Core Concepts
Insulin resistance in adolescents with obesity is associated with increased abdominal fibrogenesis, which impairs the capacity of subcutaneous adipose tissue to store lipids, leading to fat accumulation in the visceral adipose tissue and other organs.
Abstract
The study investigated the relationship between insulin resistance, lipid dynamics, fibrogenesis, and adipocyte turnover in the abdominal and gluteal regions of adolescents with obesity.
Key findings:
- The abdominal and gluteal subcutaneous adipose tissue (SAT) turnover rates were similar in insulin-resistant and insulin-sensitive adolescents with obesity.
- Insulin-resistant adolescents had higher levels of insoluble collagen (type I, subunit α 2) in the abdominal adipose tissue, indicating increased abdominal fibrogenesis.
- Abdominal insoluble collagen I α 2 was associated with higher fasting plasma insulin levels, a higher visceral to total adipose tissue ratio, and lower whole-body insulin sensitivity.
- There was no evidence of increased collagen production in the gluteal adipose tissue.
The increased abdominal fibrogenesis in insulin-resistant adolescents with obesity contributes to lipid spillover from subcutaneous adipose tissue to visceral adipose tissue, leading to metabolic and liver disease pathology.
Stats
Insulin-resistant adolescents with obesity had a higher fractional synthesis rate of insoluble collagen (type I, subunit α 2) in the abdominal adipose tissue compared to insulin-sensitive adolescents (difference of 0.611, p < .001).
Abdominal insoluble collagen I α 2 was positively correlated with fasting plasma insulin levels (r = 0.579, p = 0.015) and visceral to total adipose tissue ratio (r = 0.643, p = 0.007), and negatively correlated with whole-body insulin sensitivity index (r = -0.540, p = 0.023).
Quotes
"The increased formation of insoluble collagen observed in insulin-resistant compared with insulin-sensitive individuals contributes to lipid spillover from SAT to VAT and, in turn, serves as a critically important mechanism involved in the complex sequelae of obesity-related metabolic and liver disease pathology."