Effect of lncRNA uc.48 + on liver glycogen in type 2 diabetic rats

YU Ke-hua1 LI Lin2 WANG Meng-ke2 LIU Shuang-mei2 LIANG Shang-dong

(1.Medical Lab Teaching Center, Nanchang University, Nanchang, China 330006)
(2.Dept of Physiology, School of Basic Medicine, Nanchang University, Nanchang, China 330006)
【Knowledge Link】glycolysis; gluconeogenesis

【Abstract】 Aim To observe the effect of uc.48 + small interference RNA (siRNA) on liver glycogen abnormality in type 2 diabetic rats and its possible mechanism. Methods The diabetes model was established by feeding high glucose and high fat diet combined with streptozotocin (STZ). After the success of the model, the long noncoding RNA uc.48 + siRNA was injected into the rat body via tail vein. The changes of blood glucose and the content of liver glycogen were detected dynamically, and the liver glycogen was detected one week after injection. Glucokinase (GK) mRNA and protein expression in liver tissues of each group were detected by qPCR and Western blot. Results It was observed that postprandial blood glucose and fasting blood glucose decreased in diabetic model rats after treated with uc.48 + siRNA compared with those in model rats. The level of liver glycogen in diabetic model rats was significantly lower than that in control group. The synthesis of liver glycogen in diabetic model rats with uc.48 + siRNA treatment increased compared with that in diabetic model group. The expressions of GK mRNA and protein in the diabetic model group were significantly lower than those in control group. The expression of GK mRNA and protein markedly increased after uc.48 + siRNA treatment. Conclusions uc.48 + siRNA reduced blood glucose and increased glycogen synthesis in type 2 diabetic rats, and its mechanism may involve in increasing GK expression and Akt1 phosphorylation.

【Keywords】 long noncoding RNA; type 2 diabetic rats; liver glycogen; glucokinase; uc.48 +; siRNA;

【DOI】

【Funds】 National Natural Science Foundation of China (81460200, 81701114, 81570735, 81870574, 31560276)

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(Translated by YI T)

    References

    [1] Li L, Sheng X, Zhao S H, et al. Nanoparticle-encapsulated emodin decreases diabetic neuropathic pain probably via a mechanism involving P2X3 receptor in the dorsal root ganglia [J]. Purinergic Signal, 2017, 13 (4): 559–68.

    [2] Malecki M T. Type 2 diabetes mellitus and its complications: from the molecular biology to the clinical practice [J]. Rev Diabet Stud, 2004, 1 (1): 5–8.

    [3] Peng H Y, Zou L F, Xie J Y, et al. lncRNA NONRATT021972 siRNA decreases diabetic neuropathic pain mediated by the P2X3 receptor in dorsal root ganglia [J]. Mol Neurobiol, 2017, 54 (1): 511–23.

    [4] Whiting D R, Guariguata L, Weil C, et al. IDF diabetes atlas: global estimates of the prevalence of diabetes for 2011 and 2030 [J]. Diabetes Res Clin Pract, 2011, 94 (3): 311–21.

    [5] Song M M, Zou L F, Peng L C, et al. LncRNA NONRATT021972 siRNA normalized the dysfunction of hepatic glucokinase through AKT signaling in T2DM rats [J]. Endocr Res, 2017, 42 (3): 180–90.

    [6] Zuo L Q, Wang H, Wang Y H, et al. Effect of diabetes on CCl4-induced rats liver fibrosis [J]. Chin Pharmacol Bull, 2018, 34 (4): 479–84 (in Chinese).

    [7] Iynedjian P B. Molecular physiology of mammalian glucokinase [J]. Cell Mol Life Sci, 2009, 66 (1): 27–42.

    [8] Haeusler R A, Camastra S, Astiarraga B, et al. Decreased expression of hepatic glucokinase in type 2 diabetes [J]. Mol Metab, 2015, 4 (3): 222–6.

    [9] Wang S Y, Xu H, Zou L F, et al. LncRNA uc.48 + is involved in diabetic neuropathic pain mediated by the P2X3 receptor in the dorsal root ganglia [J]. Purinergic Signal, 2016, 12 (1): 139–48.

    [10] Fan B, Xu C S, Liang S D. Research development of long noncoding RNA related to the regulation mechenisms of human diseases [J]. Chin Pharmacol Bull, 2013, 29 (12): 1629–33 (in Chinese).

    [11] Bejerano G, Pheasant M, Makunin I, et al. Ultraconserved elements in the human genome [J]. Science, 2004, 304 (5657): 1 321–5.

    [12] Cho H, Thorvaldsen J, Chu Q, et al. Akt1/PKB alpha is required for normal growth but dispensable for maintenance of glucose homeostasis in mice [J]. J Biol Chem, 2001, 276 (42): 38349–52.

    [13] Iynedjian P B, Roth R A, Fleischmann M, et al. Activation of protein kinase B/cAkt in hepatocytes is sufficient for the induction of expression of the gene encoding glucokinase [J]. Biochem J, 2000, 351 (3): 621–7.

This Article

ISSN:1001-1978

CN: 34-1086/R

Vol 35, No. 02, Pages 187-191

February 2019

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Abstract

  • 1 Materials and methods
  • 2 Results
  • 3 Discussion
  • References