A brief review of vitamin D as a potential target for the regulation of blood glucose and inflammation in diabetes-associated periodontitis.

Diabetes is a metabolic disorder associated with various complications, including periodontitis. The risk of periodontitis is increased in patients with diabetes, while vitamin D deficiency is associated with both diabetes and periodontitis. Thus, there is a need to identify the molecular effects of vitamin D on the regulation of inflammation and glucose in diabetes-associated periodontitis. The Web of Science, Scopus, and PubMed databases were searched for studies of the molecular effects of vitamin D. Molecular effects were reportedly mediated by salivary secretions, interactions of advanced glycation end products (AGEs) with receptors of AGEs (RAGEs), cytokines, and oxidative stress pathways linking diabetes with periodontitis. Vitamin D supplementation attenuates inflammation in diabetes-associated periodontitis by reducing the levels of inflammatory cytokines and numbers of immune cells; it also has antibacterial effects. Vitamin D reduces cytokine levels through regulation of the extracellular signal-related kinase 1/2 and Toll-like receptor 1/2 pathways, along with the suppression of interleukin expression. Glucose homeostasis is altered in diabetes either because of reduced insulin production or decreased insulin sensitivity. These vitamin D-related alterations of glucoregulatory factors may contribute to hyperglycaemia; hyperglycaemia may also lead to alterations of glucoregulatory factors. This review discusses the pathways involved in glucose regulation and effects of vitamin D supplementation on glucose regulation. Further studies are needed to characterise the effects of vitamin D on diabetes-associated periodontitis.

Protective effect of Celastrus paniculatus on cognitive function in glutamate-induced brain-injured mice by reducing the intracellular influx of Ca.

Present investigation evaluates the protective effect of Celastrus paniculatus (CP) on the cognitive function in neuronal injured mice. Neuronal injury was induced by oral administration of monosodium glutamate (MSG) at a dose of 1.66 g/kg/day for 30 days. Mice in the CP-treated group receives CP 30 mg/kg ip and CP + GGA-treated group received CP 30 mg/kg ip and glutamic acid (GGA, 1.5 mg/kg, ip) 30 min prior to the administration of MSG for 30 days. Assessment of cognitive function was done using Morris water maze. Level of inflammatory cytokines and production of reactive oxygen species (ROS) was estimated in the brain tissue of brain-injured mice. Moreover, intracellular concentration of Ca+ ion was estimated in the brain tissue and expression of Bcl-2, Bax, and caspase-3 protein was estimated in the brain tissue by western blot assay. Cognitive function was attenuated in CP-treated glutamate-injured mice. Data of the study suggest that treatment with CP reduces the level of inflammatory cytokines and production of ROS in the brain tissue compared to negative control group. There was reduction in the concentration of Ca+ ion in the neuronal cells in CP-treated group than negative control group of mice. Treatment with CP ameliorates the expression of Bax, Bcl-2, and caspase-3 in the brain tissue of glutamate-induced brain-injured mice. In conclusion, data of the study suggest that treatment with CP attenuates the cognitive function and neuronal apoptosis in glutamate-induced neuronal injury by reducing the concentration of intracellular Ca+ ion.

Is Regular Probiotic Practice Safe for Management of Sepsis?

For decades, the gut has been thought to play an important role in sepsis pathogenesis. Sepsis is a serious life-threatening, chronic condition of an infection caused by dysregulated host immune response in most of the intensive care unit patients. Probiotics have dual roles in polymicrobial sepsis i.e. probiotics may induce sepsis in many cases and may prevent its prognosis in many cases. Experimental evidence from both pre-clinical and clinical studies have demonstrated that probiotic therapy ameliorates various inflammatory mediators such as tumor necrosis factor, interleukin-10 (IL-10), IL-6, etc., in septicemia. In addition, probiotic use was also found to reduce the severity of pathological conditions associated with irritable bowel disorder and prevent development of endocarditis in septicemia. On contrary, probiotic therapy in neonatal and athymic adult mice fail to provide any beneficial effects on mortality and sepsis-induced inflammation. Importantly, in few clinical trials probiotic use was found to aggravate sepsis by promoting inflammatory cascade rather than suppressing it. This review discusses various studies regarding the beneficial or harmful effects associated with probiotic therapy in sepsis.

Influence of Musa sapientum L. on pharmacokinetic of metformin in diabetic gastroparesis.

OBJECTIVE: To investigate the effect of Musa sapientum L. (MS) bark juice in diabetic gastroparesis and its effect on pharmacokinetic of metformin (MET). METHODS: Diabetes was induced in rats by administering alloxan (120 mg/kg) saline solution and maintained for 8 week. All the 18 Sprague-Dawley rats were divided into three groups (n =6 in each group): normal control, diabetic control and MS bark juice. Assessment of diabetes was done by glucose oxidase-peroxidase method on the 3rd day of alloxan administration. The effects of MS bark juice (100 mL/kg) on gastric emptying time, intestinal transit time, contractility of fundus and pylorus as well as gastric acid secretion in chronic diabetic rats were observed after 8 weeks of alloxan administration. The effect of MS bark juice on the pharmacokinetic of orally administered single dose of MET (350 mg/kg) was evaluated on the 57th day of protocol. Any drugs that may reduce the blood glucose level or influence the fibrinolytic system were not used in this study. RESULTS: The MS bark juice significantly reduced the blood glucose level in the diabetic rats (P<0.01). There was significant decrease in the pylorus motility and increase in the gastric emptying time, intestinal transit time, contractility of fundus, gastric acid secretion in the MS bark juice treated group (P<0.01). There was significant decrease in the time at which drug at a maximum concentration, half life of drug and increase in the maximum concentration of drug in the plasma of MET in MS bark juice treated group as compared to diabetic control group (P<0.01). CONCLUSION: MS bark juice effectively manages diabetic gastroparesis and thereby improves the bioavailabilty of MET when administered with MS bark juice.