Adipose tissue autophagy status in obesity: Expression and flux—two faces of the picture

Soussi, Hedi; Clément, Karine; Dugail, Isabelle

doi:10.1080/15548627.2015.1106667

Cited by 35 publications

(22 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Weight loss by bariatric surgery can partly reverse flux attenuation, likely through the normalized expression of an autophagy regulator, DAPK2. 19 In the present study, we did not find any transcriptional change in the expression of genes involved in the initiation complex or autolysosome stage. Therefore, our findings, together with those of others, 9,13,14,18 suggest that overweight and obesity is accompanied by an upregulation of the autophagic flux in adipose tissue, predominantly due to an increase in the autophagic conjugation cascade.…”

Section: Discussioncontrasting

confidence: 63%

“…Of interest, recent data showed that in human adipocytes isolated from adipose tissue biopsies, the obese group showed higher p62 and lower LC3II indicating that the autophagic flux might rather be blunted in human obese adipocytes. 19 In conclusion, our results show that autophagy conjugation genes are up-regulated in subcutaneous adipose tissue of overweight/obese subjects. We further showed that the autophagy and classical lipolytic pathway are coordinately regulated in an opposite manner.…”

Section: Discussionmentioning

confidence: 52%

See 1 more Smart Citation

Adipose tissue autophagy related gene expression is associated with glucometabolic status in human obesity

Mariman

Roumans

et al. 2018

Adipocyte

View full text Add to dashboard Cite

Adipose tissue autophagy (AT) is associated with human obesity and increased metabolic risk. Recent findings establish a role for autophagy in lipid metabolism. Here, we compared the expression of autophagy-related and lipolysis genes in human abdominal subcutaneous AT (SCAT) in overweight/obese subjects (n = 17) with or without impaired glucose tolerance in comparison with lean normal glucose tolerant individuals (n = 9), and investigated the association between AT autophagy and lipolysis. Human multipotent adipose-derived stem cells (hMADS) were used to investigate the effect of pharmacological HSL inhibition on changes in the autophagic flux. The expression of autophagy-related genes (ATG) 5, 7 and 12 in SCAT was significantly higher (p = 0.043, p = 0.015, p = 0.004, respectively) in overweight/obese compared to lean men, while expression of the classical lipases HSL (p = 0.092) and ATGL (p = 0.084) tended to be lower. ATG12 mRNA was positively correlated with BMI (r = 0.407, p = 0.039). ATG7 mRNA correlated positively with waist/hip ratio (WHR) (r = 0.420, p = 0.041), 2 h glucose concentration (r = 0.488, p = 0.011) and insulin (r = 0.419, p = 0.033). Multiple linear regressions revealed that ATG7 gene expression was positively related to 2 h glucose, independent of BMI, WHR and insulin. Gene expression interaction analysis showed that ATG7 mRNA negatively correlated with HSL (p<0.01) and ATGL mRNA expression (p<0.01). In line, treatment of differentiated hMADS with an HSL inhibitor increased LC3 accumulation, a marker of increased autophagic flux. Collectively, the present study demonstrated that a low expression of classical lipases in abdominal SCAT is accompanied by an increased expression of ATGs in overweight/obese subjects, which seems to be mainly related to glucose tolerance.

show abstract

Section: Discussioncontrasting

confidence: 63%

Section: Discussionmentioning

confidence: 52%

Adipose tissue autophagy related gene expression is associated with glucometabolic status in human obesity

Mariman

Roumans

et al. 2018

Adipocyte

View full text Add to dashboard Cite

show abstract

“…In independent study settings and cohorts, we found generally higher markers of autophagy in visceral compared with SC adipose tissue and significant correlations with obesity, insulin resistance and adipose tissue inflammation [49,50,81]. However, since these associations have not been consistently found across different cohorts the dynamic changes due to autophagic flux need to be considered in the discussion of whether autophagy protects against obesity associated adipocyte dysfunction or could contribute to adipose tissue inflammation [82].…”

Section: Autophagy Apoptosis and Immune Cell Infiltration In Adiposementioning

confidence: 68%

Adipose tissue inflammation: a cause or consequence of obesity-related insulin resistance?

2016

View full text Add to dashboard Cite

The worldwide obesity epidemic has become a major health concern, because it contributes to higher mortality due to an increased risk for noncommunicable diseases including cardiovascular diseases, type 2 diabetes, musculoskeletal disorders and some cancers. Insulin resistance may link accumulation of adipose tissue in obesity to metabolic diseases, although the underlying mechanisms are not completely understood. In the past decades, data from human studies and transgenic animal models strongly suggested correlative, but also causative associations between activation of proinflammatory pathways and insulin resistance. Particularly chronic inflammation in adipose tissue seems to play an important role in the development of obesity-related insulin resistance. On the other hand, adipose tissue inflammation has been shown to be essential for healthy adipose tissue expansion and remodelling. However, whether adipose tissue inflammation represents a consequence or a cause of impaired insulin sensitivity remains an open question. A better understanding of the molecular pathways linking excess adipose tissue storage to chronic inflammation and insulin resistance may provide the basis for the future development of anti-inflammatory treatment strategies to improve adverse metabolic consequences of obesity. In this review, potential mechanisms of adipose tissue inflammation and how adipose tissue inflammation may cause insulin resistance are discussed.

show abstract

“…Although autophagy is considered as a housekeeping cell process, abnormalities of autophagy have increasingly been associated with metabolic disorders such as obesity 27,28 , insulin resistance 29 , T2D onset 30 , nonalcoholic steatohepatitis 31 , atherosclerosis, and heart disease 32 , which are pathologically linked to autophagy dysfunction and may influence the onset of MetS. Yet the involvement of autophagy in these diseases remains to be properly recognized with additional experiments.…”

Section: Autophagy and Metabolic Dysfunction Onsetmentioning

confidence: 99%

Autophagy in metabolic syndrome: breaking the wheel by targeting the renin–angiotensin system

et al. 2020

View full text Add to dashboard Cite

Metabolic syndrome (MetS) is a complex, emerging epidemic which disrupts the metabolic homeostasis of several organs, including liver, heart, pancreas, and adipose tissue. While studies have been conducted in these research areas, the pathogenesis and mechanisms of MetS remain debatable. Lines of evidence show that physiological systems, such as the renin-angiotensin system (RAS) and autophagy play vital regulatory roles in MetS. RAS is a pivotal system known for controlling blood pressure and fluid balance, whereas autophagy is involved in the degradation and recycling of cellular components, including proteins. Although RAS is activated in MetS, the interrelationship between RAS and autophagy varies in glucose homeostatic organs and their cross talk is poorly understood. Interestingly, autophagy is attenuated in the liver during MetS, whereas autophagic activity is induced in adipose tissue during MetS, indicating tissue-specific discordant roles. We discuss in vivo and in vitro studies conducted in metabolic tissues and dissect their tissue-specific effects. Moreover, our review will focus on the molecular mechanisms by which autophagy orchestrates MetS and the ways future treatments could target RAS in order to achieve metabolic homeostasis. Facts • The renin-angiotensin system (RAS) is a pivotal endocrine system classically known for controlling blood pressure and fluid balance.

show abstract

Adipose tissue autophagy status in obesity: Expression and flux—two faces of the picture

Cited by 35 publications

References 0 publications

Adipose tissue autophagy related gene expression is associated with glucometabolic status in human obesity

Adipose tissue autophagy related gene expression is associated with glucometabolic status in human obesity

Adipose tissue inflammation: a cause or consequence of obesity-related insulin resistance?

Autophagy in metabolic syndrome: breaking the wheel by targeting the renin–angiotensin system

Contact Info

Product

Resources

About