Bifidobacterium longum (B. longum) could accumulate Selenium (Se) and nano-Se in the form of Se-B. longum and Nano-Se-B. longum, respectively. In this study, the effect of Nano-Se-B. longum in diabetic mice was evaluated. Physiological and metabolic parameters such as blood glucose, body weight, serum insulin level, intraperitoneal glucose tolerance test (IPGTT), food intake, water consumption and urine output were evaluated. The expression of insulin signalling pathway-related proteins was evaluated by western blotting. Haematoxylin and eosin (H&E) was used for histological examination of the liver, pancreas and kidney sections. Creatinine levels in serum (SCr) and blood urea nitrogen (BUN) were measured. Nano-Se-B. longum was the best in terms of delaying the onset of diabetes. Nano-Se-B. longum decreased blood glucose and body weight compared with those noted for the model group. IPGTT, food intake, water consumption and urine output significantly increased and serum insulin levels significantly decreased in the model group compared with those in all the Nano-Se-B. longum-treated mice. Histological results showed that the Nano-Se-B. longum-treated mice were better than the model group mice in terms of pathological changes. The expression of insulin signalling pathway-related proteins was upregulated in the Nano-Se-B. longum-treated groups. A significant increase in SCr and BUN levels was noted in the model group. This study for the first time reported the dose-dependent preventive effect of Nano-Se-B. longum on the onset of diabetes and renal damage. The mechanism may be related to changes in insulin signalling.

OBJECTIVE: Acetaldehyde dehydrogenase 2 (ALDH2) was reported for its protective properties on myocardial damage, stroke and neurodegeneration disease, but the effects and mechanisms of ALDH2 in the modulation of diabetic retinopathy remain unclear. The present study evaluated the protection effects of ALDH2 on streptozocin (STZ)-induced aged diabetic rats retinas damage.
METHODS: 24 aged male diabetic Sprague-Dawley (SD) rats induced by a single intraperitoneal injection of STZ were randomly divided into Alda1-treated group and dimethylsulfoxide (DMSO) group. Rats were intraperitoneally injected with 10 mg/kg ALDH2 activator Alda1 (or DMSO) 3 days before STZ injection and 30 days afterwards. A series of detections on retinal structural, functional and molecular levels were applied at 1 d, 7 d and 30 d after aged diabetic rats model established.
RESULTS: Optical coherence tomography (OCT) revealed that the thickness of outer nuclear layer (ONL) and whole retinas in Alda1-treated group were thicker than DMSO group. Full field electroretinograms (ffERG) showed a higher amplitude wave (dark-adaptation 3.0 and OPs) in Alda1-treated group. In addition, the levels of retinal tumor necrosis factor (TNF-α) and interleukin-6 (IL-6) from Alda1-treated group were lower whereas superoxide dismutase (SOD) activity was notably higher. Moreover, the expressions of ALDH2, silence information regulation factor 2 related enzyme I (Sirt1) and nuclear factor erythroid 2-related factor 2 (Nrf2) in Alda1-treated group retinas were significantly increased, while the expression of vascular endothelial growth factor (VEGF-α) was dramatically decreased.
CONCLUSIONS: ALDH2 could ameliorate early-stage STZ-induced aged diabetic rats retinas damage possibly via increasing Sirt1 and Nrf2 expression.

Myostatin (MSTN) is not only a key negative regulator of skeletal muscle secretion, however is also an endocrine factor that is transmitted to bone. To investigate the effect and possible mechanism of weight-bearing treadmill running on bone with poorly controlled Type 1 diabetes, rats were randomly divided into three groups: Normal control (NC), diabetic mellitus (DM) and diabetic exercise training groups (DM-WTR). The DM-WTR rats were trained with weight-bearing running. The results demonstrated that the levels of serum insulin, body weight, bone mass, muscle mass, grip strength, and serum calcium in the DM-WTR rats were significantly increased, whereas the levels of blood glucose, alkaline phosphatase, and tartrate-resistant acid phosphatase were markedly reduced in the DM-WTR rats compared with the DM rats. Weight-bearing running inhibited streptozocin (STZ)-induced MSTN mRNA and protein expression in the diabetic rats. The mRNA and protein expression levels of activin type IIB receptor and mothers against decapentaplegic homolog 2/3 and its phosphorylation in femur DM-WTR rats were reduced compared with DM rats. In addition, weight-bearing running enhanced the STZ-induced Wnt and β-catenin expression levels and reduced the STZ-induced glycogen synthase kinase (GSK)-3β expression in diabetic rats\' femora. In conclusion, the results suggested that weight-bearing running could partially ameliorate STZ-induced femur atrophy via MSTN downregulation, and this may be associated with the inactivation of Activin A Receptor Type 2B/Smad2/3 signaling pathways and the activation of the Wnt/GSK3β/β-catenin signaling pathway. Further studies are needed to verify these conclusions.