Electroacupuncture regulates glucose-inhibited neurons in treatment of simple obesity

Zhi Yu, Youbing Xia, Chuanhui Ju, Qinghua Shao, Zhen Mao, Yun Gu, Bin Xu, Zhi Yu, Youbing Xia, Chuanhui Ju, Qinghua Shao, Zhen Mao, Yun Gu, Bin Xu

Abstract

The glucose-inhibited neurons present in the lateral hypothalamic area are regarded as glucose detectors. This structure is involved in the regulation of food intake through extracellular blood glucose concentrations, and plays a crucial role in obesity onset. In the present study, obesity models established with high fat feeding were treated with electroacupuncture at Zusanli (ST36)/Inner Court (ST44) on the left side and Tianshu (ST25) bilaterally. We found that electroacupuncture could effectively reduce body weight and the fat-weight ratio, and decrease serum leptin, resistin, tumor necrosis factor alpha, and neuropeptide Y levels, while increase serum adiponectin and cholecystokinin-8 levels. This treatment altered the electrical activity of glucose-inhibited neurons in the lateral hypothalamic area, with electroacupuncture at Zusanli/Inner Court exerting an inhibitory effect, while electroacupuncture at bilateral Tianshu exerting an excitatory effect. These data suggest that electroacupuncture at the lower limbs and abdominal cavity is an effective means for regulating the activity of glucose-inhibited neurons in the lateral hypothalamic area and for improving the secretory function of adipose tissue.

Keywords: acupoint; acupuncture; acupuncture and moxibustion; adipose tissue; electroacupuncture; feeding center; grants-supported paper; hypothalamus; neural regeneration; neuroregeneration; obesity; regeneration.

Conflict of interest statement

Conflicts of interest: None declared.

Figures

Figure 1
Figure 1
Effect of electroacupuncture on adipocyte factors of obese rats. Data are expressed as mean ± SD (n = 10 rats per group). Differences between the two groups were compared using independent samples t-test. aP < 0.05, vs. normal group; bP < 0.01, vs. model group; cP < 0.01, vs. Zusanli/Inner Court acupoint group.
Figure 2
Figure 2
Effect of electroacupuncture at various acupoints on the feeding related peptide in obese rats. Data are expressed as mean ± SD (n =10 rats per group). Comparison before and after treatment was performed using a paired sample t-test, and differences between the two groups were compared using an independent samples t-test. aP < 0.05, vs. normal group; bP < 0.01, vs. model group.
Figure 3
Figure 3
Effect of electroacupuncture at Zusanli (ST36)/Inner Court (ST44) and Tianshu (ST25)/Tianshu acupoints on activity of glucose-inhibited neurons. (A) In the electroacupuncture at Zusanli/Inner Court point group, the discharge frequency of glucose-inhibited neurons decreased significantly after intravenous injection of glucose, and was not changed after saline injection, while glucose-inhibited neurons were inhibited by electroacupuncture at Zusanli/Inner Court points. (B) In the electroacupuncture at Tianshu/Tianshu acupoint group, glucose-inhibited neurons were excited by electroacupuncture at Tianshu. (C) After the experiment was complete, pontamine sky blue was applied to label the microelectrode recording sites. Arrow indicates pontamine sky blue exudation point (lateral hypothalamic area). The intervals are denoted by “-”.

References

    1. Wozniak SE, Gee LL, Wachtel MS, et al. Adipose tissue: the new endocrine organ? A review article. Dig Dis Sci. 2009;54(9):1847–1856.
    1. Galic S, Oakhill JS, Steinberg GR. Adipose tissue as an endocrine organ. Mol Cell Endocrinol. 2010;316(2):129–139.
    1. Cammisotto PG, Levy E, Bukowiecki LJ, et al. Cross-talk between adipose and gastric leptins for the control of food intake and energy metabolism. Prog Histochem Cytochem. 2010;45(3):143–200.
    1. Valassi E, Scacchi M, Cavagnini F. Neuroendocrine control of food intake. Nutr Metab Cardiovasc Dis. 2008;18(2):158–168.
    1. Burdakov D, González JA. Physiological functions of glucose-inhibited neurones. Acta Physiol (Oxf) 2009;195(1):71–78.
    1. Shiraishi T, Oomura Y, Sasaki K, et al. Effects of leptin and orexin-A on food intake and feeding related hypothalamic neurons. Physiol Behav. 2000;71(3-4):251–261.
    1. Li B, Guo CL, Tang J, et al. Cerebellar fastigial nuclear inputs and peripheral feeding signals converge on neurons in the dorsomedial hypothalamic nucleus. Neurosignals. 2009;17(2):132–143.
    1. Blüher M. Adipose tissue dysfunction in obesity. Exp Clin Endocrinol Diabetes. 2009;117(6):241–250.
    1. Sui Y, Zhao HL, Wong VC, et al. A systematic review on use of Chinese medicine and acupuncture for treatment of obesity. Obes Rev. 2012;13(5):409–430.
    1. Cho SH, Lee JS, Thabane L, et al. Acupuncture for obesity: a systematic review and meta-analysis. Int J Obes (Lond) 2009;33(2):183–196.
    1. Wang F, Tian DR, Han JS. Electroacupuncture in the treatment of obesity. Neurochem Res. 2008;33(10):2023–2027.
    1. Tong J, Chen JX, Zhang ZQ, et al. Clinical observation on simple obesity treated by acupuncture. Zhongguo Zhen Jiu. 2011;31(8):697–701.
    1. Abdi H, Zhao B, Darbandi M, et al. The effects of body acupuncture on obesity: anthropometric parameters, lipid profile, and inflammatory and immunologic markers. ScientificWorldJournal 2012. 2012 603539.
    1. Yang JJ, Xing HJ, Wang SJ, et al. Effects of acupuncture combined with dietary adjustments and aerobic exercise on body weight, body mass index and serum leptin level in simple obesity patients. Zhen Ci Yan Jiu. 2010;35(6):453–457.
    1. Kim SK, Bae H, Lee G, et al. The endogenous CCK mediation of electroacupuncture stimulation-induced satiety in rats. Peptides. 2008;29(4):564–570.
    1. Zhao M, Yuan JH, Li J, et al. Effect of acupuncture on feeding center of hypothalamus in experimental fat rats. Zhongguo Zhen Jiu. 2001;21(5):305–306.
    1. Liu ZC, Sun FM. The experimental study on acupuncture treatment of simple obesity in rats. Zhen Ci Yan Jiu. 1998;23(1):69–74.
    1. Jordan SD, Könner AC, Brüning JC. Sensing the fuels: glucose and lipid signaling in the CNS controlling energy homeostasis. Cell Mol Life Sci. 2010;67(19):3255–3273.
    1. Corbett SW, Keesey RE. Energy balance of rats with lateral hypothalamic lesions. Am J Physiol. 1982;242(4):E273–279.
    1. Zhang YP, Ma C, Wen YQ, et al. Convergence of gastric vagal and cerebellar fastigial nuclear inputs on glycemiasensitive neurons of lateral hypothalamic area in the rat. Neurosci Res. 2003;45(1):9–16.
    1. Mountjoy PD, Bailey SJ, Rutter GA. Inhibition by glucose or leptin of hypothalamic neurons expressing neuropeptide Y requires changes in AMP-activated protein kinase activity. Diabetologia. 2007;50(1):168–177.
    1. Fioramonti X, Contié S, Song Z, et al. Characterization of glucosensing neuron subpopulations in the arcuate nucleus: integration in neuropeptide Y and pro-opio melanocortin networks? Diabetes. 2007;56(5):1219–1227.
    1. Gozali M, Pavia JM, Morris MJ. Involvement of neuropeptide Y in glucose sensing in the dorsal hypothalamus of streptozotocin diabetic rats - in vitro and in vivo studies of transmitter release. Diabetologia. 2002;45(9):1332–1339.
    1. Murphy BA, Fioramonti X, Jochnowitz N, et al. Fasting enhances the response of arcuate neuropeptide Y-glucose-inhibited neurons to decreased extracellular glucose. Am J Physiol Cell Physiol. 2009;296(4):C746–756.
    1. Levin BE, Routh VH, Kang L, et al. Neuronal glucosensing: what do we know after 50 years? Diabetes. 2004;53(10):2521–2528.
    1. Morton GJ, Cummings DE, Baskin DG, et al. Central nervous system control of food intake and body weight. Nature. 2006;443(7109):289–295.
    1. Dockray GJ. Cholecystokinin and gut-brain signalling. Regul Pept. 2009;155(1-3):6–10.
    1. Emond M, Schwartz GJ, Ladenheim EE, et al. Central leptin modulates behavioral and neural responsivity to CCK. Am J Physiol. 1999;276(5 Pt 2):R1545–1549.
    1. Elmquist JK, Bjørbaek C, Ahima RS, et al. Distributions of leptin receptor mRNA isoforms in the rat brain. J Comp Neurol. 1998;395(4):535–547.
    1. Grill HJ, Schwartz MW, Kaplan JM, et al. Evidence that the caudal brainstem is a target for the inhibitory effect of leptin on food intake. Endocrinology. 2002;143(1):239–246.
    1. Gong M, Wang X, Mao Z, et al. Effect of electroacupuncture on leptin resistance in rats with diet-induced obesity. Am J Chin Med. 2012;40(3):511–520.
    1. Fonseca-Alaniz MH, Takada J, Alonso-Vale MI, et al. Adipose tissue as an endocrine organ: from theory to practice. J Pediatr (Rio J) 2007;83(5 Suppl):S192–203.
    1. Zeyda M, Stulnig TM. Obesity, inflammation, and insulin resistance--a mini-review. Gerontology. 2009;55(4):379–386.
    1. Maury E, Brichard SM. Adipokine dysregulation, adipose tissue inflammation and metabolic syndrome. Mol Cell Endocrinol. 2010;314(1):1–16.
    1. Antuna-Puente B, Feve B, Fellahi S, et al. Adipokines: the missing link between insulin resistance and obesity. Diabetes Metab. 2008;34(1):2–11.
    1. Barnes KM, Miner JL. Role of resistin in insulin sensitivity in rodents and humans. Curr Protein Pept Sci. 2009;10(1):96–107.
    1. Fan YJ, Xu B, Xiang XR, et al. Effects of electroacupuncture versus sibutramine on adipocyte products in obesity rats. Zhongguo Zuzhi Gongcheng Yanjiu yu Linchuang Kangfu. 2008;12(11):2189–2192.
    1. Sun DY, Sun LH, Liang YL, et al. Effect of electroacupuncture on lipid metabolism in male and female obesity rats. Zhen Ci Yan Jiu. 2012;37(3):206–210.
    1. China: People's Government of Jiangsu Province. Regulations for the Administration of Affairs Concerning Experimental Animals in Jiangsu Province. 2008-09-02.
    1. Sun Z, Zhang ZC, Liu ZC. Experimental study of diet-induced obesity animal model. Zhongyao Tongbao. 2002;18(4):466–467.
    1. Paxinos G, Watson C. 5th ed. London: Academic Press; 2005. The Rat Brain in Stereotaxic Coordinates.
    1. Min BI, Oomura Y, Katafuchi T. Responses of rat lateral hypothalamic neuronal activity to fastigial nucleus stimulation. J Neurophysiol. 1989;61(6):1178–1184.
    1. Pu YM, Wang JJ, Wang T, et al. Cerebellar interpositus nucleus modulates neuronal activity of lateral hypothalamic area. Neuroreport. 1995;6(7):985–988.

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