Leptin and zinc relation : In regulation of food intake and immunity

Abstract

Leptin is synthesized and released by the adipose tissue. Leptin, which carries the information about energy reserves of the body to the brain, controls food intake by acting on neuropeptide Y (NPY), which exercises a food-intake-increasing effect through relevant receptors in the hypothalamus. Zinc deficiency is claimed to result in anorexia, weight loss, poor food efficiency, and growth impairment. The fact that obese individuals have low zinc and high leptin levels suggests that there is a relation between zinc and nutrition, and consequently also between zinc and leptin. Leptin deficiency increases the predisposition to infections and this increase is associated with the impairments in the production of cytokines. Zinc has a key role in the sustenance of immune resistance against infections. Dietary zinc deficiency negatively affects CD+4 cells, Th functions, and consequently, cell-mediated immunity by causing a decrease in the production of IL-2, IF-γ, and TNF-α, which are Th1 products. The relation between zinc and the concerned cytokines in particular, and the fact that leptin has a part in the immune responses mediated by these cytokines demonstrate that an interaction among cellular immunity, leptin and zinc is inevitable. An overall evaluation of the information presented above suggests that there are complex relations among food intake, leptin and zinc on one hand and among cellular immunity, leptin and zinc on the other. The aim of the present review was to draw attention to the possible relation between zinc and leptin in dietary regulation and cellular immunity.

Orexigenic action of oral zinc: metabolomic analysis in the rat hypothalamus

“…In seeking explanations for the dopamine results, we note that high-dose zinc administration has been shown to inhibit the binding of dopamine to D1 and D2 receptors, which acts as antagonistic to dopamine activation, and are important interactions for dopamine's food intake-inhibiting effect (= food intake acceleration by zinc). This theory suggests that zinc could be playing a regulatory role in food intake by an action on neurotransmitter receptors [12]. Applying this theory to our results, we speculate that orally administered zinc partly binds to D1 and D2 receptors in the intestinal epithelium, and the resulting free dopamine would lead to an observation of increased dopamine in the Zn-PO group, although this idea must be investigated further in detail [13].…”

Investigation changes in production, some blood hormones, and metabolites, serum and colostrum IgG of calves of Holstein cows fed with two levels of zinc supplement in transitional period

“…The pancreas is very sensitive to Zn metabolism and losses Zn as soon as dietary level of zinc decreases (Roth and Kirchgessner 1981). Zinc is more necessary in β than α cells for the production, storage and release of insulin (Baltaci and Mogulkoc 2012). Zinc is accompanied with insulin in the pancreas and pancreatic concentrations are severely reduced by dietary deficiency.…”

“…In vivo zinc deficiency causes not only a decrease in insulin secretion but also decreases cellular reaction to insulin. Therefore, zinc deficiency may decrease the ob gene expression, which is stimulated by insulin (Baltaci and Mogulkoc 2012). In the study performed by Delavaud et al (2002), insulin had no effect on plasma leptin and they claimed that glucose might be involved in the regulation of leptin released by adipose tissue.…”

Data quantification procedures for a bench‐top elemental microimaging of brain specimens for the clinical studies on the obesity treatment by transcranial direct current brain stimulation

“…[7] In turn, another recent study provided compelling evidence suggesting that obese individuals have low brain zinc coincided with high leptin levels. [8] However, to date, the levels of chemical major trace and trace elements in different brain structures have not been shown. Hence, the methods for the in situ quantitative assessment of the elemental changes in brain tissue is still pending, as the previous studies utilized either a bulk analysis or made use of homogenized samples.…”