What question did this study set out to answer?

To determine the neuroprotective effects of liraglutide against cognitive impairment in type 2 diabetic rats and elucidate the underlying molecular mechanisms.

June 18, 2018Molecular Medicine ReportsOpen Access

Liraglutide improves cognitive impairment via the AMPK and PI3K/Akt signaling pathways in type 2 diabetic rats

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Authors

YYYing Yang HFHui Fang GXGang Xu

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Overview

Preclinical study reveals liraglutide alleviates cognitive deficits in diabetic rats, suggesting neuroprotection mediated by AMPK and PI3K/Akt pathway activation.

Key Points

To determine the neuroprotective effects of liraglutide against cognitive impairment in type 2 diabetic rats and elucidate the underlying molecular mechanisms.
Male diabetic Goto-Kakizaki (GK) rats (N=30, age 32 weeks) were randomly assigned to receive vehicle, low-dose liraglutide (75 µg/kg), or high-dose liraglutide (200 µg/kg) daily for 28 days, compared with vehicle-treated male Wistar control rats (N=10).
Spatial learning and memory were evaluated using the Morris water maze test.
Western blot analysis quantified hippocampal expression of PI3K, Akt, p-Akt, AMPK, p-AMPK, mTOR, Beclin-1, LC3-II, caspase-3, Bax, and Bcl-2.
Liraglutide treatment alleviated diabetes-induced learning and memory deficits in GK rats, with the greatest improvement observed in the high-dose group.
Liraglutide restored suppressed autophagy markers (Beclin-1 and LC3-II) and reversed diabetes-induced changes in p-AMPK, PI3K, p-Akt, and mTOR expression.
Treatment modulated apoptosis-related proteins, inhibiting cell death and preserving neuronal function via autophagy activation.

Cite This Study

Yang et al. (2018) studied this question.

synapsesocial.com/papers/6a9880aa1ec081155cd317da https://doi.org/10.3892/mmr.2018.9180

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June 18, 2018Molecular Medicine ReportsOpen Access

Liraglutide improves cognitive impairment via the AMPK and PI3K/Akt signaling pathways in type 2 diabetic rats

View Full Paper

Ask AI

Bookmark

Authors

YYYing Yang HFHui Fang GXGang Xu

Discussion

Member takes

Overview

Preclinical study reveals liraglutide alleviates cognitive deficits in diabetic rats, suggesting neuroprotection mediated by AMPK and PI3K/Akt pathway activation.

Key Points

To determine the neuroprotective effects of liraglutide against cognitive impairment in type 2 diabetic rats and elucidate the underlying molecular mechanisms.
Male diabetic Goto-Kakizaki (GK) rats (N=30, age 32 weeks) were randomly assigned to receive vehicle, low-dose liraglutide (75 µg/kg), or high-dose liraglutide (200 µg/kg) daily for 28 days, compared with vehicle-treated male Wistar control rats (N=10).
Spatial learning and memory were evaluated using the Morris water maze test.
Western blot analysis quantified hippocampal expression of PI3K, Akt, p-Akt, AMPK, p-AMPK, mTOR, Beclin-1, LC3-II, caspase-3, Bax, and Bcl-2.
Liraglutide treatment alleviated diabetes-induced learning and memory deficits in GK rats, with the greatest improvement observed in the high-dose group.
Liraglutide restored suppressed autophagy markers (Beclin-1 and LC3-II) and reversed diabetes-induced changes in p-AMPK, PI3K, p-Akt, and mTOR expression.
Treatment modulated apoptosis-related proteins, inhibiting cell death and preserving neuronal function via autophagy activation.

Cite This Study

Yang et al. (2018) studied this question.

synapsesocial.com/papers/6a9880aa1ec081155cd317da https://doi.org/10.3892/mmr.2018.9180

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