The Effects of Chromium Histidinate on Mineral Status of Serum and Tissue in Fat-Fed and Streptozotocin-Treated Type II Diabetic Rats

Abstract

The present study was conducted to investigate the effects of chromium histidinate (CrHis) against experimentally induced type II diabetes and on chromium (Cr), zinc (Zn), selenium (Se), manganese (Mn), iron (Fe), and copper (Cu) in serum, liver, and kidney of diabetic rats. The male Wistar rats (n = 60, 8 weeks old) were divided into four groups. Group I received a standard diet (12% of calories as fat); group II were fed standard diet and received CrHis (110 mcg CrHis/kg body weight per day); group III received a high-fat diet (HFD; 40% of calories as fat) for 2 weeks and then were injected with streptozotocin (STZ) on day 14 (STZ, 40 mg/kg i.p.; HFD/STZ); group IV were treated as group III (HFD/STZ) but supplemented with 110 mcg CrHis/kg body weight per day. The mineral concentrations in the serum and tissue were determined by atomic absorption spectrometry. Compared to the HFD/STZ group, CrHis significantly increased body weight and reduced blood glucose in diabetic rats (p < 0.001). Concentrations of Cr, Zn, Se, and Mn in serum, liver, and kidney of the diabetic rats were significantly lower than in the control rats (p < 0.0001). In contrast, higher Fe and Cu levels were found in serum and tissues from diabetic versus the non-diabetic rats (p < 0.001). Chromium histidinate supplementation increased serum, liver, and kidney concentrations of Cr and Zn both in diabetic and non-diabetic rats (p < 0.001). Chromium supplementation increased Mn and Se levels in diabetic rats (p < 0.001); however, it decreased Cu levels in STZ-treated group (p < 0.001). Chromium histidinate supplementation did not affect Fe levels in both groups (p > 0.05). The results of the present study conclude that supplementing Cr to the diet of diabetic rats influences serum and tissue Cr, Zn, Se, Mn, and Cu concentrations.

Evaluation of trace elements and oxidative stress levels in the liver and kidney of streptozotocin-induced experimental diabetic rat model

“…In accordance with the findings of the present study, Dogukan et al (2009) found that concentrations of Zn in liver and kidney of the diabetic rats were significantly lower than in the control rats. In contrast, higher Fe and Cu levels were found in tissues from diabetic versus the non-diabetic rats.…”

Syzygium cumini Ameliorates Insulin Resistance and ^|^beta;-Cell Dysfunction via Modulation of PPAR^|^gamma;, Dyslipidemia, Oxidative Stress, and TNF-^|^alpha; in Type 2 Diabetic Rats

“…Moreover, we also demonstrated that this beneficial effect of SC could also be due to attenuation of oxidative stress, TNF-α, β-cell damage and dysfunction. Our findings was in consonance with the previous studies demonstrating that animals fed with HFD and injected a low dose STZ display many characteristics of IR including significant obesity, fasting hyperglycemia, hyperinsulinemia, β-cell dysfunction, hyperlipidemia, and increased serum TNF-α levels (20,21). Furthermore, we also observed increased lipid peroxidation, decreased antioxidant enzyme activity and deleterious changes in pancreatic β-cells in HFD-STZtreated rats.…”

Hepcidin Is Directly Regulated by Insulin and Plays an Important Role in Iron Overload in Streptozotocin-Induced Diabetic Rats

“…STZ-induced elevation of iron storage was also observed in the proximal tubular lysosomes (27), myocardium (28), and artery (29), while studies of Silva et al (30) and Saravanan et al (31) showed that serum iron was increased in STZ rats. Additionally, Dogukan et al (32) reported that STZ injection following HFD induction markedly increased the hepatic and serum iron levels. Our results demonstrated that insulin therapy effectively released HIO, manifested by the recovery of liver iron content and serum ferritin and the improvement tendency of serum sTfR, and lowered serum iron to normal level in STZ-induced both type 1 and type 2 diabetic rats.…”