Korean J Obes 2010; 19(4): 119-129
Published online December 1, 2010
Copyright © Korean Society for the Study of Obesity.
Sang-Mo Hong, Ho Han, You-Hern Ahn, Woong-Hwan Choi*
Department of Internal Medicine, Hanyang University College of Medicine
Background: Some cross-sectional studies have established an association between the morphological change of visceral adipocyte and insulin resistance. This study was undertaken to investigate the differences of the morphological change of visceral adipocyte and myostatin
expressions according to insulin resistance.
Methods: Thirty four patients who underwent elective abdominal surgery were enrolled. Patients were classified
into either normal glucose tolerance (NGT) group, impaired fasting glucose (IFG) group, or type 2 DM
(DM) group. Adipose tissue was obtained from omental fat deposits. Morphological changes of visceral adipocyte
were examined through light and electron microscopy.Real-time quantitative PCR was performed to compare the
mRNA expression level of myostatin in obtained adipose tissue among NGT, IFG and type 2 DM patients.
Results: Mean visceral adipocyte size (μm2) was larger in IFG and DM than those with NGT. Log-transformed
mean visceral adipocyte size was significantly associated with insulin resistance (P < 0.05) even after controlling
for the effect of age, sex, BMI and visceral fat area. Infiltration of macrophages was more frequently observed
around the visceral adipocyte of IFG and DM group compared to the NGT group. The adipocytes surrounded
by macrophages showed the features of apoptosis such as chromatin condensation rather than necrosis. mRNA
expression level of myostatin was not significantly different between NGT patients and patients with
abnormal glucose metabolism.
Conclusion: Enlarged visceral adipocyte and apoptotic adipocyte death appear to be a causative factor for
development of type 2 DM by inducing infiltration of macrophage, although the mechanism is still unclear.
Keywords: Adipocyte, Apoptosis, Insulin resistance,
Online ISSN : 2508-7576Print ISSN : 2508-6235
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