**Author details**

dyslipidemia. This observation has been observed both in human clinical and experimental models [77, 78]. Cr plasma concentrations can be explained by its mobilization from its storage site (liver, kidneys) to the blood by chromodulin binding (intracellular transport protein) [79]. However, Cr bioavailability depends on the nutrients with which it is associated: Cr/ phenylalanine, Cr/cysteine, Cr/biotin and Cr/vitamin E or Cr/vitamin C complexes have been described [80–83]. Cr acts as carbohydrate tolerance factor, increases insulin sensitivity, particularly in the skeletal muscle. Indeed, trivalent chromium is an insulin pathway signaling. Cr increases insulin receptors number, insulin internalization and an activation of the GLUT4 and GLUT1 glucose carriers translocation [84]. The insulin binding to the α-subunit receptor is induced by a phosphorylation reactions cascade catalyzed by tyrosine kinase that is activated by Cr; however, phosphotyrosine phosphatase which inactivates the insulin receptor is inhibited by Cr [85]. In type 2 diabetes and obesity, the Cr deficiency can be observed in subjects consuming excessively rapid absorption carbohydrates that increase the urinary elimination of chromium. Cr Supplementation during 6 months may be prescribed in a forms variety: Cr-chloride, Cr-nicotinate, Cr-propionate, Cr-histidinate or Cr-picolinate leads to a significant decrease HbA1c and AGE [86, 87]. Cr supplementation effects appear to be mediated by AMP kinase activation and p38 MAP kinase signaling pathway [88]. Cr controls body fat and body weight by satiety mechanisms (food intake control) and thermogenesis [89]. The Cr effects are observed via the resistin and *uncoupling protein* (UCP) decoupling proteins signaling pathway [84, 90]. Otherwise, experimental animal studies have shown that Cr modulates the inflammatory state during diabetes by decreasing proinflammatory cytokines production such as

Glycemic homeostasis is not only dependent on hormonal control, especially insulin; but also the micronutrients such as Chromium, Zinc, Selenium, Manganese and Copper. These Antioxidant Trace Elements act as cofactors of antioxidant enzymes (SOD, GPx) which protect the glucose-dependent tissues from the deleterious effects of reactive oxygen species fol-

The research was supported by the General Division for Algerian Scientific Research and

*tumor necrosis factor* (TNF-α), and interleukin IL-6 [91].

Technological Development (DG-RSDT). www: www.dgrsdt.dz.

The authors declare that there is no conflict of interests regarding this paper.

**7. Conclusions**

98 Diabetes Food Plan

lowing oxidation of glucose.

**Acknowledgements**

**Conflict of interests**

Ines Gouaref and Elhadj-Ahmed Koceir

\*Address all correspondence to: e.koceir@gmail.com

Department of Bioenergetics and Intermediary Metabolism, Biology and Organisms Physiology Laboratory, Biological Sciences Faculty, University of Sciences and Technology Houari Boumediene (USTHB), Algiers, Algeria
