The presence of fat cells outside the fat tissue disrupts metabolism and promotes the development of complications such as type 2 diabetes. By describing the underlying mechanism, based on the release of adipocyte precursors from subcutaneous tissue, researchers identified a biomarker potential for individual diabetes risk.
The presence of fat cells (or adipocytes) in tissues other than fat tissue is abnormal. It is even known to be harmful to metabolism, with an increased risk of developing type 2 diabetes in overweight or obese people. Until now, it has been accepted that these “ectopic” adipocytes were derived from local precursors. But researchers at StromaLab* in Toulouse have just described that this abnormal presence is set up at a distance, from adipocyte precursors – adipocyte stromal cells (ASCs) – released by subcutaneous adipose tissue and able to migrate, for example, into skeletal muscle tissue.
Reproducing human fat tissue in the laboratory? This is now possible thanks to a research team bringing together Inserm, CNRS, Toulouse III-Paul-Sabatier University, the French Blood Establishment and the Toulouse National Veterinary School (ENVT) within the STROMALab laboratory. This team has developed – via 3-dimensional culture – small cellular units that mimic the characteristics and organization of adipose tissue as it appears in vivo: the organoids of adipose tissue or “adipospheres”. In their article in Scientific Reports, the researchers detail the different stages of the experimental conditions necessary to obtain these adipospheres from human cells. This innovation could make it possible, in particular, to study pathologies associated with the dysfunction of this tissue such as obesity and type 2 diabetes, but also to develop new drugs to treat these diseases.
The presence of ectopic adipocytes in the muscle is known to be detrimental to the metabolism. Until now it has been accepted that these fat cells came from the maturation of a local population of fat progenitors. This study published in Cell Reports shows that in mice in a context of caloric overload, subcutaneous adipose tissue abnormally releases adipose progenitors migrating to muscle, which participate in the formation of ectopic adipocytes and associated metabolic damage.
Adipose tissue has a remarkable plasticity that allows it to adapt to large variations in energy storage. This capacity, based on the increase in the size and number of adipocytes, is however limited and in a prolonged situation of energy imbalance it is frequent to observe an accumulation of lipids called “ectopic” because not associated with adipose tissue. This is particularly the case in skeletal muscle where, in addition to the appearance of small lipid droplets within the muscle fibres, real fat cells form between the muscle fibres and are associated with metabolic disorders such as insulin resistance.
In most mammals, the scarring process is fast-paced but alters the normal functioning of the tissue, unlike regeneration. In a study published in August 2018 in Scientific Reports, a team from the StromaLab laboratory (UMR 1031 – UT3 Paul Sabatier/EFS/ENVT/Inserm/ERL CNRS 5311), shows that the painkillers currently used are leading tissue repair towards scar healing and not regeneration. These results question about the actual pain relief strategy.
Regeneration is a complex biological process that allows an organism to restore a damaged tissue close to its original state. While spectacular examples exist in nature, such as the salamander capable of re-forming an entire limb after its amputation, regeneration in adult mammals is an exceptional phenomenon. In the vast majority of cases, the repair of an organ following a massive injury leads to scar healing that will frequently be associated with functional loss. From an evolutionary point of view, the scarring process leads more quickly to the reconstitution of a barrier against subsequent aggressions compared to the regeneration process.