Expansion of fat mass mainly occurs through cellular hypertrophic mechanisms leading to an increase in adipocyte size. This has focused attention on the role of the extracellular matrix of adipose cells. The extracellular matrix has been sometimes pointed out as a factor that could prevent adipocyte growth, indeed COL6A3 synthesis is increased in insulin resistant patients. In the present study, insulin deprivation reduced the transcription of genes coding for COL6A3, without restoration by insulin replacement but even additional reduction in rWAT. Similarly, FN1 transcript levels were reduced during type 1 diabetes and further lowered in scWAT and rWAT and only slightly increased in eWAT by insulin. These results suggest that the extracellular matrix of adipose cell is not directly involved in the changes of adipose cell sizes during highly dynamic modifications related to insulin action. Numerous studies have shown that not only the mass of adipose tissue is important but also its quality is of major importance. The present study shows that insulin is a major regulator of adipose cell size distribution and of its bimodal repartition. The mechanisms involved in that regulation are not yet fully deciphered. Understanding these mechanisms may help to identify the self organisation of adipose tissue and could bring original insights to identify new therapeutic targets for the treatment of metabolic complications induced by inappropriate fat storages. ATP plays important roles in sensory and motor functions of the urinary bladder. ATP co-released with acetylcholine from parasympathetic fibers can directly excite the EX 527 bladder detrusor muscle, and ATP released from the urothelium in response to stretch of the bladder wall as it fills with urine has been proposed to convey information to the CNS regarding the degree of bladder distension by activating suburothelial afferent nerve fibers. The participation of urothelial-derived ATP and purinergic receptors in the bladder mechanosensory and transduction systems is supported by an ever growing body of evidence, starting with the identification of a population of suburothelial afferents that express purinergic P2X3 receptors, observations that desensitization of P2X receptors or administration of P2R blockers significantly depress the activity of the bladder afferents in response to distension, and demonstrations that stretchinduced urothelial ATP release is not altered in P2X3R-null mice but absence of this receptor results in marked bladder hyporeflexia with the animals displaying increased voiding volume and reduced voiding frequency. Urothelial ATP release has been shown to be increased in humans with several bladder conditions, such as interstitial cystitis, irritative voiding from benign prostatic hyperplasia, painful bladder syndrome, bladder overactivity and also in animal models of spinal cord injury, diabetes and cystitis. These findings not only emphasize the importance of urothelial ATP release and signaling for proper bladder function, but also highlight the need to better understand the cellular mechanisms whereby urothelial cells respond to bladder wall distension with ATP release. In general, regulated cellular ATP release can occur through vesicular and non-vesicular mechanisms.