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Amelioration of insulin resistance by rosiglitazone is associated with increased adipose cell size in obese type 2 diabetics
Author(s) -
Yang Jian,
Eliasson Bjorn,
Smith Ulf,
Cushman Samuel W.,
Sherman Arthur
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.869.1
Subject(s) - adipose tissue , rosiglitazone , medicine , endocrinology , insulin resistance , adiponectin , type 2 diabetes , glut4 , adipogenesis , insulin , obesity , diabetes mellitus
Whereas early studies reported that having large adipose cells correlates with insulin resistance, this is not always seen. A recent study with BMI‐matched moderately insulin‐sensitive or –resistant obese subjects found a correlation with the proportion of small adipose cells, rather than the size of the large adipose cells, suggesting impaired adipogenesis. To further test this hypothesis, we recruited and treated eleven type 2 diabetic patients for 90 days with an insulin‐sensitizing drug rosiglitazone. Needle biopsies of the abdominal subcutaneous fat from the patients were assayed by fitting the adipose cell size distribution with two exponentials and a Gaussian function. The fraction of large adipose cells was defined as the area of the Gaussian peak and the size of the large cells was defined as its center. Insulin resistance was ameliorated as shown by lowered fasting plasma glucose and increased plasma adiponectin. Rosiglitazone also increased mRNA expression of Adiponectin and GLUT4 in adipose tissue. We observed multimodal adipose cell size distributions similar to those seen previously in non‐diabetic, moderately obese subjects. Contrary to expectations, the main effect of rosiglitazone was increased size of the large adipose cells. We conclude that improved insulin sensitivity is associated with increased size of large adipose cells in rosiglitazone‐treated type 2 diabetics.