The impact of nesfatin-1 on autophagy in brain tissue and dopamine secretion in fasting mice

Intermittent fasting is known to affect metabolic and neuroendocrine pathways, and Nesfatin-1, a peptide in- volved in appetite regulation and metabolism, may play a crucial role in these processes. This study investigates the impact of Nesfatin-1 on brain tissue autophagy and dopamine secretion in fasting mice. Forty C57BL/6 mice were randomly assigned to the control group, 24 h fasting group, 48 h fasting group, Nesfatin-1+24 h fasting group, and Nesfatin-1+48 h fasting group. Following intraperitoneal injections of 1.25 nmol/g Nesfatin-1 after the respective fasting periods, serum levels of Nesfatin-1 and dopamine, as well as mRNA and protein expression of tyrosine hydroxylase and autophagy factors in brain tissues, were assessed using enzyme-linked immunosorbent assay, re- al-time quantitative polymerase chain reaction, and Western blot. The results showed significant decreases in serum Nesfatin-1 and dopamine levels (P<0.05) compared to the control group, along with increased mRNA and protein expression of Beclin-1 and microtubule-associated protein 1 light chain 3 in brain tissues (P<0.05), and decreased p62 and tyrosine hydroxylase levels (P<0.01) in fasting groups. However, Nesfatin-1 intervention led to significant increases in serum Nesfatin-1 and dopamine levels (P<0.01), while decreasing Beclin-1 and protein 1 light chain 3 expression (P<0.01), and increasing p62 and tyrosine hydroxylase levels (P<0.01). These findings suggest that acute fasting reduces Nesfatin-1 and dopamine levels, while increasing autophagy in mice, whereas Nesfatin-1 intervention not only effectively diminishes autophagy levels in the brain but also boosts dopamine secretion.