Therapeutic interventions to reduce the risk of progression from prediabetes to type 2 diabetes mellitus

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Type-2 diabetes mellitus and the frequency of the G22A polymorphism of the adenosine deaminase gene in a mixed population in Brazil

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Heart rate variability in children with type 1 diabetes mellitus

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Avaliação da expressão gênica e de lesões no DNA de índividuos portadores de diabetes mellitus tipo 2, dislipidemia e periodontite crônica

Pós-graduação em Odontologia - FOAR

Diabetes Mellitus em cães e suas complicações

Diabetes mellitus is one of the most common endocrinopathies among dogs characterized by hyperglycemia and if not treated properly can be fatal. It occurs by an absolute or relative insulin deficiency, which alters the metabolism of carbohydrates, lipids and proteins Complications such as cataracts, recurrent infections, pancreatitis and ketoacidosis can arise with the development of the disease. Recognizing these will help the diagnosis, once in some dogs it is not always detected the classical signs of polyuria, polydipsia, polyphagia and weight loss

Terapia do diabetes mellitus em cães

Diabetes Mellitus is caracterized by a disturbance on endocrine pâncreas with reduction in serum levels of insulin. The deficiency or absence of insulin promotes alterations in the metabolism of carbohydrates, lipidis and proteins. The most common clinical signs of disease are polyuria, polydipsia, polyphagia and loses of weight. The diagnosis is made based on clinical symptoms, with laboratory confirmation through persistent hyperglycemia on fasting and glycosuria. Treatment includes insulin therapy, diet, exercise and oral hypoglycemic agents in an attempt to reverse the catabolic effects associated with deficiency or antagonism of insulin and restore normal homeostasis of the metabolism of proteins, lipids and carbohydrates

Avaliação da expressão gênica em pacientes com Diabetes Mellitus tipo 2

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Angiotensin converting enzyme polymorphism in type 2 diabetes mellitus

This study was undertaken to assess the frequency of angiotensin converting enzyme (ACE) insertion/deletion (I/D) polymorphism in patients with type 2 diabetes mellitus. A total of 162 patients with type 2 diabetes and 160 individuals without this disease were analyzed. From the diabetes group, 81 patients with cardiovascular risk (according to American Diabetes Association parameters) were selected to form another subgroup. For polymorphism identification, two polymerase chain reactions were performed: one reaction to identify all genotypes and a second one to confirm the presence of the I allele. The observed genotype frequencies were as follows: diabetes group I/I (19.1%), I/D (52.5%), D/D (28.4%); control group I/I (12.5%), I/D (55.6%), D/D (31.9%); and diabetes with cardiovascular risk group I/I (16.0%), I/ D (59.3%), D/D (24.7%). No statistically significant difference was observed between the allelic and genotypic frequencies in the analyzed groups. Previous studies reported an association between the D allele and type 2 diabetes in Caucasian and East Asian populations. However, in mixed populations, such as those found in Brazil, such an association was not found. This fact does not discard the need for more studies on the frequencies of this polymorphism in the Brazilian population and the associations with risk factors, which can compromise the quality of life of diabetes patients

Dinâmica linear e não linear da variabilidade da frequência cardíaca: sensibilidade, especificidade, valor preditivo e correlação de características físicas e clínicas no Diabetes Mellitus tipo 1

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Doença periodontal em pacientes com Diabetes Mellitus: influência de polimorfismos genéticos?

Currently it is clear that there are several factors that can act as modifiers of diseases, without causing them directly, but having the potential to make these conditions to progress faster and more severe. There is a growing number of studies investigating the relationship between Diabetes Mellitus (DM) and Periodontal Disease (PD), including some studies focusing on the influence of genetic factors in this process. The aim of this study was to verify through a literature review, the influence of genetic polymorphisms in the development of PD in patients with DM. PubMed and BIREME were used as databases and the terms Periodontitis or Periodontal Disease, Polymorphism, Diabetes Mellitus were searched. After a refinement in the literature, five studies were selected and they were related to chronic PD with DM and polymorphisms in cytokine genes, especially interleukin 1 (IL1) e IL6. Polymorphisms were associated with a higher concentration of pro-inflammatory cytokines in the gingival crevicular fluid of diabetic patients when compared to non-diabetic. In conclusion, it is necessary to confirm this association with longitudinal studies that must investigate a larger number of cytokine genes in order to understand the cause-effect relationship between genetic polymorphisms, DM and PD.

Periodontal disease-associated compensatory expression of osteoprotegerin is lost in type 1 diabetes mellitus and correlates with alveolar bone destruction by regulating osteoclastogenesis

Alveolar bone resorption results from the inflammatory response to periodontal pathogens. Systemic diseases that affect the host response, such as type 1 diabetes mellitus (DM1), can potentiate the severity of periodontal disease (PD) and accelerate bone resorption. However, the biological mechanisms by which DM1 modulates PD are not fully understood. The aim of this study was to determine the influence of DM1 on alveolar bone resorption and to evaluate the role of receptor activator of nuclear factor-kappaB ligand (RANKL)/osteoprotegerin (OPG) in osteoclastogenesis in rats. PD was induced by means of ligature in nondiabetic and in streptozotocyn-induced DM1 rats. Morphological and morphometric analyses, stereology and osteoclast counting were performed. RANKL and OPG mRNA levels, protein content, and location were determined. PD caused alveolar bone resorption, increased the number of osteoclasts in the alveolar bone crest and also promoted changes in RANKL/OPG mRNA expression. DM1 alone showed alveolar bone destruction and an increased number of osteoclasts at the periapical and furcal regions. DM1 exacerbated these characteristics, with a greater impact on bone structure, resulting in a low OPG content and a higher RANKL/OPG ratio, which correlated with prominent osteoclastogenesis. This work demonstrates that the effects of PD and DM1 enhance bone destruction, confirms the importance of the RANKL signaling pathway in bone destruction in DM1 in animal models and suggests the existence of alternative mechanisms potentiating bone degradation in PD.

Prevalence of Candida spp. during radiographic examination in Diabetes mellitus patients

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)