Immunological contributions to adipose tissue homeostasis

Abstract

Adipose tissue is composed of many functionally and developmentally distinct cell types, the metabolic core of which is the adipocyte. The classification of "adipocyte" encompasses three primary types - white, brown, and beige - with distinct origins, anatomic distributions, and homeostatic functions. The ability of adipocytes to store and release lipids, respond to insulin, and perform their endocrine functions (via secretion of adipokines) is heavily influenced by the immune system. Various cell populations of the innate and adaptive arms of the immune system can resist or exacerbate the development of the chronic, low-grade inflammation associated with obesity and metabolic dysfunction. Here, we discuss these interactions, with a focus on their consequences for adipocyte and adipose tissue function in the setting of chronic overnutrition. In addition, we will review the effects of diet composition on adipose tissue inflammation and recent evidence suggesting that diet-driven disruption of the gut microbiota can trigger pathologic inflammation of adipose tissue.

Keywords: Adipocyte; Hyperplasia; Hypertrophy; Immunocyte; Obesity.

Figure 1. Inflammatory cascades that contribute to adipocyte dysfunction

Diets high in saturated fatty acids, when consumed in a state of chronic caloric excess, contribute to adipocyte dysfunction. While healthy adipocytes are insulin-sensitive and have low levels of basal lipolysis, adipocytes that reach their lipid-storage limit and/or are exposed to chronically elevated levels of pro-inflammatory cytokines may exhibit the dysfunctions listed above. Chronic overnutrition also disrupts the balance of immunocyte populations present in adipose tissue. A possible contributing pathway involves diet-induced alterations in gut symbionts that, through yet unclear mechanisms, triggers pathologic adipose tissue inflammation.