Abstract
This study examined for the first time whether bee bread (BB, consisting of monofloral rape bee pollen) could alleviate lipid derangements and reduced bone quality in Zucker diabetic fatty (ZDF) rats, which are considered an appropriate animal model for type 2 diabetes mellitus (T2DM) investigation. Adult ZDF rats were segregated into four groups: lean non-diabetic rats (L group), obese diabetic rats untreated (C group), and those treated with the BB at two doses (500 and 700 mg/kg body weight, respectively, B1 and B2 groups) for 10 weeks. Significantly reduced levels of total cholesterol and triglyceride were recorded in the B2 group versus the C group. In both BB-treated groups, significantly increased relative volume of trabecular bone and trabecular thickness, enhanced density of secondary osteons, accelerated periosteal bone apposition, and improved blood flow were observed. A positive effect of higher dose of BB on femoral weight and cortical bone thickness was also demonstrated. Our results suggest a promising potential of BB to ameliorate T2DM-related complications associated with lipid and bone damages.
Highlights
Type 2 diabetes mellitus (T2DM) represents one of the most frequent public health problems with increasing prevalence worldwide
Decreased value for total cholesterol (TC) was recorded in the B1 group compared with the C group
Our findings related to blood glucose (BG), blood insulin (BI) levels, and total body weight (BW) of Zucker diabetic fatty (ZDF) rats were discussed with published researches focused on bee bread (BB) and obese Zucker diabetic rats
Summary
Type 2 diabetes mellitus (T2DM) represents one of the most frequent public health problems with increasing prevalence worldwide. Hyperlipidaemia is characterised by serum lipids alterations, especially triglyceride (TG) increase and high-density lipoprotein (HDL) cholesterol decrease [4] Another complication associated with T2DM represents diabetic bone disease. Chronic hyperglycaemia causes reduced expression of genes affecting the function of osteoblasts, downregulation of vitamin D receptors, enhanced bone marrow mesenchymal cells differentiation into adipocytes, increased production of advanced glycation end-products (AGEs) inhibiting bone remodelling, and higher oxidative stress [5,6]. All these conditions lead to altered bone morphology and increased risk of fractures
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