Periodontal conditions, oral Candida albicans and salivary proteins in type 2 diabetic subjects with emphasis on gender

<p>Abstract</p> <p>Background</p> <p>The association between periodontal conditions, oral yeast colonisation and salivary proteins in subjects with type 2 diabetes (T2D) is not yet documented. The present study aimed to assess the relationship between these variables in type 2 diabetic subjects with reference to gender.</p> <p>Methods</p> <p>Fifty-eight type 2 diabetic subjects (23 males and 35 females) with random blood glucose level ≥ 11.1 mmol/L were investigated. Periodontal conditions (plaque index [PI], bleeding on probing [BOP], probing pocket depth [PD] (4 to 6 mm and ≥ 6 mm), oral yeasts, salivary immunoglobulin (Ig) A, IgG and total protein concentrations, and number of present teeth were determined.</p> <p>Results</p> <p>Periodontal conditions (PI [<it>p </it>< 0.00001], BOP [<it>p </it>< 0.01] and PD of 4 to 6 mm [<it>p </it>< 0.001], salivary IgG (μg)/mg protein (<it>p </it>< 0.001) and salivary total protein concentrations (<it>p </it>< 0.05) were higher in type 2 diabetic females with <it>Candida albicans </it>(<it>C. albicans</it>) colonisation compared to males in the same group. Type 2 diabetic females with <it>C. albicans </it>colonisation had more teeth compared to males in the same group (<it>p </it>< 0.0001).</p> <p>Conclusion</p> <p>Clinical and salivary parameters of periodontal inflammation (BOP and IgG (μg)/mg protein) were higher in type 2 diabetic females with oral <it>C. albicans </it>colonisation compared to males in the same group. Further studies are warranted to evaluate the association of gender with these variables in subjects with T2D.</p

Leptin: a review of its peripheral actions and interactions

Following the discovery of leptin in 1994, the scientific and clinical communities have held great hope that manipulation of the leptin axis may lead to the successful treatment of obesity. This hope is not yet dashed; however the role of the leptin axis is now being shown to be ever more complex than was first envisaged. It is now well established that leptin interacts with pathways in the central nervous system and through direct peripheral mechanisms. In this review, we consider the tissues in which leptin is synthesized and the mechanisms which mediate leptin synthesis, the structure of leptin and the knowledge gained from cloning leptin genes in aiding our understanding of the role of leptin in the periphery. The discoveries of expression of leptin receptor isotypes in a wide range of tissues in the body have encouraged investigation of leptin interactions in the periphery. Many of these interactions appear to be direct, however many are also centrally mediated. Discovery of the relative importance of the centrally mediated and peripheral interactions of leptin under different physiological states and the variations between species is beginning to show the complexity of the leptin axis. Leptin appears to have a range of roles as a growth factor in a range of cell types: as be a mediator of energy expenditure; as a permissive factor for puberty; as a signal of metabolic status and modulation between the foetus and the maternal metabolism; and perhaps importantly in all of these interactions, to also interact with other hormonal mediators and regulators of energy status and metabolism such as insulin, glucagon, the insulin-like growth factors, growth hormone and glucocorticoids. Surely, more interactions are yet to be discovered. Leptin appears to act as an endocrine and a paracrine factor and perhaps also as an autocrine factor. Although the complexity of the leptin axis indicates that it is unlikely that effective treatments for obesity will be simply derived, our improving knowledge and understanding of these complex interactions may point the way to the underlying physiology which predisposes some individuals to apparently unregulated weight gain