Key result
Obesity is linked to ~18% larger subcutaneous adipocytes, increased inflammation, and insulin resistance.
Why the study?
The fat storage capability of adipose tissue depends on adipogenic gene expression and angiogenesis to prevent ectopic lipid deposition, prompting evaluation of subcutaneous white adipose tissue hyperplasia and hypertrophy across different obesity classes.
Cross-Sectional (n=80)
No
Absolute Event Rate: 21144% vs 17892%
p-value: p=0.02
Subcutaneous adipocyte hypertrophy, rather than total adiposity, is associated with inflammation, insulin resistance, and ER stress in obesity.
Larger adipocytes may flag metabolic risk beyond BMI in obesity; hypothesis-generating and requires prospective validation before clinical use.
Background: The fat storage capability of the adipose tissue prevents ectopic lipid deposition, which is one of the risk factors for metabolic abnormalities in obesity. This capability depends on the adipogenic gene expression and blood supply provision for tissue expansion through angiogenesis. Here, we studied hyperplasia/hypertrophy of subcutaneous white adipose tissue (scWAT) concerning adipogenic gene expression, angiogenic status, and metabolic parameters in non-obese, Class I, and Class II+III obese subjects. Methods: The scWAT samples were collected from 80 subjects. The anthropometric parameters, adipose tissue cell size, serum biochemistry, ER stress induced XBP1 splicing, PPARγ2, SFRP1, WNT10B, and VEGFA gene expression levels were studied. In addition, the CD31 level was investigated by Western blotting. Results: The obese subjects had greater waist circumferences and higher serum TG, TC, insulin, and HOMA-IR than the non-obese group. The Class I obese group showed the largest adipocyte size, increased TNFα, insulin, HOMA-IR, and sXBP-1, WNT10B, and VEGFAexpression. In contrast, the expression of SFRP1 was not significantly different between all studied groups. The Class II+III obesity group showed high PPARγ2 expression and CD31 levels. Class I obesity, with hypertrophic scWAT adipocytes and limited capability of adipose tissue expansion, showed inflammation, insulin resistance, and ER stress. Conclusion: The results suggest that the capability of adipogenesis with inadequate angiogenesis is related to metabolic status, inflammation, and ER function. Therefore, therapeutic strategies to simultaneously promote angiogenesis and adipogenesis can effectively prevent obesity complications.
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Pourdashti et al. (2023) conducted a cross-sectional in Obesity (n=80). Obesity (BMI ≥ 30) vs. Non-obese (BMI < 30) was evaluated on Subcutaneous abdominal adipocyte size (µm2) (p=0.02). Obesity was associated with significantly larger subcutaneous adipocytes compared to non-obese subjects (21144 vs 17892 µm2, p=0.02), with Class I obesity specifically linked to increased inflammation and insulin resistance.
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