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

Abstract

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.

Characterisation of the relationship between Heme-oxygenase-1 and adiponectin

“…We observed comparable, albeit more moderate, effects in liver and suggest that these are explained by a similar mechanism [204,316]. The role of adipose tissue inflammation in the aetiology of insulin resistance is far from clear [308,317] and our observations provide further evidence that adipose tissue inflammation does not correlate with changes in insulin sensitivity.…”

“…One possibility is that the mechanism by which CoPP affects weight gain, and other parameters, in the context of obesity may differ over time. Obesity is a progressive state with temporal alterations in stressors of specific cell-types and tissues, as evidenced by the dynamics of adipose tissue inflammation and development of ectopic lipid accumulation and insulin resistance [308,[312][313][314].…”

“…Perhaps surprisingly, in light of other publications [217,237,241,242,272,279,306] and the effects of CoPP on circulating adiponectin levels, CoPP administration reduced Adipoq expression by 30-40%, and this reached significance in the obese mice (Fig 4.3g). We also examined the effects of CoPP administration on markers of immune cell infiltration and inflammation, which has been widely reported to play a causative role in the aetiology of obesity induced adipose tissue dysfunction and insulin resistance [204,[308][309][310][311].…”

Metabolic Vascular Syndrome: New Insights into a Multidimensional Network of Risk Factors and Diseases

“…Low-grade inflammation stimulated by dysfunctional adipose tissue was one of the most accepted working hypotheses to explain the connection between (central) obesity and vascular dysfunction [34]. 10 years later, in a scientifically profound recent review, it was convincingly worked out that there are reasonable arguments to conclude that adipose tissue inflammation following adipocyte hypertrophy after long-term positive energy balance is a main driving force for insulin resistance in fat tissue itself but also for systemic insulin resistance and probably also for an obesogenic memory [35]. Key factors which determine monocyte infiltration and the development of an inflammatorily active macrophage phenotype are positive energy balance, lipid accumulation in adipocytes, adipocyte hypertrophy, reduced insulin sensitivity of hypertrophic adipocytes, and processes related to hypoxia, autophagia, and apoptosis.…”

<b>Avaliação da frutosamina em cavalos com e sem resistência à insulina</b>

“…Em muitos casos, o acúmulo de gordura é consequência direta da resistência à insulina, pois o depósito de gordura no tecido adiposo e fígado é aumentado quando há hiperglicemia (SOUZA et al, 2007;FRANK, 2010;BLUHER, 2016;BRANFORD et al, 2016). No presente estudo, os cavalos foram classificados segundo critérios estabelecidos por Henneke (1983) e não houve diferença estatística quanto ao escore corporal dos animais, considerados resistentes ou não resistentes pelo método TCGI.…”