Abstract
To the Editor: Obesity is associated with insulin resistance and type 2 diabetes, with accumulation of intra-abdominal fat carrying a more severe disease risk than accumulation of subcutaneous fat. It remains unclear whether increased visceral fat has an adverse metabolic effect due to its location or to the unique properties of intra-abdominal adipocytes. Konrad et al. [1] reported that increasing intra-abdominal fat mass by transplantation of epididymal fat from normal mice into lean recipients improved fasting glucose tolerance and insulin sensitivity, achieving an effect opposite to the expectedmetabolicconsequenceofincreasedintra-abdominal fat. This suggests that obesity-induced alterations in adipose tissue function rather than mass are responsible for the adverse metabolic consequences of obesity. We hypothesised that the intrinsic properties of adipocytes are responsible for their metabolic effects, irrespective of their anatomical location. We have addressed this using regional adipose tissue cross-transplantation in which subcutaneous (inguinal) and intra-abdominal (epididymal) fat pads from donor mice were transplanted into the subcutaneous (group 1) or intra-abdominal (group 2) compartment of recipient mice on a high-fat diet. Our studies revealed that transplantation of intra-abdominal fat into either the intraabdominal or subcutaneous space had no effect on the metabolism of a recipient animal, whereas transplantation of subcutaneous fat into the intra-abdominal space had a significant protective effect on adiposity, insulin sensitivity and glucose tolerance.
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