ABSTRACT
The ability to expand adipose tissue mass may prevent ectopic lipid accumulation and insulin resistance in response to energy oversupply and high-fat diet. Indeed, mice fed with a high-fat diet that overexpresses adiponectin (a lipogenic gene) and are leptin-deficient develop massive obesity; however, have better metabolic profile than leptin-deficient control mice. Furthermore, mice with a deletion of PPARg2 gene (an adipogenic transcription factor) have impaired adipogenic capacity and ability to expand fat mass. These animals in response to a high-fat diet are leaner and present severe insulin resistance. In humans, some of the most striking relevance of adipose tissue for metabolic control came from patients suffering of generalized lipodystrophy. On them, there is an inability to develop subcutaneous adipose tissue, which is accompanied by elevated ectopic lipid accumulation and insulin resistance. Based on this and other evidence, the role of adipose tissue as a buffering lipid tissue controlling whole-body glucose and lipid homeostasis has gained relevance. I hereby further expand on this concept and highlight future research...