The purpose of the present study was to evaluate the impact of long-term honey ingestionon metabolic disorders and neurodegeneration in mice fed a high-fat diet (HFD). Three groups of micewere fed with a standard diet (STD), HFD or HFD supplemented with honey (HFD-H) for 16 weeks.Biochemical, histological, Western blotting, RT-PCR and Profiler PCR array were performed toassess metabolic parameters, peripheral and central insulin resistance and neurodegeneration. Dailyhoney intake prevented the HFD-induced glucose dysmetabolism. In fact, it reduced plasma fastingglucose, insulin and leptin concentrations and increased adiponectin levels. It improved glucosetolerance, insulin sensitivity and HOMA index without affecting plasma lipid concentration. HFDmice showed a significantly higher number of apoptotic nuclei in the superficial and deep cerebralcortex, upregulation of Fas-L, Bim and P27 (neuronal pro-apoptotic markers) and downregulationof Bcl-2 and BDNF (anti-apoptotic factors) in comparison with STD- and HFD-H mice, providingevidence for honey neuroprotective effects. PCR-array analysis showed that long-term honey intakeincreased the expression of genes involved in insulin sensitivity and decreased genes involvedin neuroinflammation or lipogenesis, suggesting improvement of central insulin resistance. Theexpressions of p-AKT and p-GSK3 in HFD-H mice, which were decreased and increased, respectively,in HFD mouse brain, index of central insulin resistance, were similar to STD animals supporting theability of regular honey intake to protect brain neurons from insulin resistance. In conclusion, thepresent results provide evidence for the beneficial preventative impact of regular honey ingestion onneuronal damage caused by HFD.
|Number of pages||14|
|Publication status||Published - 2022|
- Food Science
- Nutrition and Dietetics