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The objective of the present study was to evaluate anti-diabetic effects of chromium picolinate (CrPic) and biotin supplementations in type 2 diabetic rats. The type 2 diabetic rat model was induced by high-fat diet (HFD) and low-dose streptozotocin. The rats were divided into five groups as follows: (1) non-diabetic rats fed a regular diet; (2) diabetic rats fed a HFD; (3) diabetic rats fed a HFD and supplemented with CrPic (80 mg/kg body weight (BW) per d); (4) diabetic rats fed a HFD and supplemented with biotin (300 mg/kg BW per d); (5) diabetic rats fed a HFD and supplemented with both CrPic and biotin. Circulating glucose, cortisol, total cholesterol, TAG, NEFA and malondialdehyde concentrations decreased (P, 0·05), but serum insulin concentrations increased (P,0·05) in diabetic rats treated with biotin and CrPic, particularly with a combination of the supplements. Feeding a HFD to diabetic rats decreased PPAR-g expression in adipose tissue and phosphorylated insulin receptor substrate 1 (p-IRS-1) expression of liver, kidney and muscle tissues, while the supplements increased (P, 0·001) PPAR-g and p-IRS-1 expressions in relevant tissues. Expression of NF-kB in the liver and kidney was greater in diabetic rats fed a HFD, as compared with rats fed a regular diet (P, 0·01). The supplements decreased the expression of NF-kB in diabetic rats (P,0·05). Results of the present study revealed that supplementing CrPic and biotin alone or in a combination exerts anti-diabetic activities, probably through modulation of PPAR-g, IRS-1 and NF-kB proteins.

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.

This experiment was conducted to investigate effects of the organic complex form of supplemental chromium (Cr) on performance, oxidative stress markers, and serum profile in broilers exposed to heat stress (HS). A total of 1,200 10-day-old boilers (Ross-308) was divided into one of the 6 treatments (2 environmental temperatures x 3 diets with different Cr forms). The birds were kept in temperature-controlled rooms at either 22 ± 2°C 24 h/d (thermoneutral, TN group) or 34 ± 2°C for 8 h/d, 08:00 to 17:00 h, followed by 22°C for 16 h (HS group) and fed either a basal diet (C) or the basal diet supplemented with Cr (200 μg/kg) through 1.600 mg of CrPic (12.43% Cr) and 0.788 mg of CrHis (25.22% Cr). Feed intake and body weight were recorded weekly. After cervical dislocation, liver samples were harvested to analyze Cr concentration and glucose transporter-2,4 (GLUT-2,4) expression. The breast meat also was sampled for the concentration of Cr and expressions of nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor kappa B (NF-κB). Data were analyzed by 2-way ANOVA. Heat stress caused depressions in feed intake (12.1%) and weight gain (21.1%) as well as elevations in feed conversion (11.2%) and abdominal fat (32.8%). It was also associated with depletion of Cr reserves and increases in serum concentrations of glucose, cholesterol, creatine, and enzymes. Exposure to HS was accompanied by suppression of the expressions of Nrf2 and GLUT-2 in muscle and GLUT-4 in the liver and amplification of the expression of NF-κB in muscle. Both Cr sources partially alleviated detrimental effects of HS on performance and metabolic profile. The efficacy of Cr as CrHis was more notable than Cr as CrPic, which could be attributed to higher bioavailability. In conclusion, CrHis can be added into the diet of broilers during hot seasons to overcome deteriorations in performance and wellbeing related to oxidative stress.

BackgroundChromium (Cr) is an essential trace element that has garnered interest for use as a weight loss aid, but its molecular mechanism in obesity is not clear. In this study, an attempt has been made to investigate the effects of chromium histidinate (CrHis) on glucose transporter-2 (GLUT-2), nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), nuclear factor-kappa B (NF-κB p65) and the oxidative stress marker 4-hydroxynonenal adducts (HNE) expressions in liver of rats fed high fat diet (HFD).MethodsMale Wistar rats (n = 40, 8 wk-old) were divided into four groups. Group I was fed a standard diet (12% of calories as fat); Group II was fed a standard diet and supplemented with 110 μg CrHis/kg BW/d; Group III was fed a HFD (40% of calories as fat); Group IV was fed HFD and supplemented with 110 μg CrHis/kg BW/d.ResultsRats fed HFD possessed greater serum insulin (40 vs.33 pmol/L) and glucose (158 vs. 143 mg/dL) concentration and less liver Cr (44 vs.82 μg/g) concentration than rats fed the control diet. However, rats supplemented with CrHis had greater liver Cr and serum insulin and lower glucose concentration in rats fed HFD (P < 0.05). The hepatic nuclear factor-kappa B (NF-κB p65) and HNE were increased in high fat group compared to control group, but reduced by the CrHis administration (P < 0.05). The levels of hepatic Nrf2 and HO-1 were increased by supplementation of CrHis (P < 0.05).ConclusionThese findings demonstrate that supplementation of CrHis is protective against obesity, at least in part, through Nrf2-mediated induction of HO-1 in rats fed high fat diet.