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Increased Abdominal Fibrogenesis Linked to Insulin Resistance in Adolescents with Obesity


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."

Deeper Inquiries

How do the mechanisms of abdominal fibrogenesis differ between adolescents and adults with obesity?

In adults with obesity, abdominal fibrogenesis is known to increase and reduce insulin sensitivity. However, in adolescents with obesity, particularly those who are insulin-resistant, there is a significant increase in insoluble collagen (type I, subunit α 2) in the abdominal adipose tissue. This heightened fibrogenesis impairs the storage capacity of abdominal subcutaneous adipose tissue, leading to fat accumulation in visceral adipose tissue and other organs like the liver. This mechanism differs from adults as it showcases a more pronounced impact on lipid dynamics and insulin sensitivity in adolescents with obesity.

What interventions could potentially reverse or mitigate the adverse effects of increased abdominal fibrogenesis in insulin-resistant adolescents with obesity?

Interventions aimed at mitigating the adverse effects of increased abdominal fibrogenesis in insulin-resistant adolescents with obesity could include lifestyle modifications such as dietary changes and increased physical activity to address obesity and insulin resistance. Additionally, targeted therapies focusing on reducing fibrogenesis, such as anti-fibrotic medications or interventions to improve adipose tissue expandability, could be beneficial. Moreover, early detection and management of insulin resistance through pharmacological interventions like insulin sensitizers may help in reducing the progression of fibrogenesis and its associated metabolic complications in this population.

What are the long-term implications of elevated abdominal fibrogenesis on the development of metabolic and liver diseases in this population?

Elevated abdominal fibrogenesis in insulin-resistant adolescents with obesity can have significant long-term implications on the development of metabolic and liver diseases. The increased formation of insoluble collagen in the abdominal adipose tissue can lead to lipid spillover from subcutaneous adipose tissue to visceral adipose tissue, contributing to a higher risk of metabolic complications such as insulin resistance and dyslipidemia. This process can further exacerbate the development of non-alcoholic fatty liver disease (NAFLD) and other liver-related disorders. Therefore, elevated abdominal fibrogenesis serves as a crucial mechanism in the pathophysiology of obesity-related metabolic and liver diseases in this population, highlighting the importance of early intervention and management strategies to prevent long-term health consequences.
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