Adipose tissue dysregulation and metabolic consequences in childhood and adolescent obesity: potential impact of dietary fat quality

Abstract

Evidence suggests that at a population level, childhood and adolescent obesity increase the long-term risk of chronic diseases such as type 2 diabetes and CVD. At an individual level, however, the metabolic consequences of obesity in youth vary immensely. Despite comparable BMI, some adolescents develop impaired glucose tolerance while others maintain normal glucose homeostasis. It has been proposed that the variation in the capacity to store lipid in the subcutaneous adipose tissue (SAT) may partially discriminate metabolically healthy from unhealthy obesity. In positive energy balance, a decreased capacity to expand SAT may drive lipid accumulation to visceral adipose tissue, liver and skeletal muscle. This state of lipotoxicity is associated with chronic low-grade inflammation, insulin resistance and dyslipidaemia. The present review examines the differential adipose tissue development and function in children and adolescents who exhibit metabolic dysregulation compared with those who are protected. Additionally, the role of manipulating dietary fat quality to potentially prevent and treat metabolic dysfunction in obesity will be discussed. The findings of the present review highlight the need for further randomised controlled trials to establish the effect of dietary n-3 PUFA on the metabolic phenotype of obese children and adolescents. Furthermore, using a personalised nutrition approach to target interventions to those at risk of, or those with established metabolic dysregulation may optimise the efficacy of modifying dietary fat quality.

Iron Status and Metabolically Unhealthy Obesity in Prepubertal Children

“…However, given that CRP levels affected the MUOV–ferritin association but did not affect the MUO–ferritin association, subclinical inflammation appears to exert influence to a lesser extent. In people with overweight or obesity and cardiometabolic risk factors, the adipose tissue phenotype is clearly different, with fat tending to centrally accumulate in the form of visceral fat , which is known to secrete proinflammatory cytokines . This was consistent with the fact that in the group of children with overweight and obesity, WC and CRP levels were significant predictors of serum ferritin in univariate analyses.…”

Metabolically healthy obesity across the life course: epidemiology, determinants, and implications

“…The pathway to MUO may be characterized by dysfunctional adipose tissue (larger fat cells), increased immune cell infiltration, elevated proinflammatory status, and reduced capacity of subcutaneous adipose tissue to expand and leading to increased ectopic fat deposition, resulting in lipotoxicity, insulin resistance in peripheral tissues, and a range of metabolic derangements (Fig. ) . In MHO individuals, the excess calories are channeled into insulin‐sensitive subcutaneous adipose tissue, which is capable of expansion; thus, visceral and ectopic adiposity are reduced, macrophage infiltration and raised proinflammatory state are attenuated, insulin sensitivity is preserved, and the individual is protected from development of the MetS …”

Impact of anti-inflammatory nutrients on obesity-associated metabolic-inflammation from childhood through to adulthood

“…α-Tocopherol supplementation, in conjunction with vitamin D 3 , was demonstrated to decrease IL-6 concentrations in vitro and in a mouse model of obesity (72) . In a cohort of T2D patients, while α-tocopherol supplementation ameliorated systemic oxidative stress, no positive effect was seen on plasma markers of inflammation (97) .…”