ± 6.5% was associated with significantly reduced GPX3 serum concentrations. GPX3 mRNA is significantly higher expressed in AT from individuals with normal glucose metabolism compared to T2D patients. SC AT GPX3 expression is significantly higher in lean compared to obese as well as in insulin-sensitive compared insulin-resistant individuals with obesity. Weight loss after bariatric surgery causes a significant increase in SC AT GPX3 expression. AT GPX3 expression significantly correlates with age, BMI, fat distribution, insulin sensitivity (only SC AT), but not with circulating GPX3. Conclusion: Our data support the notion that SC AT GPX3 expression is associated with obesity, fat distribution and related to whole body insulin resistance.

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“…13 There is a close relationship between autophagic activity and energy metabolism. [14][15][16] Complex intracellular pathways regulate autophagic activity by controlling different protein interactions, like those involving autophagy-related (Atg) protein conjugation cascades, as well as post-translational protein modifications involved in autophagosome formation and substrate recognition. Recent data indicate that transcriptional regulation of genes encoding autophagy components also plays a role in the regulation of autophagy by metabolic and endocrine signals.…”

Section: Introductionmentioning

confidence: 99%