Adipose Tissue, Non-Communicable Diseases, and Physical Exercise: An Imperfect Triangle

Abstract

The study of adipose tissue has received considerable attention due to its importance not just in maintaining body energy homeostasis but also in playing a role in a number of other physiological processes. Beyond storing energy, adipose tissue is important in endocrine, immunological, and neuromodulatory functions, secreting hormones that participate in the regulation of energy homeostasis. An imbalance of these functions will generate structural and functional changes in the adipose tissue, favoring the secretion of deleterious adipocytokines that induce a pro-inflammatory state, allowing the development of metabolic and cardiovascular diseases and even some types of cancer. A common theme worldwide has been the development of professional guidelines for the control and treatment of obesity, with emphasis on hypocaloric diets and exercise. The aim of this review is to examine the pathophysiological mechanisms of obesity, considering the relationship among adipose tissue and two aspects that contribute positively or negatively to keeping a healthy body homeostasis, namely, exercise and noninfectious diseases. We conclude that the relationship of these aspects does not have homogeneous effects among individuals. Nevertheless, it is possible to establish some common mechanisms, like a decrease in pro-inflammatory markers in the case of exercise, and an increase in chronic inflammation in non-communicable diseases. An accurate diagnosis might consider the particular variables of a patient, namely their molecular profile and how it affects its metabolism, routines, and lifestyle; their underling health conditions; and probably even the constitution of their microbiome. We foresee that the development and accessibility of omics approaches and precision medicine will greatly improve the diagnosis, treatment, and successful outcomes for obese patients.

Keywords: adipocytokines; adipose tissue; molecular mechanism; myokines; obesity; overweight; treatments.

Figure 1

Adipocytokines and other molecules are secreted by adipose tissue. (+) Beneficial effect on energy homeostasis; (−) Negative effect on energy homeostasis.

Figure 2

Some pathways by which excess adipose tissue produces risk factors or chronic diseases. ANS, Autonomic Nervous System; RAAs, Renin–Angiotensin–Aldosterone System. ↑ imply an increase.

Figure 3

Insulin-resistance systemic level model. FFA, Free Fatty Acids; ER, Endoplasmic Reticulum; ROS, Reactive Oxygen Species; GluT4, Glucose Transporter 4; IRS-1, Insulin Receptor Substrate type 1, MAPK, Mitogen-Activated Protein Kinase; PI3K, Phosphatidyl Inositol 3 Kinase; PBK, Protein Kinase B or Akt; JNK, c-Jun N-terminal kinase; ↑ imply an increase.

Figure 4

Complications and Comorbidities associated with overweight-obesity.

Figure 5

Pharmacological and non-pharmacological management of the overweight–obese patient.

Figure 6

Myokines and their potential role on metabolism. Skeletal muscle produces and secretes myokines into the circulation. Adipose tissue, under conditions of metabolic diseases, secretes proinflammatory adipocytokines that promote pathological processes such as insulin resistance. However, physical exercise promotes the secretion of myocytokines which can counteract the effects of adipocytokines. IL, Interleukin; LIF, Leukemia Inhibitory Factor; BDNF, Brain-derived Neurotrophic Factor; FGF-21, Fibroblast Growth Factor 21; SPARC, Secreted Protein Rich in Acid and Cysteine; ↑ imply an increase; ↓ imply a decrease.