scholarly journals Obesity and Breast Cancer: A Case of Inflamed Adipose Tissue

Cancers ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1686 ◽  
Author(s):  
Ryan Kolb ◽  
Weizhou Zhang
Keyword(s):  
Breast Cancer ◽  
Adipose Tissue ◽  
Molecular Mechanisms ◽  
Breast Cancer Incidence ◽  
Menopausal Status ◽  
Epidemiological Data ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Cancer Subtypes ◽  
Increased Risk

Obesity is associated with an increased risk of estrogen receptor-positive breast cancer in postmenopausal women and a worse prognosis for all major breast cancer subtypes regardless of menopausal status. While the link between obesity and the pathogenesis of breast cancer is clear, the molecular mechanism of this association is not completely understood due to the complexity of both obesity and breast cancer. The aim of this review is to highlight the association between obesity and breast cancer and discuss the literature, which indicates that this association is due to chronic adipose tissue inflammation. We will discuss the epidemiological data for the association between breast cancer incidence and progression as well as the potential molecular mechanisms for this association. We will focus on the role of inflammation within the adipose tissue during the pathogenesis of breast cancer. A better understanding of how obesity and adipose tissue inflammation affects the pathogenesis of breast cancer will lead to new strategies to reduce breast cancer risk and improve patient outcomes for obese patients.

scholarly journals SGLT2i and GLP-1RA in Cardiometabolic and Renal Diseases: From Glycemic Control to Adipose Tissue Inflammation and Senescence

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Luis D'Marco ◽  
Valery Morillo ◽  
José Luis Gorriz ◽  
María K. Suarez ◽  
Manuel Nava ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Glycemic Control ◽  
Molecular Mechanisms ◽  
Metabolic Diseases ◽  
Renal Diseases ◽  
Diabetic Patients ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
First Line Therapy ◽  
Anti Inflammatory

Background. Over the last few years, the use of sodium-glucose cotransporter 2 inhibitors (SGLT2i) and glucagon-like peptide 1 receptor agonists (GLP-1RA) has increased substantially in medical practice due to their documented benefits in cardiorenal and metabolic health. In this sense, and in addition to being used for glycemic control in diabetic patients, these drugs also have other favorable effects such as weight loss and lowering blood pressure, and more recently, they have been shown to have cardio and renoprotective effects with anti-inflammatory properties. Concerning the latter, the individual or associated use of these antihyperglycemic agents has been linked with a decrease in proinflammatory cytokines and with an improvement in the inflammatory profile in chronic endocrine-metabolic diseases. Hence, these drugs have been positioned as first-line therapy in the management of diabetes and its multiple comorbidities, such as obesity, which has been associated with persistent inflammatory states that induce dysfunction of the adipose tissue. Moreover, other frequent comorbidities in long-standing diabetic patients are chronic complications such as diabetic kidney disease, whose progression can be slowed by SGLT2i and/or GLP-1RA. The neuroendocrine and immunometabolism mechanisms underlying adipose tissue inflammation in individuals with diabetes and cardiometabolic and renal diseases are complex and not fully understood. Summary. This review intends to expose the probable molecular mechanisms and compile evidence of the synergistic or additive anti-inflammatory effects of SGLT2i and GLP-1RA and their potential impact on the management of patients with obesity and cardiorenal compromise.

scholarly journals Obesity and Cancer Mechanisms: Tumor Microenvironment and Inflammation

2016 ◽  
Vol 34 (35) ◽  
pp. 4270-4276 ◽  
Author(s):  
Neil M. Iyengar ◽  
Ayca Gucalp ◽  
Andrew J. Dannenberg ◽  
Clifford A. Hudis
Keyword(s):  
Body Mass Index ◽  
Adipose Tissue ◽  
Tumor Growth ◽  
Body Mass ◽  
Low Grade ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
The Metabolic Syndrome ◽  
Increased Risk ◽  
Adipose Inflammation

Purpose There is growing evidence that inflammation is a central and reversible mechanism through which obesity promotes cancer risk and progression. Methods We review recent findings regarding obesity-associated alterations in the microenvironment and the local and systemic mechanisms through which these changes support tumor growth. Results Locally, hyperadiposity is associated with altered adipose tissue function, adipocyte death, and chronic low-grade inflammation. Most individuals who are obese harbor inflamed adipose tissue, which resembles chronically injured tissue, with immune cell infiltration and remodeling. Within this distinctly altered local environment, several pathophysiologic changes are found that may promote breast and other cancers. Consistently, adipose tissue inflammation is associated with a worse prognosis in patients with breast and tongue cancers. Systemically, the metabolic syndrome, including dyslipidemia and insulin resistance, occurs in the setting of adipose inflammation and operates in concert with local mechanisms to sustain the inflamed microenvironment and promote tumor growth. Importantly, adipose inflammation and its protumor consequences can be found in some individuals who are not considered to be obese or overweight by body mass index. Conclusion The tumor-promoting effects of obesity occur at the local level via adipose inflammation and associated alterations in the microenvironment, as well as systemically via circulating metabolic and inflammatory mediators associated with adipose inflammation. Accurately characterizing the obese state and identifying patients at increased risk for cancer development and progression will likely require more precise assessments than body mass index alone. Biomarkers of adipose tissue inflammation would help to identify high-risk populations. Moreover, adipose inflammation is a reversible process and represents a novel therapeutic target that warrants further study to break the obesity-cancer link.

scholarly journals Systemic Correlates of White Adipose Tissue Inflammation in Early-Stage Breast Cancer

2015 ◽  
Vol 22 (9) ◽  
pp. 2283-2289 ◽  
Author(s):  
Neil M. Iyengar ◽  
Xi Kathy Zhou ◽  
Ayca Gucalp ◽  
Patrick G. Morris ◽  
Louise R. Howe ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Early Stage ◽  
Early Stage Breast Cancer ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation

White adipose tissue inflammation and breast cancer progression.

2015 ◽  
Vol 33 (15_suppl) ◽  
pp. 11001-11001
Author(s):  
Neil M. Iyengar ◽  
Patrick G. Morris ◽  
Xi Kathy Zhou ◽  
Hanhan Wang ◽  
Ayca Gucalp ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Adipose Tissue ◽  
Cancer Progression ◽  
White Adipose Tissue ◽  
Breast Cancer Progression ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation

scholarly journals Characterization, Pathogenesis, and Clinical Implications of Inflammation‐Related Atrial Myopathy as an Important Cause of Atrial Fibrillation

2020 ◽  
Vol 9 (7) ◽  
Author(s):  
Milton Packer
Keyword(s):  
Atrial Fibrillation ◽  
Adipose Tissue ◽  
Left Atrium ◽  
Left Ventricular ◽  
Risk Scores ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Proinflammatory Mediators ◽  
Obesity And Diabetes ◽  
Increased Risk

Abstract Historically, atrial fibrillation has been observed in clinical settings of prolonged hemodynamic stress, eg, hypertension and valvular heart disease. However, recently, the most prominent precedents to atrial fibrillation are metabolic diseases that are associated with adipose tissue inflammation (ie, obesity and diabetes mellitus) and systemic inflammatory disorders (ie, rheumatoid arthritis and psoriasis). These patients typically have little evidence of left ventricular hypertrophy or dilatation; instead, imaging reveals abnormalities of the structure or function of the atria, particularly the left atrium, indicative of an atrial myopathy. The left atrium is enlarged, fibrotic and noncompliant, potentially because the predisposing disorder leads to an expansion of epicardial adipose tissue, which transmits proinflammatory mediators to the underlying left atrium. The development of an atrial myopathy not only leads to atrial fibrillation, but also contributes to pulmonary venous hypertension and systemic thromboembolism. These mechanisms explain why disorders of systemic or adipose tissue inflammation are accompanied an increased risk of atrial fibrillation, abnormalities of left atrium geometry and an enhanced risk of stroke. The risk of stroke exceeds that predicted by conventional cardiovascular risk factors or thromboembolism risk scores used to guide the use of anticoagulation, but it is strongly linked to clinical evidence and biomarkers of systemic inflammation.

scholarly journals Voluntary exercise improves insulin sensitivity and adipose tissue inflammation in diet-induced obese mice

2008 ◽  
Vol 295 (3) ◽  
pp. E586-E594 ◽  
Author(s):  
Richard L. Bradley ◽  
Justin Y. Jeon ◽  
Fen-Fen Liu ◽  
Eleftheria Maratos-Flier
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Inflammatory Cytokines ◽  
Molecular Mechanisms ◽  
Voluntary Exercise ◽  
Adipose Tissue Inflammation ◽  
Obese Mice ◽  
Tissue Inflammation

Exercise promotes weight loss and improves insulin sensitivity. However, the molecular mechanisms mediating its beneficial effects are not fully understood. Obesity correlates with increased production of inflammatory cytokines, which in turn, contributes to systemic insulin resistance. To test the hypothesis that exercise mitigates this inflammatory response, thereby improving insulin sensitivity, we developed a model of voluntary exercise in mice made obese by feeding of a high fat/high sucrose diet (HFD). Over four wk, mice fed chow gained 2.3 ± 0.3 g, while HFD mice gained 6.8 ± 0.5 g. After 4 wk, mice were subdivided into four groups: chow-no exercise, chow-exercise, HFD-no exercise, HFD-exercise and monitored for an additional 6 wk. Chow-no exercise and HFD-no exercise mice gained an additional 1.2 ± 0.3 g and 3.3 ± 0.5 g respectively. Exercising mice had higher food consumption, but did not gain additional weight. As expected, GTT and ITT showed impaired glucose tolerance and insulin resistance in HFD-no exercise mice. However, glucose tolerance improved significantly and insulin sensitivity was completely normalized in HFD-exercise animals. Furthermore, expression of TNF-α, MCP-1, PAI-1 and IKKβ was increased in adipose tissue from HFD mice compared with chow mice, whereas exercise reversed the increased expression of these inflammatory cytokines. In contrast, expression of these cytokines in liver was unchanged among the four groups. These results suggest that exercise partially reduces adiposity, reverses insulin resistance and decreases adipose tissue inflammation in diet-induced obese mice, despite continued consumption of HFD.

Incidence of periprostatic white adipose tissue inflammation in men with prostate cancer.

2017 ◽  
Vol 35 (6_suppl) ◽  
pp. 63-63 ◽  
Author(s):  
Ayca Gucalp ◽  
Neil M. Iyengar ◽  
Xi K. Zhou ◽  
Dilip D. Giri ◽  
Domenick J. Falcone ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Host Factors ◽  
Gleason Grade ◽  
High Grade ◽  
Adipose Tissue Inflammation ◽  
Grade Group ◽  
Tissue Inflammation ◽  
Increased Risk

63 Background: Obesity, a common cause of chronic inflammation, is associated with an increased risk of high grade, lethal prostate cancer (PC) and poor outcomes. The existence or clinical importance of periprostatic white adipose tissue inflammation (WATi) in patients (pts) with PC has not been previously described. We examined the relationships among periprostatic WATi and 1) tumor clinicopathologic features, and 2) host factors including age, body mass index (BMI), and circulating metabolic factors. Methods: Periprostatic WAT was collected prospectively from men with PC undergoing radical prostatectomy. WATi was defined by the presence of dead/dying adipocytes surrounded by macrophages forming crown-like structures (CLS). Tumor characteristics and host factors were measured. Wilcoxon rank-sum, Chi-square, or Fisher’s exact tests were used to examine the relationship between WATi and tumor and host characteristics. Results: From 11/2011-8/2015, periprostatic WAT was obtained from 169 pts (median age 62 years, range: 39 -77). Fasting blood samples were collected from 154 pts. CLS were present in 84 (49.7%) of pts. Presence of CLS was associated with higher median BMI (P = 0.02); 40/65 (61.5%) obese pts, 36/83 (43.4 %) overweight pts, and 8/21 (38.1 %) normal weight pts had CLS. Pts with CLS were more likely to have high grade prostate cancer (Gleason grade group IV/V, P = 0.02), larger adipocytes (P = 0.004), and positive surgical margins at the time of surgery (P = 0.04). WATi correlated with higher circulating levels of insulin, triglycerides, and leptin/adiponectin ratio, and lower high density lipoprotein cholesterol, compared to pts without WATi (P’s < 0.05). Conclusions: Periprostatic WATi is common in men with PC. It is associated with high grade PC and alterations in systemic factors that contribute to PC development and progression. Periprostatic WATi may represent a therapeutic target for improving PC risk and outcomes.

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

2016 ◽  
Vol 130 (18) ◽  
pp. 1603-1614 ◽  
Author(s):  
Matthias Blüher
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Chronic Inflammation ◽  
Metabolic Diseases ◽  
Health Concern ◽  
Noncommunicable Diseases ◽  
Adipose Tissue Inflammation ◽  
Tissue Storage ◽  
Tissue Inflammation ◽  
Increased Risk

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.

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