Title : Metformin treatment ameliorates diabetes-associated decline in hippocampal neurogenesis and memory via phosphorylation of insulin receptor substrate 1.

Pub. Date : 2018 Jul

PMID : 29988567






3 Functional Relationships(s)
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1 Although chronic therapy with metformin fails to achieve recovery from hyperglycemia, a key feature of diabetes in middle-aged diabetic mice, it improves hippocampal-dependent spatial memory functions accompanied by increased phosphorylation of adenosine monophosphate-activated protein kinase (AMPK), atypical protein kinase C zeta (aPKC zeta), and insulin receptor substrate 1 (IRS1) at selective serine residues in the hippocampus. Metformin protein kinase C, zeta Mus musculus
2 Although chronic therapy with metformin fails to achieve recovery from hyperglycemia, a key feature of diabetes in middle-aged diabetic mice, it improves hippocampal-dependent spatial memory functions accompanied by increased phosphorylation of adenosine monophosphate-activated protein kinase (AMPK), atypical protein kinase C zeta (aPKC zeta), and insulin receptor substrate 1 (IRS1) at selective serine residues in the hippocampus. Metformin protein kinase C, zeta Mus musculus
3 Our findings suggest that signaling networks acting through long-term metformin-stimulated phosphorylation of AMPK, aPKC zeta/lambda, and IRS1 serine sites contribute to neuroprotective effects on hippocampal neurogenesis and cognitive function independent of a hypoglycemic effect. Metformin protein kinase C, zeta Mus musculus