Different adipose tissue depots: Metabolic implications and effects of surgical removal

Marcadenti, Aline; Abreu-Silva, Erlon Oliveira de

doi:10.1016/j.endonu.2015.05.010

Cited by 25 publications

(27 citation statements)

References 29 publications

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“…Deleterious consequences of chronic inflammation and oxidative stress are known to increase tumor progression and metastasis, and also facilitate tumor resistance to both chemotherapy and radiotherapy [7,20,[23][24][25][26][27][28]. Studies have documented that the visceral adipose tissue secreted inflammatory cytokines can promote insulin resistance in vascular cells [29][30][31][32]. Metabolic complications of insulin resistance make individuals more susceptible to chronic oxidative stress, neoplastic transformation and aggressive tumor growth.…”

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confidence: 99%

Tripping on TRIB3 at the junction of health, metabolic dysfunction and cancer

2016

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Metabolic diseases like obesity, atherosclerosis and diabetes are frequently associated with increased risk of aggressive cancers. Although metabolic dysfunctions in normal cells are manifested due to defective signaling networks that control cellular homeostasis, malignant cells utilize these signaling networks for their increased survival, growth and metastasis. Despite decades of research, a common mechanistic link between these chronic pathologies is still not well delineated. Evidences show that the unfolded protein response (UPR) and the endoplasmic reticulum stress (ERS) pathways are often dysregulated in both metabolic diseases and cancer. The UPR also triggers coordinated signaling with both PI3K/AKT/mTOR and Autophagy pathways in order to promote stress-adaptive mechanisms. Whereas, uncontrolled UPR and the resultant ERS escalates cells towards metabolic dysfunctions and ultimately cell death. In this review, we will discuss findings that implicate a crucial role for the multifunctional ERS-induced protein, TRIB3. The 'pseudokinase' function of TRIB3 facilitates the inactivation of multiple transcription factors and signaling proteins. The MEK1 binding domain of TRIB3 enables it to deactivate multiple MAP-kinases. In addition, the COP1 motif of TRIB3 assists ubiquitination and proteasomal degradation of numerous TRIB3 associated proteins. The most well studied action of TRIB3 has been on the PI3K/AKT/mTOR pathway, where TRIB3-mediated inhibition of AKT phosphorylation decreases insulin signaling and cell survival. Conversely, cancer cells can either upregulate the AKT survival pathway by suppressing TRIB3 expression or alter TRIB3 localization to degrade differentiation inducing nuclear transcription factors such as C/EBPα and PPARγ. The gain-of-function Q84R polymorphism in TRIB3 is associated with increased risk of diabetes and atherosclerosis. TRIB3 acts as a crucial 'stress adjusting switch' that links homeostasis, metabolic disease and cancer; and is being actively investigated as a disease biomarker and therapeutic target.

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confidence: 99%

Tripping on TRIB3 at the junction of health, metabolic dysfunction and cancer

2016

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“…No changes were observed in the gWAT for neither cdk2 nor p27 expression. This result suggests a possible implication of p27 and cdk2 on the expansion of scWAT and not gWAT in obesity, which could be due to the physiological difference of both depots [ 52 ]. The higher expression of p27 in scWAT of aged obese mice might make difficult the hyperplasia and fat accumulation in this depot, favoring unhealthy fat accumulation in vWAT.…”

Section: Discussionmentioning

confidence: 99%

Regulation of p27 and Cdk2 Expression in Different Adipose Tissue Depots in Aging and Obesity

Colón-Mesa

Fernández‐Galilea

Sáinz

et al. 2021

IJMS

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Aging usually comes associated with increased visceral fat accumulation, reaching even an obesity state, and favoring its associated comorbidities. One of the processes involved in aging is cellular senescence, which is highly dependent on the activity of the regulators of the cell cycle. The aim of this study was to analyze the changes in the expression of p27 and cdk2 in different adipose tissue depots during aging, as well as their regulation by obesity in mice. Changes in the expression of p27 and CDK2 in visceral and subcutaneous white adipose tissue (WAT) biopsies were also analyzed in a human cohort of obesity and type 2 diabetes. p27, but not cdk2, exhibits a lower expression in subcutaneous than in visceral WAT in mice and humans. p27 is drastically downregulated by aging in subcutaneous WAT (scWAT), but not in gonadal WAT, of female mice. Obesity upregulates p27 and cdk2 expression in scWAT, but not in other fat depots of aged mice. In humans, a significant upregulation of p27 was observed in visceral WAT of subjects with obesity. Taken together, these results show a differential adipose depot-dependent regulation of p27 and cdk2 in aging and obesity, suggesting that p27 and cdk2 could contribute to the adipose-tissue depot’s metabolic differences. Further studies are necessary to fully corroborate this hypothesis.

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“…Adipose tissue is an important metabolic organ, which expands in terms of cell size and number to permit greater lipid storage during long-term positive energy imbalance [5]. Abdominal white adipose tissue (WAT) fat has a vital role in the regulation of systemic energy homeostasis [6], and can be classified as visceral (VAT) and subcutaneous (SAT) [7]. If excess lipid principally accumulates in VAT, which is the more metabolically active depot, glucose intolerance is more likely to develop than if this accumulation occurs in SAT.…”

Section: Introductionmentioning

confidence: 99%

Effect of Dietary Silk Peptide on Obesity, Hyperglycemia, and Skeletal Muscle Regeneration in High-Fat Diet-Fed Mice

Lee

Jin

Chei

et al. 2020

Cells

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Obesity is associated with excess body fat accumulation that can cause hyperglycemia and reduce skeletal muscle function and strength, which characterize the development of sarcopenic obesity. In this study, we aimed to determine the mechanism whereby acid-hydrolyzed silk peptide (SP) prevents high-fat diet (HFD)-induced obesity and whether it regulates glucose uptake and muscle differentiation using in vivo and in vitro approaches. Our findings demonstrate that SP inhibits body mass gain and the expression of adipogenic transcription factors in visceral adipose tissue (VAT). SP also had an anti-diabetic effect in VAT and skeletal muscle because it upregulated glucose transporter type 4 (GLUT4) and uncoupling protein 3 (UCP3) expression. Furthermore, SP reduced ubiquitin proteasome and promoted myoblast determination protein 1 (MyoD)/myogenic factor 4 (myogenin) expression, implying that it may have potential for the treatment of obesity-induced hyperglycemia and obesity-associated sarcopenia.

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Different adipose tissue depots: Metabolic implications and effects of surgical removal

Cited by 25 publications

References 29 publications

Tripping on TRIB3 at the junction of health, metabolic dysfunction and cancer

Tripping on TRIB3 at the junction of health, metabolic dysfunction and cancer

Regulation of p27 and Cdk2 Expression in Different Adipose Tissue Depots in Aging and Obesity

Effect of Dietary Silk Peptide on Obesity, Hyperglycemia, and Skeletal Muscle Regeneration in High-Fat Diet-Fed Mice

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