Publication

Fat cell enlargement is an independent marker of insulin resistance and 'hyperleptinaemia'

Journal Paper/Review - Jan 10, 2007

Units
PubMed
Doi

Citation
Lundgren M, Svensson M, Lindmark S, Renström F, Ruge T, Eriksson J. Fat cell enlargement is an independent marker of insulin resistance and 'hyperleptinaemia'. Diabetologia 2007; 50:625-33.
Type
Journal Paper/Review (English)
Journal
Diabetologia 2007; 50
Publication Date
Jan 10, 2007
Issn Print
0012-186X
Pages
625-33
Brief description/objective

AIMS/HYPOTHESIS
The aim of this study was to explore whether fat cell size in human subcutaneous and omental adipose tissue is independently related to insulin action and adipokine levels.

MATERIALS AND METHODS
Fat cells were prepared from abdominal subcutaneous biopsies obtained from 49 type 2 diabetic and 83 non-diabetic subjects and from omental biopsies obtained from 37 non-diabetic subjects. Cell size and insulin action on glucose uptake capacity in vitro were assessed in isolated fat cells. Insulin sensitivity in vivo was assessed with euglycaemic-hyperinsulinaemic clamps. Fasting blood samples were collected and adipokines and NEFA were measured.

RESULTS
Negative correlations were found between subcutaneous fat cell size and insulin sensitivity assessed as M-value during clamp and as insulin action on glucose uptake in fat cells in vitro. This was seen in non-diabetic subjects after including age, sex and BMI in the analyses. No such relationship was found in type 2 diabetic subjects. In both groups, subcutaneous fat cell size correlated positively and independently with plasma levels of leptin but not to any of the other assessed adipokines. In non-diabetic subjects, omental fat cell size was independently and negatively correlated with insulin action in subcutaneous, but not omental, fat cells in vitro.

CONCLUSIONS/INTERPRETATION
Fat cell enlargement is associated with insulin resistance in non-diabetic individuals independently of BMI. This was not seen in type 2 diabetic subjects, suggesting that after development of type 2 diabetes other factors, not related to fat cell size, become more important for the modulation of insulin resistance.