Effects of dietary vitamin D3 and carbohydrate levels on growth performance, carbohydrate metabolism, and intestinal health of yellow catfish (Pelteobagrus fulvidraco)

The study was performed to determine effects of vitamin D3 (VD3) and carbohydrate levels in the diets on growth, carbohydrate absorption and metabolism, and intestinal health of yellow catfish (Pelteobagrus fulvidraco). Four groups of yellow catfish with an average weight of 4.12 ± 0.00 g were provided with diets containing varying proportions of VD3 and carbohydrate. These diets included two VD3 levels at 1000 IU/kg (basic VD3) and 16,100 IU/kg diet (high VD3), each containing carbohydrate levels of 25% and 35%, respectively. After analyzing dietary VD3 and carbohydrate contents, these groups were labeled as follows: the control (30.78% carbohydrates +1040 IU/kg), the VD3 group (30.67% carbohydrates +16,041 IU/kg), the high-carbohydrate group (HCD group, 39.65% carbohydrates +1017 IU/kg), and the HCD + VD3 group (39.67% carbohydrates +16,061 IU/kg). Each tank consisted of three replicates, with each replicate containing 30 fish. The experiment continued for 10 weeks. Compared with the control, HCD group reduced growth performance, the muscular layer thickness, the zonulae occludentes1 and 3 (zo1, zo3), junctional adhesion molecules 3a (jam3a), claudin1, occludin, phosphoglucomutase 1 (pgm1) mRNA expression, but increased intestinal villi height, glycogen content, glycogen synthase (gs), glycogen branching enzyme (gbe), sodium/glucose cotransporter 1 and 2 (sglt1, sglt2) and glucose transporter 2 (glut2) mRNA expression, solute carrier family 5 member 1 (SGLT1) protein expression, and dietary VD3 group alleviated HCD-induced variations of these indices mentioned above. Compared to the control, HCD group significantly suppressed pyruvate carboxylase b (pcxb), phosphoenolpyruvate carboxykinase (pepck), interleukin10 (il10), NFE2 like bZIP transcription factor 2 (nrf2), superoxide dismutase 2 (sod2) and catalase 1 (cat1) mRNA expression, and also inhibited the activities of glutathione peroxidase (GPX), catalase (CAT), total superoxide dismutase (T-SOD) and total antioxidant capacity (T-AOC), but increased hexokinase 1 (hk1), glucokinase (gk), 1-phosphofructokinase (pfkb), interleukin 1β (il1β), interleukin 6 (il6), tumor necrosis factor a and β (tnfa, tnfβ) mRNA expression, and malondialdehyde (MDA) content; dietary VD3 group further suppressed gluconeogenic genes (pcxb, pepck) expression, but significantly enhanced the expression of glycolytic genes (hk1, gk, pfkp). Dietary VD3 also alleviated HCD-induced variations of these indices involved in antioxidant and inflammatory responses in yellow catfish intestine. Based on these results, our study indicated that dietary VD3 contributed to alleviate HCD-induced adverse effects on intestinal carbohydrate utilization and health. Our study also elucidated the innovative insights into the interaction of HCD and VD3 in fish, and provided the potential strategies for improving dietary carbohydrate utilization of fish via VD3 addition in aquafeeds. These findings can potentially contribute to cost savings for businesses and serve as a reference for optimizing feed formulations.