The classical diagnostic strategy of internal medicine, including medical history, physical examination and additional diagnostic test, is unable to assess the activity of the autonomous nervous system in detail and, consequently, has resulted in negligence of the involvement of the autonomic nervous system. Nonetheless, evidence is emerging that the autonomous nervous system is involved in the pathophysiology of complex diseases. These conditions include insulin resistance, type 2 diabetes mellitus and dyslipidemia, which have traditionally been interpreted in brainless concepts of disease. Several lines of evidence obtained in rodent studies have provided support for this involvement of the autonomous nervous system. These include experiments emploing retrograde neuronal tracers, which have documented for instance tissue specific neuroanatomical representation of different fat compartments in hypothalamic nuclei (Kreier et al., Endocrinology 2007). Conversely, experiments using tissue specific denervation in combination with neuroendocrine interventions have documented that hypothalamic nuclei and the two branches of the autonomic nervous system are powerful modulators of tissue specific hormone sensitivity. For instrance, NPY induces hepatic insulin resistance of VLDL production through neuronal activity of hepatic sympathetic nerves (van den Hoek et al. Diabetes 2008). In humans the involvement the hypothalamus in the pathophysiology of type 2 diabetes mellitus was proven by functional MRI (Vidarsdottir et al. Diabetes 2007). These observations support the notion that the metabolic syndrome is getting nervous, even though we lack the tools to assess this involvement in all details in humans in vivo.
25 - 29 Apr 2009
European Society of Endocrinology