Current Issue : January - March Volume : 2018 Issue Number : 1 Articles : 5 Articles
Aims. To explore the differences in salivary BPI fold containing family A, member 1 (BPIFA1) concentration among type 2 diabetes\nmellitus (T2DM) subjects with various severities of chronic periodontitis and to determine whether BPIFA1 in saliva can be used as\na potential biomarker of T2DM. Methods. Unstimulated saliva samples were collected from 44 subjects with T2DM and 44 without\nT2DM (NDM). Additionally, demographic data and general health parameters, including fasting blood glucose (FBG) and body\nmass index (BMI), were collected. We also detected full-mouth clinical periodontal parameters including probing pocket depth\n(PPD), clinical attachment level (CAL), bleeding index (BI), and plaque index (PLI). Salivary BPIFA1, tumor necrosis factor-�±\n(TNF-�±), and interleukin-6 (IL-6) concentrations were also detected. Results. BPIFA1 in saliva was detected at relatively high\nlevels. T2DM subjects had decreased salivary BPIFA1 concentrations (P = 0 031). In T2DM subjects with nonperiodontitis or\nsevere periodontitis, the level of BPIFA1 was significantly lower compared with that of NDM. Salivary TNF-�± concentration\ndisplayed a similar trend to BPIFA1 in the NDM group. Conclusions. BPIFA1 protein is rich in saliva and might be used as a\npotential predictive biomarker of T2DM, especially in patients with severe periodontitis and nonperiodontitis. This trial is\nregistered with ChiCTR-ROC-17010310....
Background. Primary hyperaldosteronism is a known cause for secondary hypertension. In addition to its effect on blood pressure,\naldosterone exhibits proinflammatory actions and plays a role in immunomodulation/development of autoimmunity. Recent\nresearches also suggest significant thyroid dysfunction among patients with hyperaldosteronism, but exact causal relationship is\nnot established. Autoimmune hyperthyroidism (Graves� disease) and primary hyperaldosteronism rarely coexist but underlying\nmechanisms associating the two are still unclear. Case Presentation. A 32-year-old Sri Lankan female was evaluated for new onset\nhypertension in associationwith hypokalemia. She also had features of hyperthyroidism together with high TSHreceptor antibodies\nsuggestive ofGraves� disease.On evaluation of persistent hypokalemia and hypertension, primary hyperaldosteronism due to rightsided\nadrenal adenoma was diagnosed. She was rendered euthyroid with antithyroid drugs followed by right-sided adrenalectomy.\nAntithyroid drugs were continued up to 12 months, after which the patient entered remission of Graves� disease. Conclusion.\nAutoimmune hyperthyroidism and primary hyperaldosteronism rarely coexist and this case report adds to the limited number\nof cases documented in the literature. Underlying mechanism associating the two is still unclear but possibilities of autoimmune\nmechanisms and autoantibodies warrant further evaluation and research....
Background. The aim of this study was to investigate the relationship between metabolic syndrome (MS) and nonalcoholic fatty\nliver disease (NAFLD) in obese children. One hundred and twenty-five subjects aged 11-12 years old participated in the study.\nMethods. Anthropometric and biochemical indices were measured, including lipid and liver profile, blood glucose, serum\ninsulin, and liver ultrasound. Results. Forty-four children (58.6%) were found to have MS. Insulin resistance was present in\n78 (62.4%) children. Patients with MS were more likely to have NAFLD (P < 0 001). Children with NAFLD had significantly\nhigher body mass index, waist circumference, triglycerides, fasting insulin, and lower high-density lipoprotein compared to\npatients with normal livers (P < 0 001). Insulin resistance was significantly higher in children with NAFLD (P < 0 001). Obese\nchildren presenting with MS were 3.01 (2.87ââ?¬â??3.57, P < 0 002) times more likely to develop NAFLD compared to those without\nmetabolic syndrome after adjustment of cofounders. Conclusions. Obese children with MS have a higher risk of developing\nNAFLD. Weight management and early prevention should be the first line of treatment to prevent any possible health issues\nlater on....
Previous in vitro studies demonstrated that aldosterone rapidly activates sodium-hydrogen exchangers 1 and 3 (NHE 1 and 3). In\nvitro investigations revealed that protein kinase C (PKC) regulates NHE properties. We previously demonstrated that aldosterone\nrapidly enhances PKC�± protein abundance in the rat kidney. There are no reports of renal PKC�² (I and II) protein levels related to\nthe regulation by aldosterone. There are also no in vivo data regarding the rapid effects of aldosterone on renal protein levels of NHE\n(1 and 3) and PKC�² (I and II), simultaneously. In the current study, rats received normal saline solution or aldosterone (150 �¼g/kg\nBW, i.p.). After 30 minutes, abundance and immunoreactivity of these proteins were determined by Western blot analysis and\nimmunohistochemistry, respectively. Aldosterone increased NHE1 and NHE3 protein abundance to 152% and 134%,\nrespectively (P < 0 05). PKC�²I protein level was enhanced by 30%, whereas PKC�²II declined slightly. Aldosterone increased\nNHE protein expression mostly in the medulla. PKC�²I immunostaining intensity was increased in the glomeruli, renal\nvasculature, and thin limb of the loop of Henle, while PKC�²II was reduced. This is the first in vivo study to simultaneously\ndemonstrate that aldosterone rapidly elevates PKC�²I and NHE (1 and 3) protein abundance in the rat kidney. Aldosteroneinduced\nNHE (1 and 3) protein levels may be related to PKC�²I activation....
Diabetic polyneuropathy (DPN) is the most frequent and prevalent chronic complication of diabetes mellitus (DM). The state of\npersistent hyperglycemia leads to an increase in the production of cytosolic and mitochondrial reactive oxygen species (ROS)\nand favors deregulation of the antioxidant defenses that are capable of activating diverse metabolic pathways which trigger\nthe presence of nitro-oxidative stress (NOS) and endoplasmic reticulum stress. Hyperglycemia provokes the appearance of\nmicro- and macrovascular complications and favors oxidative damage to the macromolecules (lipids, carbohydrates, and\nproteins) with an increase in products that damage the DNA. Hyperglycemia produces mitochondrial dysfunction with\nderegulation between mitochondrial fission/fusion and regulatory factors. Mitochondrial fission appears early in diabetic\nneuropathy with the ability to facilitate mitochondrial fragmentation. Autophagy is a catabolic process induced by oxidative\nstress that involves the formation of vesicles by the lysosomes. Autophagy protects cells from diverse stress factors and\nroutine deterioration. Clarification of the mechanisms involved in the appearance of complications in DM will facilitate the\nselection of specific therapeutic options based on the mechanisms involved in the metabolic pathways affected. Nowadays, the\nantioxidant agents consumed exogenously form an adjuvant therapeutic alternative in chronic degenerative metabolic\ndiseases, such as DM....
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