Extracellular matrix remodeling and matrix metalloproteinase inhibition in visceral adipose during weight cycling in mice

Caria, Cíntia Rabelo e Paiva; Gotardo, Érica Martins Ferreira; Santos, Paola Souza; Acedo, Simone Coghetto; Ribeiro, Marcelo Lima; Gambero, Alessandra

doi:10.1016/j.yexcr.2017.08.026

Cited by 14 publications

(9 citation statements)

References 39 publications

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“…Based on CR experimen cytokine, chemokine, and metabolic pathways are significantly regulated by CR the aging process. It is expected that a better understanding of senoinflam mechanisms will provide a basis for the discovery of molecular targets that modulate age-related chronic inflammatory conditions and enable the develop effective interventions to delay aging and prevent the occurrence of aging-assoc ├ Mouse, Rat [60,74,82,242] MMP9 ↑ subfamily that is expressed in adipose tissues (white and brown) [220] and Although the GPR109A receptor has protective effects, associations have b ketogenic dietary intervention use in stroke patients and neurodegenerative dis TNFα or LPS-induced inflammatory setting, HB exerts anti-inflammatory effects release of pro-inflammatory proteins (iNOS and COX-2) and cytokines (TN CCL2/MCP-1), which seems to occur partially via inhibition of NF-κB translocati pro-inflammatory gene activation [224,225]. However, in neurodegenera conditions, the effects of GPR109A-mediated HB do not appear to involve infl signaling via the MAPK pathway [224].…”

Section: Discussionmentioning

confidence: 99%

Anti-Aging Effects of Calorie Restriction (CR) and CR Mimetics Based on the Senoinflammation Concept

et al. 2020

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Chronic inflammation, a pervasive feature of the aging process, is defined by a continuous, multifarious, low-grade inflammatory response. It is a sustained and systemic phenomenon that aggravates aging and can lead to age-related chronic diseases. In recent years, our understanding of age-related chronic inflammation has advanced through a large number of investigations on aging and calorie restriction (CR). A broader view of age-related inflammation is the concept of senoinflammation, which has an outlook beyond the traditional view, as proposed in our previous work. In this review, we discuss the effects of CR on multiple phases of proinflammatory networks and inflammatory signaling pathways to elucidate the basic mechanism underlying aging. Based on studies on senoinflammation and CR, we recognized that senescence-associated secretory phenotype (SASP), which mainly comprises cytokines and chemokines, was significantly increased during aging, whereas it was suppressed during CR. Further, we recognized that cellular metabolic pathways were also dysregulated in aging; however, CR mimetics reversed these effects. These results further support and enhance our understanding of the novel concept of senoinflammation, which is related to the metabolic changes that occur in the aging process. Furthermore, a thorough elucidation of the effect of CR on senoinflammation will reveal key insights and allow possible interventions in aging mechanisms, thus contributing to the development of new therapies focused on improving health and longevity.

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Section: Discussionmentioning

confidence: 99%

Anti-Aging Effects of Calorie Restriction (CR) and CR Mimetics Based on the Senoinflammation Concept

et al. 2020

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“…Blood lipid levels were lower in women with WC than in those who maintained weight [ 24 ]. The incidence of hepatic steatosis was significantly higher in WC mice than in obese mice [ 28 ]. The pathological findings revealed that lipid droplets had entered the liver cells, and the levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) increased, leading to liver inflammation and degradation of systemic glucose metabolism, which ultimately affects systemic metabolism [ 29 ].…”

Section: Systemic Effects On Wc: Metaflammation Of the Endocrine Syst...mentioning

confidence: 99%

Weight cycling based on altered immune microenvironment as a result of metaflammation

Chen

2023

Nutr Metab (Lond)

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As a result of the obesity epidemic, more people are concerned about losing weight; however, weight regain is common, leading to repeated weight loss and weight cycling. The health benefits of early weight loss are nullified by weight regain after weight cycling, which has much more severe metabolic consequences. Weight cycling alters body composition, resulting in faster fat recovery and slower muscle reconstruction. This evident fat accumulation, muscle loss, and ectopic fat deposition destroy the intestinal barrier, increase the permeability of the small intestinal epithelium, and cause the lipotoxicity of lipid metabolites and toxins to leak into extraintestinal tissues and circulation. It causes oxidative stress and hypoxia in local tissues and immune cell infiltration in various tissues, all contributing to the adaptation to this metabolic change. Immune cells transmit inflammatory responses in adipose and skeletal muscle tissue by secreting cytokines and adipokines, which mediate immune cell pathways and cause metaflammation and inefficient metabolic degradation. In this review, we focus on the regulatory function of the immunological microenvironment in the final metabolic outcome, with a particular emphasis on the cellular and molecular processes of local and systemic metaflammation induced by weight cycling-induced changes in body composition. Metaflammation in adipose and muscle tissues that is difficult to relieve may cause weight cycling. As this chronic low-grade inflammation spreads throughout the body, metabolic complications associated with weight cycling are triggered. Inhibiting the onset and progression of metabolic inflammation and enhancing the immune microenvironment of adipose and muscle tissues may be the first step in addressing weight cycling.

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“…An elegant study demonstrated an increased expression of MMP-2 and MMP-12, gelatinase activity (MMP-2 and MMP-9) in the rats fed HFD. Interestingly, however, intense MMP activity in adipose tissue can remain during weight loss induced by caloric restriction [75]. The authors suggest that ECM could be less rigid during weight loss and that collagen deposition could be due to robust ECM remodeling and not fibrosis process [75].…”

Section: High-fat Diet-fed Animals Modelsmentioning

confidence: 99%

“…Interestingly, however, intense MMP activity in adipose tissue can remain during weight loss induced by caloric restriction [75]. The authors suggest that ECM could be less rigid during weight loss and that collagen deposition could be due to robust ECM remodeling and not fibrosis process [75]. In addition, MMP inhibition during weight loss modifies adipose tissue inflammation during weight regain, suggesting that the MMP inhibition could be an exciting target to establish weight cyclers [75].…”

Section: High-fat Diet-fed Animals Modelsmentioning

confidence: 99%

“…The authors suggest that ECM could be less rigid during weight loss and that collagen deposition could be due to robust ECM remodeling and not fibrosis process [75]. In addition, MMP inhibition during weight loss modifies adipose tissue inflammation during weight regain, suggesting that the MMP inhibition could be an exciting target to establish weight cyclers [75]. Those findings may have crucial implications for nutritional therapy and dietary management.…”

Section: High-fat Diet-fed Animals Modelsmentioning

confidence: 99%

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Adipose Tissue Extracellular Matrix Remodeling in Response to Dietary Patterns and Exercise: Molecular Landscape, Mechanistic Insights, and Therapeutic Approaches

Neto

Durigan

Silva

et al. 2022

Biology

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The extracellular matrix (ECM) is a 3-dimensional network of molecules that play a central role in differentiation, migration, and survival for maintaining normal homeostasis. It seems that ECM remodeling is required for adipose tissue expansion. Despite evidence indicating that ECM is an essential component of tissue physiology, adipose tissue ECM has received limited attention. Hence, there is great interest in approaches to neutralize the harmful effects of ECM enlargement. This review compiles and discusses the current literature on adipose tissue ECM remodeling in response to different dietary patterns and exercise training. High-calorie diets result in substantial adipose tissue ECM remodeling, which in turn could lead to fibrosis (excess deposition of collagens, elastin, and fibronectin), inflammation, and the onset of metabolic dysfunction. However, combining a nutritionally balanced diet with exercise is a remarkable potential strategy for lipolytic activity, preventing rapid ECM expansion in different adipose tissue depots. Despite the distinct exercise modalities (aerobic or resistance exercise) reversing adipose tissue fibrosis in animal models, the beneficial effect on humans remains controversial. Defining molecular pathways and specific mechanisms that mediate the positive effects on adipose tissue, ECM is essential in developing optimized interventions to improve health and clinical outcomes.

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Extracellular matrix remodeling and matrix metalloproteinase inhibition in visceral adipose during weight cycling in mice

Cited by 14 publications

References 39 publications

Anti-Aging Effects of Calorie Restriction (CR) and CR Mimetics Based on the Senoinflammation Concept

Anti-Aging Effects of Calorie Restriction (CR) and CR Mimetics Based on the Senoinflammation Concept

Weight cycling based on altered immune microenvironment as a result of metaflammation

Adipose Tissue Extracellular Matrix Remodeling in Response to Dietary Patterns and Exercise: Molecular Landscape, Mechanistic Insights, and Therapeutic Approaches

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