Abstract：Objective To investigate the effect of high-fat diet on the expression of transient receptor potential vanilloid 1 (TRPV1) in the respiratory system and the dorsal root ganglion (DRG) of mice, as well as its effect on the excitability of sensory neurons. Methods A total of 20 C57BL/6 mice were randomly divided into normal-diet (ND) group and high-fat diet (HFD) group, with 10 mice in each group. The mice were given corresponding diets and body weights were monitored. After 7 weeks of feeding, lung tissue, bronchial tissue, and DRG at thoracic segments 3-4 were collected and immunohistochemical staining was performed. A patch clamp was used to measure the number of action potentials and TRPV1 current intensity in the DRG. Results After 7 weeks of feeding, the HFD group had signifcantly greater mean weight gain than the ND group (6.4±2.6 g vs 2.3±0.5 g; P < 0.001). The HFD group had signifcantly higher expression of TRPV1 in the bronchus, pulmonary alveoli, and DRG than the ND group (P < 0.05). Compared with the ND group, the HFD group had signifcant increases in the TRPV1 current intensity and number of action potentials in the DRG (P < 0.05). Conclusions High-fat diet induces a signifcant increase in body weight and leads to high expression of TRPV1 and high excitability in the respiratory system and the peripheral sensory neurons. This suggests that TRPV1 may be an important factor in the physiopathological mechanisms of bronchial hyperresponsiveness.
ZHU Lian,XU Zhi-Liang. Effect of high-fat diet on expression of transient receptor potential vanilloid 1 in respiratory tract and dorsal root ganglion of mice[J]. CJCP, 2017, 19(7): 826-831.
Shore SA, Fredberg JJ. Obesity, smooth muscle, and airway hyperresponsiveness[J]. J Allergy Clin Immunol, 2005, 115(5):925-927.
[6]
Bonini S, Lambiase A, Lapucci G, et al. Nerve growth factor and asthma[J]. Allergy, 2002, 57 Suppl 72:13-15.
[7]
Olgart Höglund C, de Blay F, Oster JP, et al. Nerve growth factor levels and localisation in human asthmatic bronchi[J]. Eur Respir J, 2002, 20(5):1110-1116.
Baraniuk JN. Rise of the sensors:nociception and pruritus[J]. Curr Allergy Asthma Rep, 2012, 12(2):104-114.
[10]
Talbot S, Abdulnour RE, Burkett PR, et al. Silencing nociceptor neurons reduces allergic airway inflammation[J]. Neuron, 2015, 87(2):341-354.
[11]
Binshtok AM, Bean BP, Woolf CJ. Inhibition of nociceptors by TRPV1-mediated entry of impermeant sodium channel blockers[J]. Nature, 2007, 449(7162):607-610.
[12]
Enriori PJ, Evans AE, Sinnayah P, et al. Diet-induced obesity causes severe but reversible leptin resistance in arcuate melanocortin neurons[J]. Cell Metab, 2007, 5(3):181-194.
[13]
Winzell MS, Ahrén B. The high-fat diet-fed mouse:a model for studying mechanisms and treatment of impaired glucose tolerance and type 2 diabetes[J]. Diabetes, 2004, 53 Suppl 3:S215-S219.
[14]
McGarvey LP, Butler CA, Stokesberry S, et al. Increased expression of bronchial epithelial transient receptor potential vanilloid 1 channels in patients with severe asthma[J]. J Allergy Clin Immunol, 2014, 133(3):704-712.e4.
[15]
Baker K, Raemdonck K, Dekkak B, et al. Role of the ion channel, transient receptor potential cation channel subfamily V member 1(TRPV1), in allergic asthma[J]. Respir Res, 2016, 17(1):67.
