Fibroblast growth factors (FGFs) are responsible for the regulation of a wide range of biological functions, among which cellular proliferation, survival, migration, and differentiation could be pointed out. FGF19 controls the enterohepatic bile acid/cholesterol system, and FGF21 modulates fatty acid/glucose metabolism. Obesity, type 2 diabetes, coronary artery disease, and cancer, all can alter FGF21 circulating concentrations. In contrast to FGF21, metabolic diseases exhibit reduced serum FGF19 levels. Accordingly, FGF19 and FGF21 play important roles in regulating glucose and lipid metabolism. Hence, we present here a timely review on the relationship between FGF19/21 and metabolic diseases, especially obesity, and their probable role in development and treatment of obesity seems necessary.

Cadmium (Cd) is a highly toxic element, which may cause toxicity to most organs in the body. Zinc (Zn) and magnesium (Mg) are essential minerals with probable benefits on Cd harmful effects. Finding an efficient and non-pathological treatment against Cd toxicity seems promising. Fifty adult rats were divided into ten experimental groups of five rats each. The Cd group was treated with 1 mg Cd/kg and the control group received 0.5 cm normal saline. The other eight groups received Zn (0.5 and 1.5 mg/kg) and Mg (0.5 and 1.5 mg/kg) either alone or in combination with 1 mg Cd/kg through IP injection for 3 weeks. Testis malondialdehyde (MDA), sperm parameters, and testis histopathology were investigated. Cd reduced sperm parameters and increased testis MDA. Moreover, Cd exposure caused a significant histological damage in testis of male rats. However, Zn or Mg treatment prevented and reversed Cd toxic alterations in testis. These findings suggest that co-administration of Zn or Mg could improve cadmium testicular toxicity in male Wistar rats.

Cd is a toxic metal that has a destructive impact on most organ systems. This work aims to determine Zn or Mg protective effects against Cd renal toxicity. In this study, rats were divided into six groups. The Cd group was treated with 1 mg Cd/kg, and the control group received 0.5 cm normal saline, intraperitoneally. The other four groups received one of the following dosages of 1 mg/kg Cd + 0.5 mg/kg Zn, 1 mg/kg Cd + 1.5 mg/kg Zn, 1 mg/kg Cd + 0.5 mg/kg Mg, or 1 mg/kg Cd + 1.5 mg/kg Mg through IP injection for 3 weeks. Kidney malondialdehyde (MDA) and serum sodium, potassium, urea, creatinine, and protein were measured. Light microscopic examination was used for histological studies. Cd reduced serum creatinine and protein, and increased urea, sodium, and potassium. Moreover, Cd exposure caused a significant enhancement in MDA levels as well as histological damage in kidneys. Zn or Mg treatment prevented and reversed toxic alterations induced by Cd. These results suggest that Zn and Mg may have protective effects against Cd renal toxicity.