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, 9 (1), 106

Anti-diabetic Effect of Sorghum Extract on Hepatic Gluconeogenesis of Streptozotocin-Induced Diabetic Rats

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Anti-diabetic Effect of Sorghum Extract on Hepatic Gluconeogenesis of Streptozotocin-Induced Diabetic Rats

Jungmin Kim et al. Nutr Metab (Lond).

Abstract

Background: It has been suggested that Sorghum, a rich source of phytochemicals, has a hypoglycemic effect, but the mechanism is unknown. We investigated the effects of oral administration of sorghum extract (SE) on hepatic gluconeogenesis and the glucose uptake of muscle in streptozotocin-induced diabetic rats for six weeks.

Methods: Male Wistar rats were divided in five groups (n=5 per group): normal control (NC), rats with STZ-induced diabetic mellitus (DM), diabetic rats administrated 0.4 g/kg body weight of SE (DM-SE 0.4) and 0.6 g/kg body weight of SE (DM-SE 0.6), and diabetic rats administrated 0.7 mg/kg body weight of glibenclamide (DM-G).

Results: Administration of SE and G reduced the concentration of triglycerides, total and LDL-cholesterol and glucose, and the area under the curve of glucose during intraperitoneal glucose tolerance tests down to the levels observed in non-diabetic rats. In addition, administration of 0.4 and 0.6 g/kg SE and 0.7 mg/kg glibenclamide (G) significantly reduced the expression of phosphoenolpyruvate carboxykinase and the phosphor-p38/p38 ratio, while increased phosphor adenosine monophosphate activated protein kinase (AMPK)/AMPK ratio, but the glucose transporter 4 translocation and the phosphor-Akt/Akt ratio was significantly increased only by administration of G.

Conclusions: These results indicate that the hypoglycemic effect of SE was related to hepatic gluconeogenesis but not the glucose uptake of skeletal muscle, and the effect was similar to that of anti-diabetic medication.

Figures

Figure 1
Figure 1
Blood glucose levels during the intraperitoneal glucose tolerance tests. NC, normal control rats administrated saline; DM, rats with diabetes mellitus administrated saline; DM-SE 0.4, rats with diabetes mellitus administrated 0.4 g/kg body weight of sorghum extract; DM-SE 0.6, rats with diabetes mellitus administrated 0.6 g/kg body weight of sorghum extract; DM-G, rats with diabetes mellitus administrated 0.7 mg/kg body weight of glibenclamide. The values are mean ± SEM (n = 5). Values with different superscripts are significantly different at p < 0.05 using ANOVA with Duncan’s multiple range test.
Figure 2
Figure 2
Expression of phosphoenolpyruvate carboxykinase (PEPCK), adenosine monophosphate activated protein kinase (AMPK), and p38. NC, normal control rats administrated saline; DM, rats with diabetes mellitus administrated saline; DM-SE 0.4, rats with diabetes mellitus administrated 0.4 g/kg body weight of sorghum extract; DM-SE 0.6, rats with diabetes mellitus administrated 0.6 g/kg body weight of sorghum extract; DM-G, rats with diabetes mellitus administrated 0.7 mg/kg body weight of glibenclamide. The values are mean ± SEM (n = 5). The values with different superscripts are significantly different at p < 0.05 using ANOVA with Duncan’s multiple range test.
Figure 3
Figure 3
Expression of the glucose transporter (GLUT) 4 and Akt (protein kinase B). NC, normal control rats administrated saline; DM, rats with diabetes mellitus administrated saline; DM-SE 0.4, rats with diabetes mellitus administrated 0.4 g/kg body weight of sorghum extract; DM-SE 0.6, rats with diabetes mellitus administrated 0.6 g/kg body weight of sorghum extract; DM-G, rats with diabetes mellitus administrated 0.7 mg/kg body weight of glibenclamide. The values are mean ± SEM (n = 5). The values with different superscripts are significantly different at p < 0.05 using ANOVA with Duncan’s multiple range test.

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References

    1. Craig ME, Hattersley A, Donaghue KC. Definition, epidemiology and classification of diabetes in children and adolescents. Pediatr Diabetes. 2009;10:3–12. - PubMed
    1. Agius L. New hepatic targets for glycaemic control in diabetes. Best Pract Res Clin Endocrinol Metab. 2007;21:587–605. doi: 10.1016/j.beem.2007.09.001. - DOI - PubMed
    1. Standaert ML, Ortmeyer HK, Sajan MP, Kanoh Y, Bandyopadhyay G, Hansen BC, Farese RV. Skeletal muscle insulin resistance in obesity-associated type 2 diabetes in monkeys is linked to a defect in insulin activation of protein kinase C-zeta/lambda/iota. Diabetes. 2002;51:2936–2943. doi: 10.2337/diabetes.51.10.2936. - DOI - PubMed
    1. Cao W, Collins QF, Becker TC, Robidoux J, Lupo EG Jr, Lupo EG, Xiong Y, Daniel KW, Floering L, Collins S. p38 Mitogen-activated protein kinase plays a stimulatory role in hepatic gluconeogenesis. J Biol Chem. 2005;280:42731–42737. doi: 10.1074/jbc.M506223200. - DOI - PubMed
    1. Pilkis SJ, Granner DK. Molecular physiology of the regulation of hepatic gluconeogenesis and glycolysis. Annu Rev Physiol. 1992;54:885–909. doi: 10.1146/annurev.ph.54.030192.004321. - DOI - PubMed
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