Dept. of Clinical Biochemistry, Faculty of Pharmacy, University of Mansoura, Mansoura 35516, Egypt; Faculty of Pharmacy, University of Tabuk, Tabuk 71491, Saudi Arabia.
Dept. of Internal Medicine, Faculty of Medicine, University of Tabuk, Tabuk 71471, Saudi Arabia.
Life Sci. 2015 Jan 1;120:13-21. doi: 10.1016/j.lfs.2014.11.002. Epub 2014 Nov 11.
Sodium nitrite is used to inhibit the growth of microorganisms and is responsible for the desirable red color of meat; however, it can be toxic in high quantities for humans and other animals. Moreover, glycogen, a branched polysaccharide, efficiently stores and releases glucose monosaccharides to be accessible for metabolic and synthetic requirements of the cell. Therefore, we examined the impact of dietary sodium nitrite and cod liver oil on liver glycogen.
Thirty-two Sprague-Dawley rats were treated daily with sodium nitrite (80 mg/kg) in the presence/absence of cod liver oil (5 ml/kg). Liver sections were stained with Periodic acid-Schiff. Hepatic homogenates were used for measurements of glycogen, cyclic adenosine monophosphate (cAMP), protein kinase A (PKA), glycogen synthase, glycogen synthase kinase, pyruvate carboxylase, fructose 1,6-diphosphatase, glucose 6-phosphatase, phosphodiesterase and glycogen phosphorylase. Glucose, pyruvate tolerances and HOMA insulin resistance were also determined.
Sodium nitrite significantly increased plasma glucose and insulin resistance. Moreover, sodium nitrite significantly reduced hepatic glycogen content as well as activities of glycogen synthase, glycogen synthase kinase-3, and phosphodiesterase. Sodium nitrite elevated hepatic cAMP, PKA, pyruvate carboxylase, fructose 1,6-diphosphatase, glucose 6-phosphatase and phosphorylase. Cod liver oil significantly blocked all of these except pyruvate carboxylase, fructose 1,6-diphosphatase and glucose 6-phosphatase.
Sodium nitrite inhibited liver glycogenesis and enhanced liver glycogenolysis and gluconeogenesis, which is accompanied by hyperglycemia and insulin resistance through the activation of cAMP/PKA and the inhibition of phosphodiesterase. Cod liver oil blocked the sodium nitrite effects on glycogenesis and glycogenolysis without affecting gluconeogenesis.
亚硝酸钠用于抑制微生物的生长，是使肉类呈现理想红色的原因；然而，对于人类和其他动物来说，大量的亚硝酸钠是有毒的。此外，糖原是一种支链多糖，能够有效地储存和释放葡萄糖单糖，以满足细胞代谢和合成的需要。因此，我们研究了饮食中亚硝酸钠和鱼肝油对肝糖原的影响。
32 只 Sprague-Dawley 大鼠每天用亚硝酸钠（80mg/kg）处理，同时存在/不存在鱼肝油（5ml/kg）。用过碘酸希夫染色法对肝组织切片进行染色。肝匀浆用于测量糖原、环磷酸腺苷（cAMP）、蛋白激酶 A（PKA）、糖原合酶、糖原合酶激酶、丙酮酸羧化酶、果糖 1,6-二磷酸酶、葡萄糖 6-磷酸酶、磷酸二酯酶和糖原磷酸化酶。还测定了葡萄糖、丙酮酸耐量和 HOMA 胰岛素抵抗。
亚硝酸钠显著增加了血浆葡萄糖和胰岛素抵抗。此外，亚硝酸钠还显著降低了肝糖原含量以及糖原合酶、糖原合酶激酶-3 和磷酸二酯酶的活性。亚硝酸钠升高了肝 cAMP、PKA、丙酮酸羧化酶、果糖 1,6-二磷酸酶、葡萄糖 6-磷酸酶和磷酸化酶。鱼肝油显著阻断了除丙酮酸羧化酶、果糖 1,6-二磷酸酶和葡萄糖 6-磷酸酶之外的所有这些变化。
亚硝酸钠抑制肝糖原合成，增强肝糖原分解和糖异生，通过激活 cAMP/PKA 和抑制磷酸二酯酶导致高血糖和胰岛素抵抗。鱼肝油阻断了亚硝酸钠对糖原合成和糖原分解的作用，而不影响糖异生。
