Body mass index is associated with region-dependent metabolic reprogramming of adipose tissue

Figures

• 

  Fig. 1. Substrate consumption by cultured visceral (VAT) and subcutaneous (SAT) adipose tissue. The figure shows glucose and pyruvate consumption by VAT (panel A, C) and SAT (panel B, D) of patients (n = 12, F:M, 9:3) with an average age of 46.8 years (range 26–83 years, mean) and different body mass index (BMI). The association between metabolite consumption and BMI was evaluated by computing Pearson correlation coefficients (r) assuming Gaussian distribution and a confidence interval of 95%. All P values < 0.05 were considered statistically significant.

• 

  Fig. 2. Substrate production by cultured visceral (VAT) and subcutaneous (SAT) adipose tissue. The figure shows acetate, alanine and lactate production by VAT (panels A, C, E) and SAT (panels B, D, F) of patients (n = 12, F:M, 9:3) with an average age of 46.8 years (range 26–83 years, mean) and different body mass index (BMI). The association between metabolite production and BMI was evaluated by computing Pearson correlation coefficients (r) assuming Gaussian distribution and a confidence interval of 95%. All P values < 0.05 were considered statistically significant.

• 

  Fig. 3. Schematic representation of the studied metabolic pathways in adipose tissue explants, visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT). We focused on glucose metabolism independent from insulin stimuli. Our results show that tissue explants of VAT from subjects with higher BMI consumed more glucose and produced less metabolites directly derived from pyruvate (e.g. lactate and alanine) and maintained the same production of acetate. Thus, we suggest that with the increase of BMI, VAT reprograms glucose metabolism towards de novo lipogenesis. Thus, our results provide a preliminary evidence that increased BMI promotes an insulin-independent metabolic reprogramming of glucose metabolism in VAT that may be associated with increased de novo lipogenesis. (AATs-Aminoacid transporters; Ins-Dep GLUTs-Insulin dependent glucose transporters; Ins-Ind GLUTs-Insulin independent glucose transporters; MCTs-Monocarboxylic acid transporters; IR-Insulin receptors).