Photobiomodulation in diabetic rats: Effects on morphological, pancreatic parameters, and glucose homeostasis.

Photobiomodulation (PBM) has therapeutic effects on wound healing, diabetic microangiopathy, and retinopathy. However, little is known about the use of PBM for the treatment of diabetes mellitus (DM). In this context, we aimed to evaluate the effects of PBM on pancreas morphology and insulin and glucose tolerance in an experimental model of DM. Thus, DM was induced by streptozotocin (STZ) (60 mg/kg). Subsequently, the rats were treated with PBM (808 nm and 30 J/cm2 ). After euthanasia, morphometric parameters and immunoreactivity for insulin and 8-OHdG were evaluated in the pancreas. The results showed that treated animals had higher values of body mass and higher values in the number of beta cells in the pancreas. In conclusion, PBM resulted in decreased weight loss in STZ-induced diabetic rats and presented a stimulatory effect on the pancreas of the treated animals, highlighting the promising effects of this therapy in the clinical condition of DM.

Effects of photobiomodulation on glucose homeostasis and morphometric parameters in pancreatic islets of diabetic mice.

High-fat diets lead to accumulation of body fat that is associated with the onset of insulin resistance and type II diabetes mellitus. On the other hand, photobiomodulation (PBM) is an electrophysical resource that interacts with cells, stimulating mitochondrial respiration, increasing ATP production, reducing key inflammatory mediators, inhibiting apoptosis, and stimulating angiogenesis. However, little is known about its therapeutic effectiveness on the development of diabetes in diet-induced obese mice. Thus, our aim was to evaluate the effect of PBM applied single point over the pancreas area on glucose homeostasis, insulin expression, and pancreatic morphometric parameters of mice submitted to high-fat diet for 12 weeks. Male mice C57BL6/J were divided into three groups: control group (C), diabetic group (D), and diabetic + PBM (D + PBM). The treatment with PBM started at 9th week and ended in the 12th week, applied 3 × /week. Body mass, fast blood glucose, and glucose and insulin tolerance were evaluated. Immunohistochemistry to detect insulin expression and pancreatic morphometry were also performed. At the end of 12th week, both groups submitted to high-fat diet showed an increase in body mass, adiposity, disturbances on glucose homeostasis, and high insulin expression when compared to the control group. However, mice treated with PBM had more discrete impairments on glucose homeostasis during the glucose tolerance test when compared to untreated D animals. Despite modest, the results were positive and encourage future investigations to explore different doses and duration of PBM to better elucidate its role in obesity-associated type 2 diabetes development.

Cell-to-cell contact dependence and junctional protein content are correlated with in vivo maturation of pancreatic beta cells.

In this study, we investigated the cellular distribution of junctional proteins and the dependence on cell-cell contacts of pancreatic beta cells during animal development. Fetus and newborn rat islets, which display a relatively poor insulin secretory response to glucose, present an immature morphology and cytoarchitecture when compared with young and adult islets that are responsive to glucose. At the perinatal stage, beta cells display a low junctional content of neural cell adhesion molecule (N-CAM), α- and ß-catenins, ZO-1, and F-actin, while a differential distribution of N-CAM and Pan-cadherin was seen in beta cells and nonbeta cells only from young and adult islets. In the absence of intercellular contacts, the glucose-stimulated insulin secretion was completely blocked in adult beta cells, but after reaggregation they partially reestablished the secretory response to glucose. By contrast, neonatal beta cells were poorly responsive to sugar, regardless of whether they were arranged as intact islets or as isolated cells. Interestingly, after 10 days of culturing, neonatal beta cells, known to display increased junctional protein content in vitro, became responsive to glucose and concomitantly dependent on cell-cell contacts. Therefore, our data suggest that the developmental acquisition of an adult-like insulin secretory pattern is paralleled by a dependence on direct cell-cell interactions.

Histomorphology and ultrastructure of pancreatic islet tissue during in vivo maturation of rat pancreas.

In this study, we have investigated the structural and ultrastructural features of pancreatic islet tissue during rat postnatal development. For this purpose, we used neonatal (1-2 days old), young (21 days old) and adult (3-4 months old) rats. From a functional point of view, neonatal islet tissue displayed a relatively poor insulin secretory response to glucose stimulation in comparison with the adult ones. Histological analysis showed that neonatal islet cells display a less organized morphology in comparison with the young and adult ones, characterized by a less defined form and the presence of ductal structures within or nearby the islet. Regarding the islet cytoarchitecture, no differences were observed among all animal groups studied. B-cells were always typically detected within the islet core while A-cells occupied the islet periphery area. No marked differences were found during postnatal animal development regarding the ultrastructural aspect of the endocrine cells and their secretory granules. Nevertheless, quantitative analysis showed a lower B-cell/non-B-cell ratio, a higher association with ducts and an increased immunoreaction for proliferating cell nuclear antigen (PCNA) in neonatal islets as compared to young and adults. In conclusion, the acquisition of an adult pattern of insulin secretion may require an appropriate histoarchitecture and B-cell/non-B-cell proportion that may affect crucial regulatory events such as the paracrine and/or the cell-cell interaction or communication within the islet.