No abstract

The dipeptidyl peptidase IV (DPP-IV)-inhibitory bioactivity of silver carp protein (SCP) hydrolysates were investigated, and their containing efficacious DPP-IV-inhibitory peptides were explored by in silico hydrolysis analysis, peptide separation combined with liquid chromatography-tandem mass spectrometry (LC-MS/MS) identification, and chemical synthesis. SCP hydrolysates generated by six proteases all showed efficient DPP-IV-inhibitory activities, and Neutrase-generated hydrolysates had the greatest DPP-IV inhibition (IC50 of 1.12 mg/mL). In silico Neutrase hydrolysis revealed hundreds of fragments released from myosin, actin, and collagen of SCPs, which include different Pro-motif peptides but only three reported peptidic DPP-IV inhibitors with moderate or weak bioactivity. In addition, three new DPP-IV-inhibitory peptides were identified using LC-MS/MS; in particular, LPIIDI and APGPAGP showed high DPP-IV-inhibitory activity with IC50 of 105.44 and 229.14 μM, respectively, and behaved in competitive/non-competitive mixed-type DPP-IV inhibition mode. The results indicate that the SCP-derived DPP-IV-inhibitory peptides could be potential functional ingredients in the diabetic diet.

Scope The present study aims to assess the antidiabetic effect of Lactobacillus paracasei strain NL41 and its potential mechanisms in rats with type 2 diabetes mellitus (T2DM) induced by a high‐fat diet and low‐dose streptozotocin administration (HFD/STZ). Methods and results Eighteen Sprague–Dawley (SD) rats are randomly assigned to three groups: one control, one HFD/STZ model, and one HFD/STZ‐Lactobacillus protection group with administration of strain NL41 for 12 weeks. Blood is collected for biochemical parameters analysis and tissue samples for histological analysis. Treatment with strain NL41 results in excellent blood glucose regulation and significantly decreases insulin resistance, and HbA1c, glucagon, and leptin levels, accompanied by remarkable improvement of dyslipidemia and oxidative stress status in the animals. Islets of Langerhans, liver, and kidney are significantly protected in the NL41‐treated rats compared to the HFD/STZ‐T2DM model rats. Histochemistry shows that strain NL41 inhibits beta‐cell loss and alpha‐cell expansion, indicating pancreatic islets as the targeted tissues for the primary ameliorative effect of the probiotic strain on HFD/STZ‐T2DM rats. Crosstalk between the gut–liver and liver–pancreas endocrine axes is discussed. Conclusion Probiotic strain NL41 prevents HFD/STZ‐T2DM by decreasing insulin resistance and oxidative stress status, and protecting beta‐cell function.