Somatosensory neuron receptors used to form brown fat, has implications for diabetes and obesity.
Brown fat has long been investigated as a treatment for obesity and type 2 diabetes due to the fact it burns energy faster than white fat, which hoards it, leading to weight gain. Now, a study from researchers at Zurich University increases the amount of metabolism-boosting brown adipose tissue, or good fat, by employing two somatosensory neuron receptors on brown fat cells as potential therapeutic targets. The team state that their findings have implications for the treatment of obesity, diabetes, and related metabolic disorders. The study is published in The FASEB Journal.
Previous studies show that transient receptor potential channels (TRP channels) are a group of ion channels which serve a variety of functions in the peripheral and central nervous systems. These channels mediate a variety of sensations such as pain, warmth or coldness, different kinds of tastes, pressure, and vision. The TRPM8 protein is expressed in sensory neurons, and it is activated by cold temperatures and cooling agents, such as menthol. TRPP3 (TRP polycystic (P)3) is part of a family of TRP channels which can cause polycystic kidney disease when mutated. The current study shows the potential of TRPM8 and TRPP3 as druggable targets involved in human brown formation, to develop substances which can modulate energy consumption and blood sugar control in individuals.
The current study induces human bone marrow stem cells and subcutaneous belly fat cells to become white or brown fat, and also utilises undifferentiated cells as a control. All 27 TRP channels were analyzed during the process. Results show that some TRPs are not expressed, while some TRP channels are constantly present, and some TRP channels are only expressed during brown fat cell differentiation. Data findings show that TRPM8 and TRPP3 were present at high levels in differentiated brown fat, and not in the progenitor cells.
The group also investigated the role of TRPM8 using specific activator or inhibitors, and found that stimulation of TRPM8 strongly supports browning, whereas the presence of inhibitors impedes it. The function of TRPP3 was tested by using genetic manipulation to eliminate its function, which shows that its ablation prevents the formation of brown fat. The researchers stress that the ablation of TRPP3 did not prevent the formation of white fat.
The team surmise that their study shows that both the TRPM8 and TRPP3 sensory receptors are associated with the creation of brown fat in humans, and may be activated by certain foods, and envisioned new drugs. For the future, the researchers state that in the face of a growing number of diabetic and obese people, their work will hopefully contribute to the development of non-adrenergic stimulators of brown fat and the appreciation of functional food to influence brown fat physiology.