Biochemical and immunological changes in obesity

• Published in: Archives of biochemistry and biophysics 2021-09, Vol.708, p.108951, Article 108951
• Main Authors: Barakat, Beatriz, Almeida, Martha E. F
• Format: Article
• Language: English
• Subjects: Adipocytes - immunology; Adipocytes - metabolism; Adipokines - metabolism; Adipose tissue; Adipose Tissue - immunology; Adipose Tissue - metabolism; Animals; Cytokines; Diseases; Gastrointestinal Microbiome; Hormones; Humans; Inflammation; Inflammation - immunology; Inflammation - metabolism; Intestinal microbiota; Obesity - immunology; Obesity - metabolism
• ISSN: 0003-9861; 1096-0384; 1096-0384
• DOI: 10.1016/j.abb.2021.108951

Obesity is a syndemia that promotes high expenditures for public health, and is defined by the excess of adipose tissue that is classified according to its function and anatomical distribution. In obese people, this tissue generates oxidative stress associated with a chronic inflammatory response, in which there is an imbalance in relation to the release of hormones and adipokines that cause loss of body homeostasis and predisposition to the development of some comorbidities. The purpose of this review is to summarize the main events that occur during the onset and progression of obesity with a special focus on biochemical and immunological changes. Hypertrophied and hyperplasia adipocytes have biomarkers and release adipokines capable of regulating pathways and expressing genes that culminate in the development of metabolic changes, such as changes in energy balance and intestinal microbiota, and the development of some comorbidities, diabetes mellitus, dyslipidemias, arterial hypertension, liver disease, cancer, allergies, osteoporosis, sarcopenia and obstructive sleep apnea. Thus, it is necessary to treat and/or prevent pathology, using traditional methods based on healthy eating, and regular physical and leisure activities. [Display omitted] •Expansion of adipose tissue leads to a chronic inflammatory response.•Adipose tissue increases the activation of JNK and NF-κB signaling pathways.•Inflammatory cytokines act in the progression of comorbidities.•Increased SOCS3 expression disrupts hunger and body weight control.