Shams Mohamed E E, Al-Gayyar Mohammed M H, Barakat Enaase A M E
Department of Pharmaceutics, Faculty of Pharmacy, University of Mansoura, Mansoura, Egypt.
Sci Pharm. 2011 Jul-Sep;79(3):623-34. doi: 10.3797/scipharm.1104-21. Epub 2011 May 29.
Type 2 diabetes mellitus is associated with dyslipdemia, insulin resistance and non alcoholic fatty liver disease. The purpose of the current study was to assess whether type 2 diabetes mellitus-induced hyperglycemia has an effect on the lipid profile and release of oxidative stress markers and inflammatory mediators in patients with non alcoholic fatty liver disease and normal liver function tests which may in turn lead to enhancing the pathogenicity of this liver disease. For this purpose, one hundred and five outpatients, matched in age and weight, were classified into two groups: the first group consisted of patients with non alcoholic fatty liver disease and the second group consisted of patients with non alcoholic fatty liver disease in conjunction with hyperglycemia due to the presence of type 2 diabetes mellitus. In all patients, lipid profile, oxidative stress, and inflammatory mediators were assessed by measuring serum concentrations of triglycerides, low density lipoprotein, hydrogen preroxide, malondialdehyde, tumor necrosis factor-alpha and interleukin-6, respectively. In the studied population, it was found that the presence of type 2 diabetes mellitus-induced hyperglycemia significantly impaired lipid profile, and significantly enhanced the formation of hydrogen preroxide and malondialdehyde as well as significantly increased the release of tumor necrosis factor-alpha and interleukin-6 in the second group of patients. In addition, plasma glucose level showed significant positive correlation with hydrogen peroxide, malondialdehyde, tumor necrosis factor-alpha and interleukin-6. From the previous results, it was concluded that the presence of type 2 diabetes mellitus-induced hyperglycemia results in significant increase in lipid profile, oxidative stress markers and inflammatory mediators in patients with non alcoholic fatty liver disease and normal liver function tests. For this reason, further research studies may be essential to evaluate the benefit of adding suitable antioxidant and anti-inflammatory drugs to the treatment regimen for this group of patients. In addition, regular monitoring of blood glucose levels and liver function tests should be advised to this category of patients to reduce liver fat deposition and avoid the development of non alcoholic steatohepatitis, cirrhosis or liver cancer and their related complications.
2型糖尿病与血脂异常、胰岛素抵抗及非酒精性脂肪性肝病相关。本研究的目的是评估2型糖尿病诱发的高血糖是否会对非酒精性脂肪性肝病且肝功能检查正常的患者的血脂谱、氧化应激标志物及炎症介质的释放产生影响,而这反过来可能会增强这种肝病的致病性。为此,105名年龄和体重匹配的门诊患者被分为两组:第一组由非酒精性脂肪性肝病患者组成,第二组由因2型糖尿病存在而伴有高血糖的非酒精性脂肪性肝病患者组成。在所有患者中,分别通过测量血清甘油三酯、低密度脂蛋白、过氧化氢、丙二醛、肿瘤坏死因子-α和白细胞介素-6的浓度来评估血脂谱、氧化应激和炎症介质。在研究人群中,发现2型糖尿病诱发的高血糖的存在显著损害了血脂谱,显著增强了过氧化氢和丙二醛的形成,并且显著增加了第二组患者肿瘤坏死因子-α和白细胞介素-6的释放。此外,血糖水平与过氧化氢、丙二醛、肿瘤坏死因子-α和白细胞介素-6呈显著正相关。根据先前的结果得出结论,2型糖尿病诱发的高血糖的存在会导致非酒精性脂肪性肝病且肝功能检查正常的患者的血脂谱、氧化应激标志物和炎症介质显著增加。因此,进一步的研究对于评估在这类患者的治疗方案中添加合适的抗氧化剂和抗炎药物的益处可能至关重要。此外,建议对这类患者定期监测血糖水平和肝功能检查,以减少肝脏脂肪沉积,避免非酒精性脂肪性肝炎、肝硬化或肝癌及其相关并发症的发生。