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Several studies have confirmed a decrease in the quality and quantity of milk of mothers with diabetes during lactation. However, it remains unclear how maternal diabetes affects the offspring specifically during lactation. The aim of this study was to evaluate body and mandibular growth and tooth eruption in pups suckling from diabetic dams. The study was performed on 13 Wistar rat pups that were born to dams that were subjected to experimental diabetes on the day of parturition. Body weight and body size were recorded regularly throughout the study. The experimental pups and a group of eight age-matched pups suckling from nondiabetic dams were killed at weaning. Both hemimandibles were excised and fixed. Right hemimandibles were radiographed to assess mandibular growth and tooth eruption. The left hemimandibles were processed to obtain buccolingually oriented sections at the level of the first mesial root of the first lower molar. Histologic and histomorphometric studies were performed. Results showed that body weight and body size were significantly lower in experimental animals at weaning compared with their age-matched controls. Smaller mandible size and reduced tooth eruption in experimental animals compared with controls were observed. The length, width, and bone volume of the developing alveolus were reduced in experimental animals compared with controls. The results obtained in this study allow the conclusion that suckling from diabetic dams results in reduced body, mandible size, and tooth eruption of the pups at weaning. Diabetes encompasses a group of metabolic diseases characterized by hyperglycemia, which results from decreased insulin secretion, from functional deficiency of insulin action, or both. Diabetes-associated chronic hyperglycemia causes dysfunction, long-term damage, and failure of several body organs (1).When a mother has diabetes, the alterations in maternal metabolism cause damage to the offspring, not only during gestation but also during lactation. Alterations in maternal metabolism during gestation are responsible for fetal macrosomia and congenital malformations, among other consequences (2,3). There are reports of the long-term effects of neonatal breastfeeding in children of mothers with pregestational diabetes during pregnancy (4). It may result in an increased risk for becoming overweight and developing impaired glucose tolerance during childhood. Moreover, diabetic dams have decreased yield and altered composition of the milk (5-9). Alterations in maternal metabolism caused by diabetes during lactation may affect the offspring specifically when the known effects that maternal diabetes has on their pups during pregnancy are excluded. Thus, the first aim of this study was to measure the effect of reduced milk quality and quantity on body size and weight of the pups of dams that were rendered diabetic before lactation.Tooth eruption is a complex process in developmental biology and is yet to be fully understood. Tooth and periodontal development are two major events associated ...

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Little is known about the early response of bone metabolism to hyperglycemia, or transient hyperglycemia, caused by poor compliance with treatment or inadequate control of diabetes in patients with type 1 diabetes. There are no studies comparing early diabetes-related alterations in endochondral ossification with those occurring through time. In order to histomorphometrically evaluate the growth cartilage and subchondral bone of male Wistar rat tibia shortly after experimentally inducing type 1 diabetes, thirty-five male Wistar rats were divided into 5 groups: Group A: control; Group B: induction of diabetes; euthanasia at one week; Group C: induction of diabetes plus insulin treatment; euthanasia at one week; Group D: induction of diabetes; euthanasia at six weeks; Group E: induction of diabetes plus insulin treatment; euthanasia at six weeks. Diabetes was induced by single intraperitoneal injection of 60mg/kg body weight of streptozotocin dissolved in citrate buffer pH 4.0. Two days after inducing diabetes, treatment with subcutaneously injected human insulin was initiated, according to protocol. The following parameters were evaluated: Tibial subchondral bone volume; trabecular area; bone surface; trabecular number; trabecular thickness. Tibial subchondral bone volume and epiphyseal cartilage width were significantly lower in both experimental groups as compared to controls. Insulin treatment resulted in values similar to controls. As shown by the microarchitecture of subchondral trabecular bone, all parameters were lower in diabetic animals, except for trabecular width which was similar to that observed in controls. The alteration in bone metabolism manifests in long bones very early in the course of diabetes, suggesting it would be advisable to analyze bone response as soon as possible following diagnosis of the disease, in order to prescribe treatments aimed at preventing further alterations in bone architecture.

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