Sweeteners and beta-glucans improve metabolic and anthropometrics variables in well controlled type 2 diabetic patients.

UNLABELLED: The introduction of fat and carbohydrates replacers has been a revolutionary advance in treating obesity and diabetes mellitus. Since these materials have shown to have beneficial effects on the metabolic profiles of diabetic patients, they should be useful in designing specific foods for patients with diabetes. OBJECTIVE: To compare metabolic and anthropometric improvements elicited by a diet based on the American Diabetic Association's nutrition recommendations with a modified, low-energy diet incorporating fat replacers and non-sucrose sweeteners. DESIGN: A total of 16 male, well controlled type 2 diabetes patients were divided into two groups of eight; one group received the diet based on the American Diabetic Association's nutrition recommendations, and the other was fed a modified, low-calorie diet containing a fat replacer (beta-glucans derived from oats) and the sweeteners, sucralose and fructose. Both groups were maintained on their respective diets for 4 weeks. All patients performed daily aerobic exercise consisting of walking for 60 minutes. Body weight, body mass index, basal glycemia, hemoglobin HbA1C, and lipid profile were determined in each patient before starting the diets and after 4 weeks of dietary intervention. RESULTS: Both diets produced significant improvements in weight, body mass index, lipid profile, basal glucose, and HbA1C. However, the experimental diet was superior to the American Diabetic Association's diet in improving metabolic and anthropometric profile: greater increase in HDL cholesterol and larger decreases in HbA1C, weight, and body mass index. CONCLUSIONS: A diet incorporating a fat replacer and non-sucrose sweeteners produced a greater improvement in metabolic and anthropometric variables in well controlled type 2 diabetic patients when compared with a diet based on American Diabetic Association's nutrition recommendations.

Increased serum malondialdehyde and decreased nitric oxide within 24 hours of thrombotic stroke onset.

BACKGROUND AND PURPOSE: Ischemia/reperfusion generates free oxygen radicals, which react with the unsaturated lipids of biomembranes resulting in the generation products such as malondialdehyde. Malondialdehyde could be a sensor for tissue damage and reperfusion. Nitric oxide, released due to the early arrival of leukocytes in the brain parenchyma, could be a sensor for nonflow phenomenon. Thereby, the purpose of this research was to evaluate the behavior of malondialdehyde and nitric oxide within the 24 hours after the stroke onset. METHODS: Fifteen patients up to an age of 49 years, admitted to the emergency of University Hospital and Chiquinquirá Hospital in Maracaibo, Venezuela, were examined by a neurologist and underwent 12-lead electrocardiograms and computed tomography for the diagnosis of thrombotic stroke. Serum malondialdehyde and nitric oxide were measured as thiobarbituric acid adducts and total nitrites. Data were collected within the 24 hours after the stroke onset. RESULTS: Malondialdehyde for patients with stroke had a significant increase (P<0.001) when compared with healthy controls (47.9 +/- 7.1 vs. 1.7 +/- 0.2 micromol/L). Conversely, serum nitric oxide for patients with stroke had a significant decrease (P<0.001) when compared with the control group (14.5 +/- 1.4 vs. 41.3 +/- 3.7 micromol/L). The lowest values of malondialdehyde and the highest values of nitric oxide were observed in two patients, who died. CONCLUSIONS: Serum levels of malondialdehyde increase, and serum levels of nitric oxide diminish within 24 hours after the onset of thrombotic stroke onset. This suggests that serum malondialdehyde level could be used as potentially reliable and sensitive marker for reperfusion, whereas nitric oxide levels could acts as potential biochemical sensor for nonreflow phenomenon.

Trimetazidine diminishes fasting glucose in rats with fasting hyperglycemia: a preliminary study.

Trimetazidine is a drug with cardioprotective properties used in coronary artery disease. Its effect has been attributed to the inhibition of the long chain fatty acids intramitochondrial transport via carnitine-palmitoyl-transferase-1. Clinical evidence supports the possibility that trimetazidine is able to improve the fasting glycemia in diabetic patients. For this reason, the objective of the present study was to determine the effect of trimetazidine on serum glucose of Sprague-Dawley rats with fasting hyperglycemia. All animals received water and food "ad libitum." Blood glucose was measured weekly to confirm fasting hyperglycemia in rats. The rats were treated for 1 month with trimetazidine (1 mg/kg), and blood samples were collected (in the fasting period) on the last day of treatment (the 30th day); and then on the 15th day posttreatment, measurements of plasma glucose were taken. Fasting plasma levels after 30 days of trimetazidine administration decreased significantly from 141.2 +/- 3.3 mg/dL (pre-drug) to 120.9 +/- 5.8 mg/dL (P<0.01). 15 days after the end of treatment, fasting plasma glucose levels (137.0 +/- 7.0 mg/dL) were close to the pretreatment levels but significantly different (P<0.05) from levels on day 30 of treatment. These data suggest that trimetazidine improved blood glucose utilization in rats with fasting hyperglycemia.

Enfermedad periodontal como factor de riesgo para la aterosclerosis / Periodontal disease with risk factor for the atherosclerosis

La asociación entre enfermedad periodontal y la aterosclerosis ha sido sustentada gracias a varios postulados en los cuales proceso inflamatorio característico de ambas entidades pudiera ser el nexo que explique por que es frecuente que estas patologías compartan rasgos patogénicos, clínicos, y fisiopatológicos. La asociación propuesta entre ambas está ligada a los efectos sistémicos de los lipopolisacáridos bacterianos liberados en el sitio de inflamación periodontal viajando por vía circulatoria para anclarse en el sub-endotelio de la íntima lo cual conduce a la sobre-expresión de moléculas de adherencia por parte de la célula endotelial, permitiendo la fijación y la entrada de monocitos al sub-endotelio. Esta interacción estimula la unión de los LPS a receptores específicos en la superficie de los monocitos y macrófagos desencadenando la liberación de citoquinas como el TNF-& e interleuquina-1 quienes amplifican la respuesta inflamatoria inicial. Además de ocasionar disfunción endotelial, infiltración laucocitaria y profileración de células musculares lisas, todos elementos característicos del fenómeno aterogénico. Los tóxicos bacterianos como los LPS, ácidos orgánicos de bajo peso molecular, aminas y leucotoxinas inician y perpetúan una serie de eventos inmunológicos en el hospedador que pueden ser divididos en fenómeno de tipo local como la enfermedad periodontal y distancia fenómeno aterogénico