Rosemary extract increases neuronal cell glucose uptake and activates AMPK

Glucose is the primary metabolic substrate of neurons and is responsible for supporting many vital functions including neuronal signalling. Decreases in glucose uptake and utilization are common characteristics of dementia, particularly Alzheimer's disease, and thus agents that can restore neuronal glucose availability may be especially valuable to the field. Diets rich in antioxidants and polyphenols have been associated with reductions in the risk of chronic disease that are associated with aging. In previous studies, rosemary extract (RE) has been reported to have antioxidant, anti-inflammatory, anticancer, and antidiabetic properties. The purpose of the present study was to explore the effects of RE on neuronal glucose uptake. Human SH-SY5Y neuroblastoma cells exposed to varied concentrations of RE showed a dose-dependent increase in glucose uptake, with a significant increase observed following treatment with 5 mu g/mL RE for 2 h (159% +/- 20.81% of control) that was comparable to maximum insulin stimulation (135.6% +/- 3.2% of control). This increase in glucose uptake was paralleled by increases in AMP-activated protein kinase (AMPK), but not Akt, phosphorylationiactivation. The present study is the first to report that treatment with rosemary extract can stimulate glucose uptake in a neuronal cell line. These results demonstrate the potential of RE to be used as an agent to regulate neuronal glucose homeostasis. Novelty: RE increases neuronal glucose uptake. RE activates AMPK in neurons. RE increases neuronal glucose uptake independently of insulin signalling.

Automated summary

Glucose is the primary metabolic substrate of neurons, and a decrease in glucose uptake is common in dementia. This study found that rosemary extract (RE) can increase neuronal glucose uptake, activate AMP-activated protein kinase (AMPK), and independently regulate glucose uptake in neurons.