chromium-histidinate and picolinic-acid

In this study, the effect of the supplemental organic chromium (Cr) forms on the expression of ovarian orexin(hypocretin), glucose transporters (GLUTs), heat shock proteins (HSPs) andnuclear factor-kappaB (NF-κB)were investigated in laying hens (HS). Laying hens (n=1800; 16-wk-old; Lohmann LSL-Lite) were allocated to 6 random groups according to a 2 × 3 factorial trial scheme with two different environmental temperatures [Thermoneutral (TN groups; at either 22±2 °C 24 h/d)  and heat stress (HS groups; at 34±2 °C for 8 h/d, 08:00 to 17:00 h, followed by 22°C for 16 h for a period of 12 wks)], andhens reared under both environmental conditions were fed either a basal diet or the basal diet supplemented with 1.600 mg of chromium-picolinate (CrPic, 12.43% Cr) and 0.788 mg of chromium-histidinate (CrHis, 25.22% Cr) per kg of diet, delivering 200 µg elemental Cr per kg diet. HS groups showed decreased levels of orexin and GLUTs(GLUT1, GLUT4), and increased NFκB, HSP60, HSP70 and HSP90 levels compared to the TN groups in ovarian tissue of hens (P < 0.0001 for all).However, dietary chromium supplementation (CrPic-CrHis) increasedorexin and GLUTs levels and significantly reduced the NF-κB and HSPs levels making them closer to those of thermoneutral group (P < 0.0001).In conclusion, CrPic and CrHis showed supported the relief and treatment of stress complications.

Topics: Animals; Chickens; Dietary Supplements; Female; Glucose Transport Proteins, Facilitative; Heat-Shock Proteins; Histidine; NF-kappa B; Orexins; Organometallic Compounds; Ovary; Picolinic Acids; Stress, Physiological; Temperature; Up-Regulation

This experiment investigated if chromium (Cr) as Cr-histidinate (CrHis) and Cr29 picolinate (CrPic) have a protective role in rats with hypoglycemia-induced brain injury, assessed by neuronal plasticity and regeneration potential.. Male Sprague-Dawley rats were prospectively divided into 2 groups: control and hypoglycemic (induced by insulin administration, 15U/kg, i.p., n=56). Hypoglycemic rats were then received randomly 1) none, 2) dextrose (on the day of sampling), 3) CrHis, or 4) CrPic. Cr-chelates were delivered via drinking water (providing 8μg elemental Cr per day) for one week prior to the hypoglycemia induction. The expressions of neuroplasticity markers [neural cell adhesion molecule (NCAM), growth-associated protein-43 (GAP-43), glial fibrillary acidic protein (GFAP)], glucose transporters (GLUT), and nuclear transcription proteins [nuclear factor-kappa (NF-κB), nuclear factor (erythroid-derived 2)-like 2 (Nrf2), and 4-hydroxyl nonenal (HNE)] were determined using Western blot.. Hypoglycemia caused increases in the expressions of GLUT-1, GLUT-3, GFAP, NF-κB and HNE and decreases in the expression of NCAM's, GAP-43 and Nrf2 in the hippocampus, cerebellum, and cortex. Cr-chelates suppressed expressions of GLUTs, GFAP, NF-κB and HNE expressions and enhanced expressions of NCAM, GAP-43 and Nrf2, which were more notable for CrHis than for CrPic.. In conclusion, hypoglycemia leads to cerebral injury and Cr-chelates, particularly CrHis have protective and regeneration potential in cerebral tissues through modulating neuroplasticity markers and nuclear transcription proteins as well as facilitating glucose transporters.

Topics: Animals; Blood Glucose; Brain; Brain Diseases; Cerebral Cortex; GAP-43 Protein; Glial Fibrillary Acidic Protein; Glucose Transporter Type 1; Glucose Transporter Type 3; Histidine; Hypoglycemia; Insulin; Male; Nerve Regeneration; Neural Cell Adhesion Molecules; Neuronal Plasticity; NF-E2-Related Factor 2; NF-kappa B; Organometallic Compounds; Picolinic Acids; Protective Agents; Rats; Rats, Sprague-Dawley

The objective of this experiment was to investigate the effects of supplemental chromium picolinate (CrPic) and chromium histidinate (CrHis) on nuclear factor-kappa B (NF-κB p65) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2) signaling pathway in diabetic rat brain. Nondiabetic (n = 45) and diabetic (n = 45) male Wistar rats were either not supplemented or supplemented with CrPic or CrHis via drinking water to consume 8 μg elemental chromium (Cr) per day for 12 weeks. Diabetes was induced by streptozotocin injection (40 mg/kg i.p., for 2 weeks) and maintained by high-fat feeding (40 %). Diabetes was associated with increases in cerebral NF-κB and 4-hydroxynonenal (4-HNE) protein adducts and decreased in cerebral nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha (IκBα) and Nrf2 levels. Both Cr chelates were effective to decrease levels of NF-κB and 4-HNE protein adducts and to increase levels of IκBα and Nrf2 in the brain of diabetic rats. However, responses of these increases and decreases were more notable when Cr was supplemented as CrHis than as CrPic. In conclusion, Cr may play a protective role in cerebral antioxidant defense system in diabetic subjects via the Nrf2 pathway by reducing inflammation through NF-κB p65 inhibition. Histidinate form of Cr was superior to picolinate form of Cr in reducing NF-κB expression and increasing Nrf2 expression in the brain of diabetic rats.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Brain; Chelating Agents; Chromium; Diabetes Mellitus, Type 2; Dietary Supplements; Heme Oxygenase (Decyclizing); Histidine; Hypoglycemic Agents; I-kappa B Proteins; Male; Nerve Tissue Proteins; Neurons; NF-E2-Related Factor 2; NF-KappaB Inhibitor alpha; Organometallic Compounds; Picolinic Acids; Rats; Rats, Wistar; Signal Transduction; Transcription Factor RelA