Adeyemi Wale J, Olayaki Luqman A
Department of Physiology, College of Health Sciences, University of Ilorin, Ilorin, Kwara State, Nigeria.
Department of Physiology, College of Health Sciences, University of Ilorin, Ilorin, Kwara State, Nigeria.
Exp Mol Pathol. 2017 Oct;103(2):113-120. doi: 10.1016/j.yexmp.2017.07.005. Epub 2017 Jul 28.
Clinical evidences on the coexistence of diabetes mellitus (DM) and osteoarthritis (OA) dated back to the 1960s. Therefore, the study investigated the effects of induced DM and/or knee osteoarthritis (KOA) on some biochemical and haematological parameters in adult male Wistar rats. Twenty rats were used for this study. They were randomly divided into 4 groups (N=5 rats) which included: Normal control; Osteoarthritic (OA) control; Diabetic control; and, Diabetic+Osteoarthritic (D+OA) control. DM was induced in overnight fasted rats by the administration of streptozotocin (65mg/kg b.w., i.p.) 15min after the administration of nicotinamide (110mg/kg, b.w., i.p.). However, KOA was induced by the intra-articular injection of 4mg of sodium monoiodoacetate in 40μl of normal saline. In the D+OA group, KOA was induced about 12h after the induction of DM. The rats were left untreated for four weeks. Afterwards, the experiment was terminated. The results showed that both DM and OA featured hypercortisolism and dyslipidaemia. The additive effects of both conditions were observed on the lipid profile and some haematological indices in the D+OA group. Unlike DM, OA had mild adverse effects on the haematological profile. Nevertheless, it significantly contributed to hyperglycaemia in the D+OA group, even though it had no significant effect on the insulin resistance. However, the hypocalcaemic and glycogenolytic effects of DM were negated by OA. In conclusion, the coexistence of DM and OA presents a greater challenge on the biochemical and haematological profiles than the individual disease. But, this prediction could sometimes be annulled by the intervention of endogenous homeostatic mechanisms.
糖尿病(DM)与骨关节炎(OA)并存的临床证据可追溯到20世纪60年代。因此,本研究调查了诱导性糖尿病和/或膝骨关节炎(KOA)对成年雄性Wistar大鼠某些生化和血液学参数的影响。本研究使用了20只大鼠。它们被随机分为4组(每组5只大鼠),包括:正常对照组;骨关节炎(OA)对照组;糖尿病对照组;糖尿病+骨关节炎(D+OA)对照组。在禁食过夜的大鼠中,于注射烟酰胺(110mg/kg体重,腹腔注射)15分钟后,注射链脲佐菌素(65mg/kg体重,腹腔注射)诱导糖尿病。然而,通过在40μl生理盐水中关节内注射4mg一碘乙酸钠诱导KOA。在D+OA组中,KOA在糖尿病诱导后约12小时诱导。大鼠未经治疗4周。之后,实验终止。结果表明,糖尿病和骨关节炎均表现为皮质醇增多症和血脂异常。在D+OA组中,观察到两种情况对血脂谱和一些血液学指标的叠加效应。与糖尿病不同,骨关节炎对血液学指标有轻微不良影响。然而,它显著导致了D+OA组的高血糖,尽管它对胰岛素抵抗没有显著影响。然而,骨关节炎抵消了糖尿病的低钙血症和糖原分解作用。总之,糖尿病和骨关节炎并存对生化和血液学指标的挑战比单一疾病更大。但是,这种预测有时可能会被内源性稳态机制的干预所消除。