The distribution and significance of PGC-1α neurons in the centre of energy homeostasis in hypothalamus
Chinese Journal of Clinical Anatomy ›› 2015, Vol. 33 ›› Issue (5) : 558-562.
The distribution and significance of PGC-1α neurons in the centre of energy homeostasis in hypothalamus
Objective To investigate the role of high fat diet in the distribution of PGC-1α in SD rat hypothalamus. Methods 12 SD rats were randomly divided two groups, a normal diet group and a high fat diet group. HE staining was used to detect the fatty degeneration of the liver tissue; Immunofluorescence staining was used to observe the change of PGC-1α in the hypothalamusventromedial nucleus, and arcuate nucleus after 8 weeks. Results 8 weeks later, the live tissue of normal diet rats showed that hepatic cord was well organized; the boundary among hepatic cord, liver blood sinus and liver cells was clear; the nucleus were clear and cytoplasmhomogeneous; there was no liver cell lipid and necrosis. But the high fat diet rat live tissues expressed the characteristic of serious fatty degeneration, such as hepatic corddisorganized, liver blood sinus cavity became smaller, the boundary was not clear, live cells swelling with fat vacuoles in the cytoplasm which was not uniform in size. The PGC-1α cell number in the normal diet rat hypothalamusventromedial nucleus determination area was (199.96±42.95), but it was (256.08±39.25) in the high fat diet rat, and there was statistical significance(P<0.05). In the arcuate nucleus the cell number of PGC-1α was (173.25±47.19) in the normal diet rat, but high fat diet made the cell number increased to 200.48±51.44, and there was statistical significance between them( P<0.05). Conclusion High fat diet made the cell number of PGC-1α increased in ventromedial nucleus andarcuate nucleus, PGC-1α may play a role in regulating the energy metabolism balance.
PGC-1α / Hypothalamusventromedial nucleus / Arcuate nucleus / High fat diet
[1] Liu C, Lin JD. PGC-1 coactivators in the control of energy metabolism[J]. Acta Biochim Biophys Sin (Shanghai), 2011, 43(4):248-257.
[2] Finley LW, Lee J, Souza A, et al. Skeletal muscle transcriptional coactivator PGC-1alpha mediates mitochondrial, but not metabolic, changes during calorie restriction[J]. Proc Natl Acad Sci U S A, 2012,109(8):2931-2936.
[3] Tritos NA, Mastaitis JW, Kokkotou EG, et al. Characterization of the peroxisome proliferator activated receptor coactivator 1 alpha (PGC 1alpha) expression in the murine brain[J]. Brain Res, 2003, 961(2):255-260.
[4] 徐叔云, 卞如濂, 陈修. 药理实验方法学[M].第3版. 北京: 人民卫生出版社,2002:1201-1206.
[5] Morton GJ, Cummings DE, Baskin DG, et al. Central nervous system control of food intake and body weight[J]. Nature, 2006, 443(7109):289-295.
[6] Kim HJ, Kobayashi M, Sasaki T, et al. Overexpression of FoxO1 in the hypothalamus and pancreas causes obesity and glucose intolerance[J]. Endocrinology, 2012, 153(2):659-671.
[7] Sisley S, Sandoval D. Hypothalamic control of energy and glucose metabolism[J]. Rev Endocr Metab Disord, 2011, 12(3):219-233.
[8] Thaler JP, Schwartz MW. Minireview: Inflammation and obesity pathogenesis: the hypothalamus heats up[J]. Endocrinology, 2010,151(9):4109-4115.
[9] Lenard NR, Berthoud HR. Central and peripheral regulation of food intake and physical activity: pathways and genes[J]. Obesity (Silver Spring), 2008, 16 (Suppl 3):S11-22.
[10] Nilsson IA, Lindfors C, Schalling M, et al. Anorexia and hypothalamic degeneration[J]. Vitam Horm, 2013, 92:27-60.
[11] Blouet C, Schwartz GJ. Hypothalamic nutrient sensing in the control of energy homeostasis[J]. Behav Brain Res, 2010, 209(1):1-12.
[12] Benani A, Troy S, Carmona MC, et al. Role for mitochondrial reactive oxygen species in brain lipid sensing: redox regulation of food intake[J]. Diabetes, 2007, 56(1):152-160.
[13] Fujita K, Yamafuji M, Nakabeppu Y, et al. Therapeutic approach to neurodegenerative diseases by medical gases: focusing on redox signaling and related antioxidant enzymes[J]. Oxid Med Cell Longev, 2012, 2012:324256.
[14] Ciron C, Lengacher S, Dusonchet J, et al. Sustained expression of PGC-1alpha in the rat nigrostriatal system selectively impairs dopaminergic function[J]. Hum Mol Genet, 2012, 21(8):1861-1876.
[15] Kiebish MA, Young DM, Lehman JJ, et al. Chronic caloric restriction attenuates a loss of sulfatide content in PGC-1alpha-/- mouse cortex: a potential lipidomic role of PGC-1alpha in neurodegeneration[J]. J Lipid Res, 2012, 53(2):273-281.
[16] 钟立, 王邦琼, 李启富, 等. 短期高脂饮食引起大鼠下丘脑PGC1α表达下调[J]. 中华内分泌外科杂志, 2011, 5(4):242-243.
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