An fgf21-like gene from swamp eel (Monopterus albus): Recombinant expression and its potential roles in glucose and lipid homeostasis.

Fibroblast growth factor 21 (FGF21) plays important roles in the regulation of glucose and lipid metabolism and energy balance in mammals. In this study, the full-length cDNA of swamp eel fgf21 was cloned. Sequence analysis showed that swamp eel FGF21 displayed high similarity with FGF21 of other vertebrates. Subsequently, a prokaryotic expression vector for swamp eel fgf21 was constructed, and recombinant FGF21 (rFGF21) was successfully induced and purified. To investigate the potential roles of swamp eel FGF21 in glucose and lipid metabolism, we examined the effects of rFGF21 on regulation of glucose and lipid homeostasis in type 1 diabetes mellitus (T1DM) mice as well as swamp eels under glucose stress. In T1DM mice, the levels of blood glucose, serum triglyceride (TG), liver TG, serum total cholesterol (TC), and liver TC were significantly downregulated after repeated daily injection of rFGF21 for 15 days. In addition, liver pathological section analysis indicated that rFGF21 alleviated the degree of damage to liver cells in T1DM mice. Furthermore, rFGF21 significantly upregulated the mRNA expression levels of peroxisome proliferators-activated receptor alpha (Pparα), ß-Klotho, fibroblast growth factor receptor 1 (Fgfr1), phosphoenolpyruvate carboxykinase (Pepck), glucose transporter 1 (Glut1), and glucose transporter 4 (Glut4) in T1DM mouse livers. Moreover, in swamp eels, rFGF21 significantly decreased blood glucose and liver TC levels under glucose stress and upregulated the mRNA expression levels of fgf21, pparα, ß-klotho, and fgfr1 in liver tissue. These results suggested that FGF21 plays important roles in the regulation of glucose and lipid homeostasis in swamp eel.

Characterization, expression, and function analysis of AKR1A1 gene from yellow catfish (Tachysurus fulvidraco).

Aldehyde reductase (AKR1A1) is a carbonyl detoxification protein in toxic aldehyde removal. In the present study, the full-length cDNA of yellow catfish AKR1A1 (TfAKR1A1) was cloned. As expected, yellow catfish AKR1A1 showed similarities with that of other species. Subsequently, prokaryotic expression vector was constructed and recombinant TfAKR1A1 (rTfAKR1A1) was successfully induced and purified. rTfAKR1A1 exhibited reductive activity to many aldehydes and ketones. To determine whether TfAKR1A1 could confer stress tolerance in vitro, the viability of control and TfAKR1A1 expression E. coli under abiotic stress was compared by spot assay. Results showed that the recombinant strain had better stress resistance under cadmium, hydrogen peroxide, and DL-glyceraldehyde stress. Then, effects of an intraperitoneal injection of rTfAKR1A1 protein on cadmium-induced oxidative stress were evaluated. Results displayed that TfAKR1A1 and Nrf2 expression levels were significantly decreased, CAT and SOD expression levels were significantly increased, BCL-2 and IL-10 expression levels were significantly increased, and caspase3a, NF-κB, and IL-1ß expression levels were significantly decreased in protein-injection group. Furthermore, oxidative stress indexes in livers under different protein injection doses were examined by ELISA. Results showed that CAT, SOD, and GSH-Px activities were upregulated, ROS and T-AOC contents were also improved, while MDA content was significantly decreased both in lower and middle dose injection groups. Finally, liver pathological section analysis was performed. Results displayed that liver injury degree in protein-injected groups was lower than that of PBS group under cadmium stress. These results suggested that TfAKR1A1 played important roles in response to cadmium stress in yellow catfish.