Acupoint catgut embedding exerts node-dependent effects on leptin resistance-related signaling and the ghrelin-GOAT pathway in obese mice.

BACKGROUND

Obesity is a major metabolic health problem with limited effective treatments. Acupoint catgut embedding (ACE) has shown therapeutic potential; however, its underlying mechanisms remain unclear. This study aimed to investigate the effects of ACE on leptin resistance and the Ghrelin-GOAT pathway in obese mice.

METHODS

Diet-induced obesity was established in C57BL/6 J mice. A total of 51 mice were included in the final analysis across six groups: normal control, obese model control, ST36 sham ACE, ST36 verum ACE, ST25 ACE, and ST25 + ST36 ACE. ACE was administered once weekly for 5 weeks. Body weight, Lee's index, and daily food intake were recorded. Serum and cerebrospinal fluid (CSF) leptin levels were measured to assess peripheral and central leptin availability. Hypothalamic SOCS3 and PTP1B protein expression and POMC/NPY mRNA levels were evaluated. Ghrelin-related indicators in gastric tissue and hypothalamus were also assessed.

RESULTS

At week 1, body weight and Lee's index were lower in the ST36 verum ACE group than in the ST25 + ST36 group (p < 0.01), and the difference in Lee's index remained significant at week 2 (p = 0.002). Food intake decreased transiently at week 1 in all obese groups, with a significant time effect (p < 0.001) but no group or group-by-time interaction effects (p > 0.05). For leptin resistance-related parameters, serum leptin levels in the model control group were significantly higher than those in the normal control group (p < 0.001), whereas CSF leptin levels were increased in the verum ST36 ACE group compared with the model control group (p < 0.001), accompanied by downregulation of hypothalamic SOCS3 and PTP1B expression (both p < 0.01). For downstream neuropeptides, POMC expression was upregulated and NPY expression was downregulated in the verum ST36 ACE group (both p < 0.001), with effects superior to those in the model control group and the ST25 ACE group (p < 0.05). In addition, within the ghrelin-GOAT pathway, gastric ghrelin and GOAT levels as well as hypothalamic GHSR-1a were higher in the verum ST36 ACE group than in the model control group (p < 0.001) and also greater than those in the ST25 ACE group (p < 0.05).

CONCLUSION

ACE may increase central leptin availability, downregulate SOCS3 and PTP1B, regulate hypothalamic POMC/NPY expression, and modulate the ghrelin-GOAT pathway, supporting a node-dependent, multi-target mechanism underlying its anti-obesity effects.