Type 2 diabetes (T2D) is a major public health issue increasingly affecting adolescents. While glycemia control has significantly improved the quality of life for diabetic patients, some complications persist, particularly those associated with the progressive degeneration of the sensory nervous system. This process often leads to neuropathic pain, frequently associated with chronic skin ulcers that can result in amputations. A better understanding of the underlying mechanisms leading to diabetic neuropathies (DN) and chronic wounds will permit the development of effective treatments. Congenital absence of sensory neurons can lead to chronic ulcers, resembling T2D complications. Recently, we have identified a new neuro-immune axis in which subsets of c-fibers sensory neurons, including nociceptors and C-low threshold mechanoreceptors (C-LTRMs), are capable of activating the pro-reparative functions of dermal macrophages. The progression of the disease is poorly understood, but obesity is often a triggering factor for T2D. Hence, we are currently investigating the impact of obesity on these pro-regenerative neuroimmune mechanisms. We have identified specific sensory neurons, innervating the subcutaneous adipose tissue and responding to their "metabolic state." We have demonstrated that the activation of these neurons accelerated the phagocytic properties of adipose tissue macrophages. This regulatory loop is crucial for the healing process upon skin injury, but obesity could lead to the overactivation and potentially the exhaustion of this mechanism. Understanding how these sensory neurons maintain adipose tissue homeostasis could help prevent the acceleration of metabolic syndrome in overweight adolescents and treat chronic wounds in T2D patients.