Exercise Rescues Gene Pathways Involved in Vascular Expansion and Promotes Functional Angiogenesis in Subcutaneous White Adipose Tissue

Min, So Yun; Learnard, Heather; Kant, Shashi; Gealikman, Olga; Rojas-Rodriguez, Raziel; DeSouza, Tiffany; Desai, Anand; Keaney, John F.; Corvera, Silvia; Craige, Siobhan M.

doi:10.3390/ijms20082046

Cited by 22 publications

(16 citation statements)

References 35 publications

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“…In retinoic acid treatment, activation of the brown fat-associated program in white adipocytes was mediated by vascular endothelial growth factor-stimulated angiogenesis (Wang et al, 2017). With exercise, vascularization in subcutaneous WAT is increased and may mediate an improved metabolic response (Min et al, 2019). EPO exhibits angiogenic and neovascularization activity in animal models (Yasuda et al, 1998;Ribatti et al, 1999;Kertesz et al, 2004;Wang et al, 2004;Li et al, 2007).…”

Section: Epo Protection In Mouse Adipose Tissue Inflammationmentioning

confidence: 99%

Effects of Erythropoietin in White Adipose Tissue and Bone Microenvironment

Suresh

Lee

Noguchi

2020

Front. Cell Dev. Biol.

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Erythropoietin (EPO) is expressed primarily in fetal liver and adult kidney to stimulate red blood cell production. Erythropoietin receptor expression is not restricted to erythroid progenitor cells, and non-erythroid EPO activity includes immune response and bone remodeling. In bone fracture models, EPO administration promotes bone formation and accelerates bone healing. In contrast, in healthy adult mice, exogenous EPO-stimulated erythropoiesis has been concomitant with bone loss, particularly at high EPO, that may be accompanied by increased osteoclast activation. Other EPO-associated responses include reduced inflammation and loss of fat mass with high-fat diet feeding, especially in male mice. While EPO exhibited a sex-dimorphic response in regulation of fat mass and inflammation in obese mice, EPO-stimulated erythropoiesis as well as EPO-associated bone loss was comparable in males and females. EPO administration in young mice and in obese mice resulted in bone loss without increasing osteoclasts, suggesting an osteoclast-independent mechanism, while loss of endogenous EPO decreased bone development and maintenance. Ossicle formation of bone marrow stromal cell transplants showed that EPO directly regulates the balance between osteogenesis and adipogenesis. Therefore, during development, endogenous EPO contributes to normal bone development and in maintaining the balance between osteogenesis and adipogenesis in bone marrow stromal cells, while EPO treatment in mice increased erythropoiesis, promoted bone loss, decreased bone marrow adipogenesis, and increased osteoclast activity. These observations in mouse models suggest that the most prevalent use of EPO to treat anemia associated with chronic kidney disease may compromise bone health and increase fracture risk, especially at a high dose.

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Section: Epo Protection In Mouse Adipose Tissue Inflammationmentioning

confidence: 99%

Effects of Erythropoietin in White Adipose Tissue and Bone Microenvironment

Suresh

Lee

Noguchi

2020

Front. Cell Dev. Biol.

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“…Epidemiological studies and clinical trials showed that fatty acids are associated with cardiovascular diseases [ 1 , 2 , 3 , 4 , 5 ], neurological diseases [ 6 , 7 , 8 , 9 ], non-alcoholic fatty liver disease [ 10 , 11 , 12 , 13 ], allergic diseases [ 14 , 15 , 16 ], and so on. Evidence from metabolomics experiments indicates that they participate in the metabolic pathways of related diseases [ 8 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 ]. For example, the free FA profile was found to be altered in both leukemia and pre-leukemic diseases, particularly C14:0, C16:0, and C18:0 [ 26 ].…”

Section: Introductionmentioning

confidence: 99%

Nutritional Indices for Assessing Fatty Acids: A Mini-Review

Chen

Liu

2020

IJMS

586

439

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Dietary fats are generally fatty acids that may play positive or negative roles in the prevention and treatment of diseases. In nature, fatty acids occur in the form of mixtures of saturated fatty acid (SFA), monounsaturated fatty acid (MUFA), and polyunsaturated fatty acid (PUFA), so their nutritional and/or medicinal values must be determined. Herein, we do not consider the classic indices, such as ∑SFA, ∑MUFA, ∑PUFA, ∑n-6 PUFA, ∑n-3 PUFA, and n-6 PUFA/n-3 PUFA; instead, we summarize and review the definitions, implications, and applications of indices used in recent years, including the PUFA/SFA, index of atherogenicity (IA), the index of thrombogenicity (IT), the hypocholesterolemic/hypercholesterolemic ratio (HH), the health-promoting index (HPI), the unsaturation index (UI), the sum of eicosapentaenoic acid and docosahexaenoic acid (EPA + DHA), fish lipid quality/flesh lipid quality (FLQ), the linoleic acid/α-linolenic acid (LA/ALA) ratio, and trans fatty acid (TFA). Of these nutritional indices, IA and IT are the most commonly used to assess the composition of fatty acids as they outline significant implications and provide clear evidence. EPA + DHA is commonly used to assess the nutritional quality of marine animal products. All indices have their advantages and disadvantages; hence, a rational choice of which to use is critical.

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“…In this regard, chronic exercise training has been shown to attenuate adipocyte apoptosis (assessed via chromatin condensation) in inguinal AT, whereas apoptosis is increased by exercise in retroperitoneal AT. This is intriguing, given that markers of vascular expansion and capillary density in AT are reportedly increased by exercise training in rodents (56‐58) and humans (59), which is typically inversely associated with cell death. However, a prior study found that targeted deletion of mature adipocytes through apoptosis was not accompanied by aberrant inflammation in AT but rather increased the abundance of alternatively activated macrophages (60).…”

Section: Exercise and At Remodeling In Obesitymentioning

confidence: 99%

Exercise and Adipose Tissue Immunity: Outrunning Inflammation

Winn

Cottam

Wasserman

et al. 2021

Obesity

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Chronic inflammation is considered a precipitating factor and possibly an underlying cause of many noncommunicable diseases, including cardiovascular disease, metabolic diseases, and some cancers. Obesity, which manifests in more than 650 million people worldwide, is the most common chronic inflammatory condition, with visceral adiposity thought to be the major inflammatory hub that links obesity and chronic disease. Adipose tissue (AT) inflammation is triggered or heightened in large part by (1) accelerated immune cell recruitment, (2) reshaping of the AT stromal‐immuno landscape (e.g., immune cells, endothelial cells, fibroblasts, adipocyte progenitors), and (3) perturbed AT immune cell function. Exercise, along with diet management, is a cornerstone in promoting weight loss and preventing weight regain. This review focuses on evidence that increased physical activity reduces AT inflammation caused by hypercaloric diets or genetic obesity. The precise cell types and mechanisms responsible for the therapeutic effects of exercise on AT inflammation remain poorly understood. This review summarizes what is known about obesity‐induced AT inflammation and immunomodulation and highlights mechanisms by which aerobic exercise combats inflammation by remodeling the AT immune landscape. Furthermore, key areas are highlighted that require future exploration and novel discoveries into the burgeoning field of how the biology of exercise affects AT immunity.

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Exercise Rescues Gene Pathways Involved in Vascular Expansion and Promotes Functional Angiogenesis in Subcutaneous White Adipose Tissue

Cited by 22 publications

References 35 publications

Effects of Erythropoietin in White Adipose Tissue and Bone Microenvironment

Effects of Erythropoietin in White Adipose Tissue and Bone Microenvironment

Nutritional Indices for Assessing Fatty Acids: A Mini-Review

Exercise and Adipose Tissue Immunity: Outrunning Inflammation

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