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Diabetic osteoporosis (DOP) is one of the complications of diabetes, with high morbidity, and high disability rate. Here, we established a diabetic rat model and administered lycopene to observe its effect on DOP. Our results showed that ten weeks lycopene treatment lowered blood glucose, improved diabetic induced polydipsia, overeating and body weight loss. Lycopene treatment also enhanced bone mineral density, restored bone mechanical and bone Micro-CT parameters of diabetic rats. Subsequently, lycopene decreased serum inflammatory cytokines levels and increased serum anti-oxidant indicators levels. Moreover, lycopene reduced the number of bone marrow adipocytes, and osteoclasts numbers of diabetic rats. The serum bone turnover markers levels were down-regulated after lycopene treatment. Meanwhile, the bone and serum OPG, RUNX 2 expression levels were up-regulated by lycopene in diabetic rats, and the OPG/RANKL ratio was also up-regulated. This study showed that lycopene could ameliorate diabetic induced bone loss via anti-inflammatory, anti-oxidation, and increasing OPG/RANKL ratio in diabetic rats. Lycopene could be used for nutritional intervention in patients with diabetic osteoporosis.

Salidroside from Rhodiola rosea L. has hypoglycemic effects, and has anti-osteoporosis effect in diabetic rats. Whether it has beneficial effects on diabetic nephropathy (DN) has not been fully reported. Here, a DN rat model was established by streptozotocin (STZ). Salidroside (10, and 20 mg kg−1 d−1) were orally giving for eight weeks. The purity of salidroside was 99%. The results showed that eight weeks salidroside supplementation dose-dependently decreased blood glucose, serum insulin, serum creatinine, blood urea nitrogen (BUN), as well as urinary albumin of DN rats, repaired the pathological changes of kidney tissue, the renal sclerosis and fibrosis in the kidney of DN rats were improved, and the activities of oxidative defense system associated enzyme such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) were also improved. Serum inflammatory cytokines (including tumor necrosis factor-α, monocyte chemoattractant protein-1, interleukin-1β, and interleukin-6) were decreased significantly in DN rats after eight weeks salidroside supplementation. Immunohistochemical results showed that fibrosis related proteins such as transforming growth factor-β1 (TGF-β1), phospho-Smad2 (p-Smad2), and phospho-Smad3 (p-Smad3) expression levels were decreased significantly in the kidney of salidroside treated group. Our results indicate that daily salidroside consumption could alleviate DN in rats, the main mechanisms are anti-inflammatory, anti-oxidative stress, and inhibition of the TGF-β1/Smad2/3 pathway. This study suggested that salidroside could be used as a nutrient against DN, as well as diabetes.

Hyperglycemia, increased inflammation, and mitochondrial dysfunction in diabetes may eventually cause kidney damage. Black rice cyanidin-3-glucoside has anti-hyperglycemic and anti-osteoporosis effects. Whether it has preventive effects on renal dysfunction in diabetes has not been reported. In this study, a rat model of diabetic nephropathy was established, and cyanidin-3-glucoside was administered for 56 days, lisinopril was administered as the positive control. The research found that black rice cyanidin-3-glucoside supplementation decreased glucose, prevented insulin resistance, repaired kidney function of diabetic rats, prevented renal interstitial fibrosis, glomerulosclerosis, and oxidative stress of diabetic rats. The inflammatory cytokines were significantly reduced in cyanidin-3-glucoside treated group. The renal Nrf2 mRNA level was evaluated, renal TNF-α mRNA, and NF-κΒ mRNA expression levels was decreased in cyanidin-3-glucoside treated group. Immunohistochemical results showed that cyanidin-3-glucoside inhibited transforming growth factor-β1 (TGF-β1), phosphorylated Smad2 (p-Smad2), phosphorylated Smad3 (p-Smad3), type IV collagen, fibronetin, and laminin expression in the kidney of diabetic rats. Our results indicate cyanidin-3-glucoside can protect against diabetic nephropathy in rats; it is mainly attributed to its anti-insulin resistance, anti-oxidative stress, anti-inflammation, as well as inhibit TGF-β1/p-Smads expression and extracellular matrix (ECM) aggregation.