Effects of reducing postprandial hyperglycemia and metabolism of acetate wheat starch on healthy mice

Abstract Recently, the acetate wheat starch (AWS) has been prepared by acetylation with an acetyl content of 2.42%, containing of rapidly digestible starch (RDS), slowly digestible starch (SDS) and resistant starch (RS) with 25.0%; 22.9% and 34.5%, respectively. In this study, this kind of starch was continuously evaluated with the postprandial blood glucose response and determined short-chain fatty acids (SCFAs) metabolized from AWS in the gastrointestinal tract of healthy mice by HPLC. The result showed that the mice fed with AWS exhibited a very limited increase in blood glucose level and remained stable for 2 hours after meals efficiently comparing with the control group fed with natural wheat starch (NWS). Simultaneously, the content of SCFAs produced in the caecum of the mice fed with AWS was significantly higher than mice fed with NWS, especially with acetic and propionic acids by 28% and 26%, respectively. Thus, AWS has shown to limit the postprandial hyperglycemia in mice effectively through the resistance to amylase hydrolysis in the small intestine. When going into the caecum, it is fermented to form SCFAs providing a part of energy for the body's activities, avoiding rotten fermentation causing digestive disorders which are inherent restrictions of normal high cellulose and fiber food.

Cerebellar synaptopathy in streptozotocin-induced diabetic rats / Sinaptopatía cerebelosa en ratas diabéticas inducidas por estreptozotocina

SUMMARY: There is an increasing amount of evidence that supports the diabetic complications of the central nervous system structure and function. The cerebellum, which is one of the primary structure derived from the hindbrain, plays an important role in motor control, motor coordination, and non-motor functions, such as cognitive processing. The synapse is a critical structure that regulates neuronal communication, and well-defined afferent and efferent fibre connections in the cerebellum help in maintaining the proper working order. Thus, the present study sought to investigate the long-term effects of diabetes-induced synaptopathy in the cerebellum, using both histological and ultrastructural studies. Twenty Sprague-Dawley male rats were divided randomly into control and diabetic groups, and diabetes was then induced through a single intraperitoneal injection of streptozotocin (60 mg/kg body weight). Six month later, the rats were sacrificed and the cerebellum was removed. Light and electron microscopic examinations showed a degeneration of Purkinje cells (Neuron purkinjense) with shrunken cells, pyknotic nuclei, and synaptopathy, including the reduction in synapse density, number of synaptic vesicles, and maturation of synapses in the molecular layer of diabetic cerebellum. The disruptions in synaptic profiles, which observed in the diabetic condition, could be related to cerebellar dysfunction, thus leading to the defects in coordinated movement, balance, as well as cognitive learning and memory.

RESUMEN: Actualmente existe una creciente evidencia que apoya las complicaciones diabéticas de la estructura y función del sistema nervioso central. El cerebelo, una de las estructuras primarias del cerebro posterior, desempeña un papel importante en el control motor, la coordinación motora y las funciones no motoras, tanto como en el procesamiento cognitivo. La sinapsis es una estructura crítica que regula la comunicación neuronal y las conexiones de fibras aferentes y eferentes bien definidas en el cerebelo, ayudan a mantener el funcionamiento correcto. Por lo tanto, en el presente estudio se investigaron los efectos a largo plazo de la sinaptopatía inducida por la diabetes en el cerebelo, utilizando estudios histológicos y ultraestructurales. Veinte ratas SpragueDawley macho se dividieron al azar en grupos de control y diabetes, se indujó la diabetes a través de una inyección intraperitoneal única de estreptozotocina (60 mg / kg de peso corporal). Seis meses después, se sacrificaron las ratas y se extrajo el cerebelo. Los exámenes de microscopías óptica y electrónica mostraron una degeneración de las neuronas purkinjenses (células de Purkinje), con células reducidas, núcleos picnóticos y sinaptopatía, como también la densidad reducida de sinapsis, el número de vesículas sinápticas y la maduración de las sinapsis en la capa molecular del cerebelo de las ratas diabéticas. Las interrupciones en los perfiles sinápticos, que se observaron en la condición diabética, podrían estar relacionadas con la disfunción cerebelosa, lo que lleva a defectos en el movimiento coordinado, el equilibrio, así como al aprendizaje cognitivo y la memoria.

Alteraciones corneales en pacientes diabéticos / Corneal alterations in diabetic patients

La diabetes mellitus, afección frecuente a nivel mundial, tiene gran impacto en la sociedad no solo por su alta prevalencia, sino por sus complicaciones crónicas y su alta mortalidad. Afecta a unos 180 millones de personas en el mundo. La prevalencia de la diabetes (tipos I y II) se estima en el 13 % en pacientes mayores de 60 años. La estructura corneal sufre modificaciones en los pacientes diabéticos; la hiperglucemia afecta la hidratación de la córnea, y con esto varía el espesor corneal y aparecen cambios queratométricos visibles mediante topografía corneal. Las córneas de los pacientes con diabetes presentan alteraciones epiteliales, estromales y endoteliales. Además, existe una disminución de la permeabilidad endotelial durante la fase de hipoxia, que relacionan estos efectos de la diabetes en las células endoteliales. El objetivo de nuestro estudio es abordar las diferentes alteraciones corneales en los pacientes diabéticos(AU)

Diabetes Mellitus, a frequent disease worldwide, has a great impact on the society, not only for their high prevalence, but for their chronic complications and high mortality. It has an effect on 180 million people approximately in the world. The prevalence of diabetes (type I and II) is estimated to be 13 % in patients older than 60 years. The corneal structure undergoes changes in diabetic patients; the hyperglycemia affects the corneal hydration and causes variations in the corneal thickness, with occurrence of visible keratometric changes detected in the corneal topography. The corneas of diabetic patients show epithelial, stromal and endothelial alterations. Additionally, there is decrease in endothelial permeability during the phase of hypoxia that relate these effects of diabetes in the endothelial cells. The objective of our study was to deal with the different corneal alterations in diabetic patients(AU)

Type 2 Diabetes Mellitus and Its Association with the Risk of Pancreatic Carcinogenesis: A Review / 대한소화기학회지

The prevalence of diabetes mellitus (DM) and associated diseases such as cancers are substantially increasing worldwide. About 80% of the patients with pancreatic cancer have glucose metabolism alterations. This suggests an association between type 2 DM and pancreatic cancer risk and progression. There are hypotheses that show metabolic links between the diseases, due to insulin resistance, hyperglycemia, hyperinsulinemia, low grade chronic inflammation, and alteration in the insulin-insulin-like growth factor axis. The use of diabetes medications can influence the extent of carcinogenesis of the pancreas. This study briefly reviews recent literature on investigation of metabolic link of type 2 DM, risk of carcinogenesis of the pancreas and their association, as well as the current understanding of metabolic pathways implicated in metabolism and cellular growth. The main finding of this review, although there are discrepancies, is that according to most research long-term DM does not raise the risk of pancreatic cancer. The longest duration of DM may reflect hypoinsulinemia due to treatment for hyperglycemia, but recent onset diabetes was associated with increased risk for pancreatic cancer due to hyperinsulinemia and hyperglycemia. In conclusion, the review demonstrates that type 2 DM and the duration of diabetes pose a risk for pancreatic carcinogenesis, and that there is biological link between the diseases.

Expression profile of mitrogen-activated protein kinase (MAPK) signaling genes in the skeletal muscle & liver of rat with type 2 diabetes: Role in disease pathology.

Background & objectives: Type 2 diabetes (T2D) is characterized as hyperglycaemia caused by defects in insulin secretion, and it affects target tissues, such as skeletal muscle, liver and adipose tissue. Therefore, analyzing the changes of gene expression profiles in these tissues is important to elucidate the pathogenesis of T2D. We, therefore, measured the gene transcript alterations in liver and skeletal muscle of rat with induced T2D, to detect differentially expressed genes in liver and skeletal muscle and perform gene-annotation enrichment analysis. Methods: In the present study, skeletal muscle and liver tissue from 10 streptozotocin-induced diabetic rats and 10 control rats were analyzed using gene expression microarrays. KEGG pathways enriched by differentially expressed genes (DEGs) were identified by WebGestalt Expander and GATHER software. DEGs were validated by the method of real-time PCR and western blot. Results: From the 9,929 expressed genes across the genome, 1,305 and 997 differentially expressed genes (DEGs, P<0.01) were identified in comparisons of skeletal muscle and liver, respectively. large numbers of DEGs (200) were common in both comparisons, which was clearly more than the predicted number (131 genes, P<0.001). For further interpretation of the gene expression data, three over-representation analysis softwares (WebGestalt, Expander and GATHER) were used. All the tools detected one KEGG pathway (MAPK signaling) and two GO (gene ontology) biological processes (response to stress and cell death), with enrichment of DEGs in both tissues. In addition, PPI (protein-protein interaction) networks constructed using human homologues not only revealed the tendency of DEGs to form a highly connected module, but also suggested a “hub” role of p38-MAPK-related genes (such as MAPK14) in the pathogenesis of T2D. Interpretation & conclusions: Our results indicated the considerably aberrant MAPK signaling in both insulin-sensitive tissues of T2D rat, and that the p38 may play a role as a common “hub” in the gene module response to hyperglycaemia. Furthermore, our research pinpoints the role of several new T2D-associated genes (such as Srebf1 and Ppargc1) in the human population.

Comparison of thrice daily biphasic human insulin (30/70) versus basal detemir & bolus aspart in patients with poorly controlled type 2 diabetes mellitus – A pilot study.

Background & objectives: Conventionally, biphasic human insulin (30/70, BHI) is used twice daily for the management of patients with diabetes. However, this regimen is suboptimal to control post-lunch and/ or pre-dinner hyperglycaemia in some patients. This study was undertaken to compare the efficacy and safety of thrice-daily biphasic human insulin (30/70, BHI) versus basal detemir and bolus aspart (BB) in patients with poorly controlled type 2 diabetes mellitus (T2DM). Methods: In this open labelled randomized pilot study, 50 patients with uncontrolled T2DM on twicedaily BHI and insulin sensitizers were randomized either to BHI thrice-daily or BB regimen. HbA1c, six point plasma glucose profile, increment in insulin dose, weight gain, hypoglycaemic episodes and cost were compared between the two treatment groups at the end of 12 wk. Results: Mean HbAlc (±SD) decreased from 9.0±0.9 per cent at randomization to 7.9±0.8 per cent in BHI (P<0.001) and from 9.4±1.3 to 8.2±1.0 per cent in BB regimen (P<0.001) after 12 wk of treatment. The mean (±SEM) weight gain in patients in the BHI regimen was 1.5±0.33 kg compared to 1.4±0.34 kg in the BB regimen. Insulin dose increment at 12 wk was significantly more in the BB regimen 0.46±0.32 U/ kg/day compared to 0.15±0.21 U/kg/day in the BHI regimen (P<0.001). The incidence of major as well as minor hypoglycaemic episodes was not different in both the regimen. The BB regimen was more expensive than the BHI regimen (P<0.001). Interpretation & conclusions: The thrice daily biphasic human insulin regimen is non-inferior to the basal bolus insulin analogue regimen in terms efficacy and safety in patients with poorly controlled T2DM. However, these data require further substantiation in large long term prospective studies.

Valor pronóstico de la hiperglicemia de ingreso en pacientes con Ictus hemorrágico intraparenquimatoso / Prognostic value of hyperglycemia on admission in patients with intracerebral hemorrhagic stroke

Determinar la asociación entre hiperglicemia y pronóstico de pacientes con Ictus Hemorrágico Intraparenquimatoso, evaluando la gravedad, discapacidad, complicaciones y mortalidad. Estudio de tipo correlacional, de cohorte histórica, en el Hospital Del Este “Dr. Domingo Luciani”, en 233 pacientes que ingresaron entre Marzo 2006 y Septiembre 2008. Las pruebas estadísticas utilizadas para el análisis de los resultados fueron: prueba exacta de Fisher; chi-cuadrado de Pearson, U de Mann-Whitney y Kruskal-Wallis. Se observó una correlación directa entre niveles de hiperglicemia y puntuación de la escala de gravedad de NIHSS, no significativa estadísticamente. No se evidenció correlación entre hiperglicemia al ingreso y escala de discapacidad de Rankin. La complicación más frecuentemente encontrada fueron las infecciones respiratorias. La hiperglicemia constituye un marcador de mal pronóstico intrahospitalario en los pacientes con Ictus Hemorrágico Intraparenquimatoso, por su asociación a complicaciones infecciosas.

To determine if there was an association between hyperglycemia and the prognosis of intraparenquimatous hemorrhagic stroke by assesing severity, discapacity, complications and mortality. Correlacional study done at the Hospital Del Este “Dr. Domingo Luciani”, Caracas, Venezuela with a sample of 233 patients between March 2006 and September 2008. The statistics applied were Fishers exact test, Pearson`s square-chi, Mann-Whitney U and Kruskal-Wallis. A direct correlation between levels of hyperglycemia and NIHSS score was found, but with no stastitical significance. Neither did we find a correlation between admission hyperglycemia and the discapacity Rankin ìs score. Respiratory infections were the most frequent complication. Hyperglycemia is a marker of adverse prognosis in patients with acute hemorrhagic stroke, due to it`s asociation to infectious complications.

Blood glucose and ischemic brain damage.

The effect of hyperglycemia on ischemic brain damage was studied in a rat model of incomplete ischemia. Incomplete ischemia was produced by permanent occlusion of one (either left or right) common carotid artery (CCA). Hyperglycemia was induced by intraperitoneal injection of 50% glucose, and same volume of physiological saline was injected in the controls 40 min before CCA ligation. Serum glucose level, at the time of vessel ligation, was 33.3 mMol/L. After CCA ligation, the rats were allowed to wake up and survive for upto 1 month. Perfusion-fixed brains were embedded in paraffin, subserially sectioned, and stained with haematoxylin-eosin/cresyl violet. Brain from sham-operated animals showed no damage neurons. Only mild neuronal damage was observed in saline pre-treated rats in CA1 area. Histological examination 24 h after CCA occlusion revealed ischemic neuronal cell damage to be more extensive in hyperglycemic rats. Neuronal damage was found in the major brain structures vulnerable to several insults. Some of those damaged neurons recovered well, but presence of some damaged neurons at 1 month of recovery suggesting delayed recovery. The results indicate that increased blood glucose level (hyperglycemia) during brain ischemia exaggerates structural alterations and leads to delay in recovery.