The approach to the mechanism of calcitonin gene-related peptide-inducing inhibition of food intake.

The aim of this study was to investigate the anorectic mechanism of calcitonin gene-related peptide (CGRP) in rats. Intraperitoneal injection of CGRP (50 µg/kg) resulted in decline (p < 0.05) in the food intake of rats at 0.5, 1, 2 and 4 h in comparison with saline control. Compared with saline-treated group, the levels of hypothalamic 3',5'-cyclic adenosine monophosphate (cAMP) and plasma glucagon were increased (p < 0.05) in CGRP-treated group, but insulin level was decreased (p < 0.05). No significant changes (p > 0.05) in the plasma leptin were observed between two treatment groups. Calcitonin gene-related peptide injection down regulated (p < 0.05) both neuropeptide Y (NPY) and melanin-concentrating hormone (MCH) genes at mRNA levels, but up regulated (p < 0.05) the expression of cholecystokinin (CCK) gene. The correlations analysis showed that food intake was negatively correlated (p < 0.05) with CCK mRNA, cAMP and glucagon levels. Moreover, there existed negative correlations (p < 0.05) between MCH mRNA and glucagon levels, and positive correlations (p < 0.05) between insulin and leptin levels. The results showed that cAMP acting as the second messenger may play a vital role in the anorectic effects of CGRP. Calcitonin gene-related peptide could stimulate anorexigenic neuropeptides (i.e. CCK) and/or inhibit orexigenic neuropeptides (i.e. NPY and MCH) expression, and ultimately suppressed food intake that was functionally coupled to cAMP/PKA pathway activation.

Effects of zinc levels on activities of gastrointestinal enzymes in growing rats.

The present study investigated the effect of different zinc (Zn) levels on activities of gastrointestinal digestive enzymes of growing rats. Four diets including Zn-adequate (ZA; 46 mg/kg, control), Zn-deficient (ZD; 3 mg/kg), high Zn supply (ZH; 234 mg/kg) and pair-fed in which animals received the ZA diet at restricted amounts reflecting feed intake of the ZD group were fed to rats for 5 weeks. Dietary Zn was supplemented with ZnO. The results showed that Zn deficiency resulted in decreases in body weight, while ZH supply stimulated growth. The activities of sucrase, lactase and lipase were unaffected by dietary Zn levels. Maltase activity, however, was reduced in ZD group and elevated in ZH group. Amylase and protease activities were depressed by zinc deficiency. However, rats fed the Zn-repletion diet displayed higher activity of pepsin, pancreatic amylase and protease. In particular, ZH supply did have no effect on intestinal hydrolases activities. The present study suggested that zinc deficiency impaired the activities of digestive enzymes and growth of animals. However, ZH supply might improve the digestion of nutrients via increasing activities of gastrointestinal hydrolase and probably enhanced animal health.

Gene expression profiles analysis of the growing rat liver in response to different zinc status by cDNA microarray analysis.

The effects of zinc on growing rats were characterized using the dietary zinc-deficient (ZD) and Zinc-overdose (ZO) models. Zinc deficiency had negative effects on the host final body weight and liver zinc content, whereas zinc overdose had positive effects. In order to identify the molecular changes in the liver responding to dietary zinc status, cDNA microarrays were used to analyze the expression pattern of 9753 genes in the livers of rats fed ZD and ZO diet for 6 wk, compared with zinc-adequate ZA. The mRNA levels for 62 genes were affected significantly by the ZD diet, whereas 66 gene transcriptions were markedly changed in the ZO diet. Those predominant gene products involved in nitrogen metabolism (glutaminase), carbohydrate metabolism (aldolase), lipid metabolism (stearoyl-CoA desaturase), growth (insulin-like growth factor-binding protein), transcription and translation (zinc-finger protein), immune (natural-killer cell), signal transduction (mitogen- activated protein kinase), and ion transportation (ATPase Na+/K+ transporting peptide) were clustered. In conclusion, a number of mammalian genes related to zinc in the liver were identified. The characterization of the genes and their products will allow a more comprehensive analysis of the role of zinc in metabolism. Furthermore, the mRNA identified could be useful in establishing the mechanisms of zinc in the pleiotropic metabolisms in vivo.

Effects of dietary zinc levels on the activities of enzymes, weights of organs, and the concentrations of zinc and copper in growing rats.

Zinc (Zn) is an essential nutrient that is required in humans and animals for many physiological functions, including immune and antioxidant function, growth, and reproduction. The present study was performed to investigate the effects of three Zn levels, including Zn adequate (35.94 mg/kg, as a control), Zn deficiency (3.15 mg/kg), and Zn overload (347.50 mg/kg) in growing male rats for 6 wk. This allowed for evaluation of the effects that these Zn levels might have on body weight, organ weight, enzymes activities, and tissues concentrations of Zn and Cu. The results showed that Zn deficiency has negative effects on growth, organ weight, and biological parameters such as alkaline phosphatase (ALP) and Cu-Zn superoxide dismutase (Cu-Zn SOD) activities, whereas Zn overload played an effective role in promoting growth, improving the developments of organs and enhancing immune system. Hepatic metallothionein (MT) concentration showed an identical increase tendency in rats fed both Zn-deficient and Zn-overload diets. The actual mechanism of reduction of Cu concentration of jejunum in rats fed a Zn-overload diet might involve the modulation or inhibition of a Cu transporter protein by Zn and not by the induction of MT.