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ResumenLa diabetes representa un síndrome de enfermedades metabólicas complejas caracterizada por la presencia de la hiperglicemia, que muestra diversos orígenes (deficiencia y/o resistencia de insulina y consecuencias sistémicas del embarazo). Se sabe que la morbilidad y mortalidad de la diabetes es debida al desarrollo de las complicaciones macrovasculares y microvasculares. Sin embargo, la neuropatía diabética genera más hospitalizaciones que las otras complicaciones y es la causa más frecuente de amputaciones y falla autonómica. En ese sentido, la neuropatía diabética es heterogénea por sus síntomas, comprende patrones neurológicos, tiempo, riesgo y alteraciones patológicas que llevan a mecanismos que conducen al daño del nervio.El objetivo de esta revisión es presentar los mecanismos que conllevan a las complicaciones diabéticas, etiopatogenia de la neuropatía diabética y los recientes marcadores terapéuticos para disminuir el dolor en los pacientes con neuropatía diabética. La revisión se basó en publicaciones relevantes que fueron identificadas usando los siguientes términos de búsqueda en las bases de datos de Pubmed, Ebsco y Web of Science: diabetes, complicaciones diabéticas, dolor y neuropatía diabética. En esta revisión se describen las cuatro vías que conducen a la neuropatía diabética como la vía del poliol, formación de productos de glicación avanzada, activación de proteína cinasa C, que participa en el aumento de enfermedades vasculares y estrés oxidativo. Además, de los agentes farmacológicos principales para el tratamiento del dolor neuropático en la diabetes (antidepresivos tricíclicos, inhibidores de la recaptura de serotonina-adrenalina, anticonvulsivantes y medicaciones tópicas).Palabras clave: Diabetes, Complicaciones diabéticas, Dolor, Neuropatía diabética. SummaryDiabetes represents a complex metabolic diseases syndrome, united by the presence of hyperglycemia which shows diverse origins (deficiency and/ or resistance of insulin and pregnancy systematic consequences).It is known that morbidity and mortality of diabetes is due to the development of macro and micro vascular complications. However, diabetic neuropathy accounts for hospitalization more frequently than other complications of diabetes that the other complications and is also the most frequent cause of amputations and autonomic failure. In this sense, diabetes neuropathy is heterogenic because of it symptoms, includes neurologic patterns, course, risk, and pathologic alterations which lead to a nerve damage mechanism. The objective of this review is to present the mechanisms that lead to diabetic complications, etiopathogenesis of diabetic neuropathy, and the actual therapeutic markers to diminish pain in patients with diabetic neuropathy. The review was based on relevant publications, which were identified by using the following term in the data base of Pubmed, Ebsco and Web of Science: diabetes, diabetic complications, pain and diabetic neuropathy. In this review is described the for ways that conduct to diabetic neuropathy ...

The s y n t h e s i s of 3H -diosgenin, 3H -esmilagenin and 3H -tigogenin ( t h r e e p o t e n t i a l hypocholesterolemic a g e n t s ) was accomplished by low p r e s s u r e hydrogenation of commercial (Sigma D 1634) diosgenin w i t h 3H -gas. obtained w a s s e p a r a t e d by s i l i c a g e l G-60 column chromatography by use of a benzene: e t h y l a c e t a t e (8:2 v / v ) s o l u t i o n . P u r i f i c a t i o n of each sapogenin was by TLC chromatography.The mixture of 3H m a t e r i a l s

Background: Statins are the cornerstone of therapy in patients with hyperlipidemia. In high risk patients statins are employed for aggressive therapy, however part of the users are intolerant to these drugs. The aim of this study was to analyze the undesirable effects of moderate, median and high doses of rosuvastatin in CD-1 male mice that received a cholesterol-rich diet, focusing in the morphological and functional changes on hepatocyte mitochondria. Methods: We studied in a mouse model the combined administration of a cholesterol-rich diet (HD) along with a moderate high dose of rosuvastatin (Ro): 1, 2.5 or 5 mg/Kg/day during several days. Animals (n=6) were sacrificed, the liver mitochondria were isolated for analysis of respiratory function and microscopic studies. The respiratory control (state 3/state 4) and the O2 expenditure (nanoatoms/min/mg proteins) were evaluated. Results: Rosuvastatin doses higher than 20 mg/Kg/day induced premature death in hypercholesterolemic mice but not in mice with a cholesterol-free diet. Doses from 2.5 to 5 mg/Kg/day also induced morphological and functional alterations in mitochondria but the hypercholesterolemic animals survived longer. A dose of 1 mg/Kg/day, which is close to the maximal therapeutic dose employed in humans, did not affect mitochondrial architecture or respiratory function after two months of treatment. We analyzed the effect of rosuvastatin on the hepatic tissue where statins are most retained after their administration, and the main site of endogenous cholesterol synthesis. Conclusions: Our results contribute to understand the undesirable side effects of rosuvastatin in hypercholesterolemic mice, effects that can also be present in human being intolerant to statins.