Changes in fat distribution in children following severe burn injury.

BACKGROUND: Children with severe cutaneous burn injury show persistent metabolic abnormalities, including inflammation and insulin resistance. Such abnormalities could potentially increase their future risk for developing type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD). This could be related to changes in body composition and fat distribution. METHODS: We studied body composition, fat distribution, and inflammatory cytokines changes in children with severe burn injury up to 6 months from discharge. Sixty-two boys and 35 girls (burn ≥30% of total body surface area) were included. RESULTS: We found a decrease in total body fat and subcutaneous peripheral fat at 6 months (6% and 2%, respectively; P<0.05 each). An inverse correlation between the decrease in peripheral fat content at 6 months and the extent of burn injury (r=-041, P=0.02) was also observed. In addition, there was a 12% increase in serum tumor necrosis factor-α (TNF-α) (P=0.01 vs. discharge) and 9% decrease in serum interleukin-10 (IL-10) (P<0.0001 vs. discharge) over 6 months after burn. CONCLUSION: Severe burn injury in children is associated with changes in body fat content and distribution up to 6 months from hospital discharge. These changes, accompanied by persisting systemic inflammation, could possibly mediate the observed persistence of insulin resistance, predisposing burn patients to the development of T2DM and CVD.

Body fat distribution and insulin resistance.

The burden of obesity has increased globally over the last few decades and its association with insulin resistance and related cardio-metabolic problems have adversely affected our ability to reduce population morbidity and mortality. Traditionally, adipose tissue in the visceral fat depot has been considered a major culprit in the development of insulin resistance. However, there is a growing body of evidence supporting the role of subcutaneous truncal/abdominal adipose tissue in the development of insulin resistance. There are significant differences in the functional characteristics of subcutaneous abdominal/truncal vs. intraabdominal vs. gluteo-femoral fat depots. More recently, mounting evidence has been supporting the role of adipose tissue function in the development of metabolic complications independent of adipose tissue volume or distribution. Decreased capacity for adipocyte differentiation and angiogenesis along with adipocyte hypertrophy can trigger a vicious cycle of inflammation leading to subcutaneous adipose tissue dysfunction and ectopic fat deposition. Therapeutic lifestyle change continues to be the most important intervention in clinical practice to improve adipose tissue function and avoid development of insulin resistance and related cardio-metabolic complications.

Role of subcutaneous adipose tissue in the pathogenesis of insulin resistance.

Burden of obesity has increased significantly in the United States over last few decades. Association of obesity with insulin resistance and related cardiometabolic problems is well established. Traditionally, adipose tissue in visceral fat depot has been considered a major culprit in development of insulin resistance. However, growing body of the literature has suggested that adipose tissue in subcutaneous fat depot, not only due to larger volume but also due to inherent functional characteristics, can have significant impact on development of insulin resistance. There are significant differences in functional characteristics of subcutaneous abdominal/truncal versus gluteofemoral depots. Decreased capacity for adipocyte differentiation and angiogenesis along with adipocyte hypertrophy can trigger vicious cycle of inflammation in subcutaneous adipose tissue and subsequent ectopic fat deposition. It is important to shift focus from fat content to functional heterogeneity in adipose tissue depots to better understand the relative role of subcutaneous adipose tissue in metabolic complications of obesity. Therapeutic lifestyle change continues to be the most important intervention in clinical practice at any level of increased adiposity. Future pharmaceutical interventions aimed at improving adipose tissue function in various subcutaneous depots have potential to help maintain adequate insulin sensitivity and reduce risk for development of insulin resistance complications.