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

2021 ◽  
Vol 22 (21) ◽  
pp. 11745
Author(s):  
Ignacio Colón-Mesa ◽  
Marta Fernández-Galilea ◽  
Neira Sáinz ◽  
Marta Lopez-Yus ◽  
Jose M. Artigas ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Subcutaneous White Adipose Tissue ◽  
Visceral Fat Accumulation ◽  
Fat Depots ◽  
Adipose Tissue Depots ◽  
Obesity In Mice ◽  
Cdk2 Expression ◽  
Lower Expression

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.

Enhanced ROS production and oxidative damage in subcutaneous white adipose tissue mitochondria in obese and type 2 diabetes subjects

2014 ◽  
Vol 399 (1-2) ◽  
pp. 95-103 ◽  
Author(s):  
Mrittika Chattopadhyay ◽  
Vineet Kumar Khemka ◽  
Gargi Chatterjee ◽  
Anirban Ganguly ◽  
Satinath Mukhopadhyay ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Oxidative Damage ◽  
White Adipose Tissue ◽  
Ros Production ◽  
Subcutaneous White Adipose Tissue

Altered Expression of Adrenomedullin 2 and its Receptor in the Adipose Tissue of Obese Patients

2019 ◽  
Vol 105 (3) ◽  
pp. e583-e596 ◽  
Author(s):  
Jimin Kim ◽  
Seul Ki Lee ◽  
Donguk Kim ◽  
Han Choe ◽  
Yeon Jin Jang ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Bariatric Surgery ◽  
Adipose Tissue ◽  
Human Adipose Tissue ◽  
Receptor Expression ◽  
Receptor Complex ◽  
Obese Patients ◽  
Fat Depots ◽  
Receptor Component

Abstract Context Adrenomedullin 2 (AM2) plays protective roles in the renal and cardiovascular systems. Recent studies in experimental animals demonstrated that AM2 is an adipokine with beneficial effects on energy metabolism. However, there is little information regarding AM2 expression in human adipose tissue. Objective To investigate the pattern and regulation of the expression of AM2 and its receptor component in human adipose tissue, in the context of obesity and type 2 diabetes. Methods We measured metabolic parameters, serum AM2, and expression of ADM2 and its receptor component genes in abdominal subcutaneous and visceral adipose tissue in obese (with or without type 2 diabetes) and normal-weight women. Serum AM2 was assessed before and 6 to 9 months after bariatric surgery. Expression/secretion of AM2 and its receptor were assessed in human adipocytes. Results ADM2 mRNA in both fat depots was higher in obese patients, whether diabetic or not. Although serum AM2 was significantly lower in obese patients, it was not changed after bariatric surgery. AM2 and its receptor complex were predominantly expressed by adipocytes, and the expression of CALCRL, encoding a component of the AM2 receptor complex, was lower in both fat depots of obese patients. Incubating adipocytes with substances mimicking the microenvironment of obese adipose tissue increased ADM2 mRNA but reduced both AM2 secretion into culture media and CALCRL mRNA expression. Conclusions Our data indicate that AM2 signaling is suppressed in adipose tissue in obesity, involving lower receptor expression and ligand availability, likely contributing to insulin resistance and other aspects of the pathophysiology associated with obesity.

scholarly journals Epicardial adipose tissue: an emerging biomarker of cardiovascular complications in type 2 diabetes?

2020 ◽  
Vol 11 ◽  
pp. 204201882092882 ◽  
Author(s):  
Regitse Højgaard Christensen ◽  
Bernt Johan von Scholten ◽  
Louise Lang Lehrskov ◽  
Peter Rossing ◽  
Peter Godsk Jørgensen
Keyword(s):  
Heart Failure ◽  
Type 2 Diabetes ◽  
Cardiovascular Disease ◽  
Adipose Tissue ◽  
Epicardial Adipose Tissue ◽  
Fat Depots ◽  
Pericardial Adipose Tissue ◽  
Increased Risk ◽  
Fat Depot

Type 2 diabetes (T2D) is associated with an increased risk of cardiovascular disease and heart failure, which highlights the need for improved understanding of factors contributing to the pathophysiology of these complications as they are the leading cause of mortality in T2D. Patients with T2D have high levels of epicardial adipose tissue (EAT). EAT is known to secrete inflammatory factors, lipid metabolites, and has been proposed to apply mechanical stress on the cardiac muscle that may accelerate atherosclerosis, cardiac remodeling, and heart failure. High levels of EAT in patients with T2D have been associated with atherosclerosis, diastolic dysfunction, and incident cardiovascular events, and this fat depot has been suggested as an important link coupling diabetes, obesity, and cardiovascular disease. Despite this, the predictive potential of EAT in general, and in patients with diabetes, is yet to be established, and, up until now, the clinical relevance of EAT is therefore limited. Should this link be established, importantly, studies show that this fat depot can be modified both by pharmacological and lifestyle interventions. In this review, we first introduce the role of adipose tissue in T2D and present mechanisms involved in the pathophysiology of EAT and pericardial adipose tissue (PAT) in general, and in patients with T2D. Next, we summarize the evidence that these fat depots are elevated in patients with T2D, and discuss whether they might drive the high cardiometabolic risk in patients with T2D. Finally, we discuss the clinical potential of cardiac adipose tissues, address means to target this depot, and briefly touch upon underlying mechanisms and future research questions.

scholarly journals Marrow adipose tissue spectrum in obesity and type 2 diabetes mellitus

2017 ◽  
Vol 176 (1) ◽  
pp. 21-30 ◽  
Author(s):  
Iana M de Araújo ◽  
Carlos E G Salmon ◽  
Andressa K Nahas ◽  
Marcello H Nogueira-Barbosa ◽  
Jorge Elias ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Magnetic Resonance ◽  
Glycated Hemoglobin ◽  
Mineral Density ◽  
Fat Depots ◽  
Marrow Adipose Tissue ◽  
Bone Remodeling Markers

ObjectiveTo assess the association of bone mass and marrow adipose tissue (MAT) with other fat depots, insulin resistance, bone remodeling markers, adipokines and glucose control in type 2 diabetes and obesity.Design and methodsThe study groups comprised 24 controls (C), 26 obese (O) and 28 type 2 diabetes. Dual-energy X-ray absorptiometry was used to determine bone mineral density (BMD). Blood samples were collected for biochemical measurements.1H Magnetic resonance spectroscopy was used to assess MAT in the L3 vertebra, and abdominal magnetic resonance imaging was used to assess intrahepatic lipids in visceral (VAT) and subcutaneous adipose tissue. Regression analysis models were used to test the association between parameters.ResultsAt all sites tested, BMD was higher in type 2 diabetes than in O and C subjects. The C group showed lower VAT values than the type 2 diabetes group and lower IHL than the O and type 2 diabetes groups. However, MAT was similar in the 3 groups. Osteocalcin and C-terminal telopeptide of type 1 collagen were lower in type 2 diabetes than those in C and O subjects. Moreover, at all sites, BMD was negatively associated with osteocalcin. No association was observed between MAT and VAT. No relationship was observed among MAT and HOMA-IR, leptin, adiponectin or Pref-1, but MAT was positively associated with glycated hemoglobin.ConclusionsMAT is not a niche for fat accumulation under conditions of energy surplus and type 2 diabetes, also is not associated with VAT or insulin resistance. MAT is associated with glycated hemoglobin.

Lipid metabolism during lactation: a review of adipose tissue-liver interactions and the development of fatty liver

2005 ◽  
Vol 72 (4) ◽  
pp. 460-469 ◽  
Author(s):  
Richard G Vernon
Keyword(s):  
Type 2 Diabetes ◽  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Negative Energy ◽  
The Body ◽  
Unesterified Fatty Acid ◽  
Adipose Tissue Depots

Fatty acids are the major source of energy for most tissues during periods of negative energy balance; however, fatty acids can, in some circumstances, have pathological effects. Fatty acids are stored as triacylglycerols (TAG), mostly in the various adipose tissue depots of the body. However, if blood unesterified fatty acid (NEFA) levels are elevated for prolonged periods, as may occur during lactation or obesity, TAG can accumulate in other tissues including liver and muscle cells (myocytes), and this can have pathological consequences such as the development of ketosis (Grummer, 1993; Drackley et al. 2001) or type 2 diabetes (Boden & Shulman, 2002; McGarry, 2002).

scholarly journals Increased fat cell size: a major phenotype of subcutaneous white adipose tissue in non-obese individuals with type 2 diabetes

Diabetologia ◽  
2015 ◽  
Vol 59 (3) ◽  
pp. 560-570 ◽  
Author(s):  
Juan R. Acosta ◽  
Iyadh Douagi ◽  
Daniel P. Andersson ◽  
Jesper Bäckdahl ◽  
Mikael Rydén ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Cell Size ◽  
White Adipose Tissue ◽  
Fat Cell ◽  
Subcutaneous White Adipose Tissue ◽  
Fat Cell Size

scholarly journals In Patients With Obesity, the Number of Adipose Tissue Mast Cells Is Significantly Lower in Subjects With Type 2 Diabetes

2021 ◽  
Vol 12 ◽  
Author(s):  
David Lopez-Perez ◽  
Anaïs Redruello-Romero ◽  
Jesús Garcia-Rubio ◽  
Carlos Arana ◽  
Luis A. Garcia-Escudero ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Mast Cell ◽  
Adipose Tissue ◽  
Mast Cells ◽  
White Adipose Tissue ◽  
Hypoxic Cell ◽  
Subcutaneous White Adipose Tissue ◽  
Huge Impact ◽  
Endocrine Signaling

Type 2 diabetes (T2D) is a rising global health problem mainly caused by obesity and a sedentary lifestyle. In healthy individuals, white adipose tissue (WAT) has a relevant homeostatic role in glucose metabolism, energy storage, and endocrine signaling. Mast cells contribute to these functions promoting WAT angiogenesis and adipogenesis. In patients with T2D, inflammation dramatically impacts WAT functioning, which results in the recruitment of several leukocytes, including monocytes, that enhance this inflammation. Accordingly, the macrophages population rises as the WAT inflammation increases during the T2D status worsening. Since mast cell progenitors cannot arrive at WAT, the amount of WAT mast cells depends on how the new microenvironment affects progenitor and differentiated mast cells. Here, we employed a flow cytometry-based approach to analyze the number of mast cells from omental white adipose tissue (o-WAT) and subcutaneous white adipose tissue (s-WAT) in a cohort of 100 patients with obesity. Additionally, we measured the number of mast cell progenitors in a subcohort of 15 patients. The cohort was divided in three groups: non-T2D, pre-T2D, and T2D. Importantly, patients with T2D have a mild condition (HbA1c <7%). The number of mast cells and mast cell progenitors was lower in patients with T2D in both o-WAT and s-WAT in comparison to subjects from the pre-T2D and non-T2D groups. In the case of mast cells in o-WAT, there were statistically significant differences between non-T2D and T2D groups (p = 0.0031), together with pre-T2D and T2D groups (p=0.0097). However, in s-WAT, the differences are only between non-T2D and T2D groups (p=0.047). These differences have been obtained with patients with a mild T2D condition. Therefore, little changes in T2D status have a huge impact on the number of mast cells in WAT, especially in o-WAT. Due to the importance of mast cells in WAT physiology, their decrease can reduce the capacity of WAT, especially o-WAT, to store lipids and cause hypoxic cell deaths that will trigger inflammation.

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