Obesity and Adipose Tissue Dysfunction: From Pediatrics to Adults

Genes (Basel). 2022 Oct 15;13(10):1866. doi: 10.3390/genes13101866.

Abstract

Obesity is a growing health problem that affects both children and adults. The increasing prevalence of childhood obesity is associated with comorbidities such as cardiovascular disease, type 2 diabetes and metabolic syndrome due to chronic low-grade inflammation present at early stages of the disease. In pediatric patients suffering from obesity, the role of epigenetics, the gut microbiome and intrauterine environment have emerged as causative factors Interestingly, pediatric obesity is strongly associated with low birth weight. Accelerated weight gain oftentimes occurs in these individuals during the post-natal period, which can lead to increased risk of adiposity and metabolic disease. The pathophysiology of obesity is complex and involves biological and physiological factors compounded by societal factors such as family and community. On a cellular level, adipocytes contained within adipose tissue become dysregulated and further contribute to development of comorbidities similar to those present in adults with obesity. This review provides an overview of the current understanding of adipose tissue immune, inflammatory and metabolic adaptation of the adipose tissue in obesity. Early cellular changes as well as the role of immune cells and inflammation on the progression of disease in pivotal pediatric clinical trials, adult studies and mouse models are emphasized. Understanding the initial molecular and cellular changes that occur during obesity can facilitate new and improved treatments aimed at early intervention and subsequent prevention of adulthood comorbidities.

Keywords: adipose immunity; immune system; obesity; pediatric obesity; pediatric obesity and inflammatory dysregulation.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue / metabolism
  • Animals
  • Child
  • Diabetes Mellitus, Type 2* / metabolism
  • Humans
  • Inflammation / metabolism
  • Mice
  • Pediatric Obesity* / epidemiology
  • Pediatric Obesity* / genetics
  • Pediatrics*

Grants and funding

The authors will like to acknowledge support from the Amerian Society for Metabolic and Bariatric Surgery (ASMBS) for funding this work.