Defective regulation of adipose tissue autophagy in obesity

Nuñez, Carla Evelyn Coimbra; Rodrigues, Viviane Soares; Gomes, Francisco A. M.; Moura, Rodrigo Ferreira de; Victório, Sheila C.; Bombassaro, Bruna; Chaim, Élinton Adami; Pareja, José Carlos; Geloneze, Bruno; Velloso, Lı́cio A.; Araujo, Eliana P.

doi:10.1038/ijo.2013.27

Cited by 100 publications

(80 citation statements)

References 31 publications

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“…Furthermore, an increase in the autophagic flux was demonstrated. These findings were confirmed in whole adipose tissue derived from the omentum or subcutaneous depot of obese patients undergoing bariatric surgery [39][40][41]. Assessment of autophagic flux by confocal microscopy using wholetissue fragments suggested that elevated autophagy was present in both adipocytes and non-adipocytes [39].…”

Section: The Role Of Autophagy In Adipose Dysfunction and Inflammationsupporting

confidence: 61%

“…Interestingly, following bariatric surgery in obese diabetic patients, adipose tissue autophagy decreases despite continued ER stress. This suggests that other regulators of adipose tissue autophagy, such as insulin resistance, may dominate the control of adipose autophagy in response to weight loss [41].…”

Section: The Role Of Autophagy In Adipose Dysfunction and Inflammationmentioning

confidence: 99%

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Autophagy in adipose tissue and the beta cell: implications for obesity and diabetes

et al. 2014

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Autophagy is a lysosomal degradation pathway recycling intracellular long-lived proteins and damaged organelles, thereby maintaining cellular homeostasis. In addition to inflammatory processes, autophagy has been implicated in the regulation of adipose tissue and beta cell functions. In obesity and type 2 diabetes autophagic activity is modulated in a tissue-dependent manner. In this review we discuss the regulation of autophagy in adipose tissue and beta cells, exemplifying tissue-specific dysregulation of autophagy and its implications for the pathophysiology of obesity and type 2 diabetes. We will highlight common themes and outstanding gaps in our understanding, which need to be addressed before autophagy could be envisioned as a therapeutic target for the treatment of obesity and diabetes.

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Section: The Role Of Autophagy In Adipose Dysfunction and Inflammationsupporting

confidence: 61%

Section: The Role Of Autophagy In Adipose Dysfunction and Inflammationmentioning

confidence: 99%

Autophagy in adipose tissue and the beta cell: implications for obesity and diabetes

et al. 2014

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“…The most plausible explanation as to why higher BMI and UUN were associated with a decreased APOL1 risk for adaptive forms of CKD progression is that these other non-APOL1-mediated pathways were occurring. Alternatively, an incremental deleterious effect of APOL1 risk variants on CKD progression may not have been observed among individuals with obesity or high UUN, because downstream pathways (e.g., apoptosis and autophagy) involving APOL1 may already be dysregulated in these individuals (28)(29)(30)(31). Finally, it is possible that our findings related to BMI and UUN may have been due to chance or residual confounding, because their significance did not persist in sensitivity analyses.…”

Section: Discussionmentioning

confidence: 77%

Examination of Potential Modifiers of the Association of APOL1 Alleles with CKD Progression

Chen¹,

Choi²,

Kao³

et al. 2015

Clinical Journal of the American Society of Nephrology

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Background and objectives Common apolipoprotein L1 (APOL1) variants are associated with increased risk of progressive CKD; however, not all individuals with high-risk APOL1 variants experience CKD progression. Identification of factors contributing to heterogeneity has important scientific and clinical implications.Design, setting, participants, & measurements Using multivariable Cox models, we analyzed data from 693 participants in the African American Study of Kidney Disease and Hypertension to identify factors that modify the association between APOL1 genotypes and CKD progression (doubling of serum creatinine or incident ESRD).Results Participant mean age was 54 years old, median GFR was 49 ml/min per 1.73 m 2 , and 23% had the APOL1 high-risk genotype (two copies of the high-risk allele). Over a mean follow-up of 7.8 years, 288 (42%) participants experienced CKD progression. As previously reported, the high-risk genotype was associated with higher risk of CKD progression compared with the low-risk genotype (hazard ratio [HR], 1.88; 95% confidence interval [95% CI], 1.46 to 2.41). Although we found some suggestion that obesity (HR, 1.48; 95% CI, 1.05 to 2.08 and HR, 2.44; 95% CI, 1.66 to 3.57 for body mass index $30 versus ,30 kg/m 2 ; P interaction =0.04) and increased urinary excretion of urea nitrogen (HR, 1.43; 95% CI, 0.98 to 2.09 versus HR, 2.33; 95% CI, 1.65 to 3.30 for urine urea nitrogen $8 versus ,8 g/d; P interaction =0.04) were associated with lower APOL1-associated risk for CKD progression, these findings were not robust in sensitivity analyses with alternative cut points. No other sociodemographic (e.g., education and income), clinical (e.g., systolic BP and smoking), or laboratory (e.g., net endogenous acid production, urinary sodium and potassium excretions, 25-hydroxy vitamin D, intact parathyroid hormone, or fibroblast growth factor 23) variables modified the association between APOL1 and CKD progression (P interaction .0.05 for each).Conclusions Sociodemographic factors and common risk factors for CKD progression do not seem to alter APOL1-related CKD progression. Additional investigation is needed to identify nontraditional factors that may affect the association between APOL1 and progressive CKD.

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“…Alzheimer's and Parkinson's) 79 and vascular 80 diseases, cancer, 81 diabetes, 82 obesity, 83 rheumatoid arthritis, 84 and osteoarthritis. 85 Studies suggest that dysregulation of autophagy may also be associated with the process of bone loss and subsequent osteoporosis.…”

Section: Autophagy Bone Loss and Osteoporosismentioning

confidence: 99%

Osteoporosis and autophagy: What is the relationship?

Florencio‐Silva

Sasso

Simões

et al. 2017

Rev. Assoc. Med. Bras.

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Autophagy is a survival pathway wherein non-functional proteins and organelles are degraded in lysosomes for recycling and energy production. Therefore, autophagy is fundamental for the maintenance of cell viability, acting as a quality control process that prevents the accumulation of unnecessary structures and oxidative stress. Increasing evidence has shown that autophagy dysfunction is related to several pathologies including neurodegenerative diseases and cancer. Moreover, recent studies have shown that autophagy plays an important role for the maintenance of bone homeostasis. For instance, in vitro and animal and human studies indicate that autophagy dysfunction in bone cells is associated with the onset of bone diseases such as osteoporosis. This review had the purpose of discussing the issue to confirm whether a relationship between autophagy dysfunction and osteoporosis exits.

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Defective regulation of adipose tissue autophagy in obesity

Abstract: Obesity and caloric overfeeding are associated with the defective regulation of autophagy in the adipose tissue. The studies in obese-diabetic subjects undergoing improved metabolic control following calorie restriction suggest that autophagy and inflammation are regulated independently.

Cited by 100 publications

References 31 publications

Autophagy in adipose tissue and the beta cell: implications for obesity and diabetes

Autophagy in adipose tissue and the beta cell: implications for obesity and diabetes

Examination of Potential Modifiers of the Association of APOL1 Alleles with CKD Progression

Osteoporosis and autophagy: What is the relationship?

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