ABSTRACT
RESUMEN Introducción: La prueba de tolerancia de comida mixta es considerada la prueba de oro para la medición de la producción de insulina endógena en pacientes con diabetes tipo 1. Objetivo: Determinar la utilidad de la prueba de tolerancia de comida mixta con Nutrial I para evaluar la función de las células ß en diabéticos tipo 1 de diagnóstico reciente y la relación de esa función con algunas características clínicas y bioquímicas. Métodos: Se estudiaron variables bioquímicas como la glucemia, hemoglobina glucosilada (HbA1c), péptido C y fracciones lipídicas. La prueba de tolerancia de comida mixta con Nutrial I se aplicó a 18 sujetos con diabetes tipo 1 de diagnóstico reciente y a 8 voluntarios con edades comprendidas entre 19 y 35 años. El consumo del suplemento Nutrial I se calculó según el peso del paciente. Se obtuvieron muestras para glucemia y péptido C a los -10, 0, 30, 60, 90 y 120 minutos. Resultados: Se observaron concentraciones elevadas de glucemia y disminuidas de péptido C durante la prueba de tolerancia de comida mixta en los diabéticos tipo 1 de diagnóstico reciente, en comparación con los voluntarios, así como, diferencias en las áreas bajo la curva de péptido C (AUC-pc) (p= 0,001). En los diabéticos tipo 1 de diagnóstico reciente se evidenció una correlación negativa entre el AUC-pc con los niveles de glucemia en ayunas (r= -0,747; p ( 0,0001) y la HbA1c (r= -0,535; p= 0,022). Por el contrario, se encontró una correlación positiva entre el AUC-pc y el péptido C en ayunas (r= 0,722; p= 0,001). El AUC-pc después de la prueba de tolerancia de comida mixta es mayor en los sujetos con glucemia en ayunas si GA < 7 mmol/L con respecto a los sujetos con glucemia en ayunas ( 7 mmol/L (p= 0,012). Conclusiones: El empleo del Nutrial I en la prueba de tolerancia de comida mixta fue útil en la evaluación de la función de las células β en diabéticos tipo 1 de diagnóstico reciente. Los valores bajos de glucemia en ayunas durante esta prueba son marcadores indirectos de una función residual de células ( más conservada en los diabéticos tipo 1 de diagnóstico reciente(AU)
ABSTRACT Introduction: The tolerance test of mixed food is considered the gold standard for the measurement of endogenous insulin production in patients with diabetes type 1. Objective: To determine the usefulness of the tolerance test of mixed food with Nutrial I to assess the ß-cells function in patients with diabetes type 1 of recent diagnosis and the relation of this function with some clinical and biochemical characteristics. Methods: There were studied biochemical variables as the blood glucose, glycosylated haemoglobin (HbA1c), C-peptide and lipid fractions. The tolerance test of mixed food with Nutrial I was applied to 18 individuals with diabetes type 1 of recent diagnosis and in 8 volunteers aged between 19 and 35 years old. The consumption of Nutrial I supplement was calculated according to the weight of the patient. Samples were obtained for blood glucose and C-peptide at -10, 0, 30, 60, 90 and 120 minutes. Results: There were observed high concentrations of glycemia and decreased amounts of C-peptide during the tolerance test of mixed food in recently diagnosed type 1 diabetics in comparison with the volunteers, as well as differences in areas under the curve of C-peptide (AUC-pc) (p= 0.001). In the recently diagnosed type 1 diabetics was evident a negative correlation between the AUC-pc with fasting plasma glucose levels (r= -0,747; p(0.0001) and HbA1c (r= -0,535; p= 0.022). On the contrary, it was found a positive correlation between the AUC-pc and fasting C-peptide (r = 0.722; p = 0.001). The AUC-pc after the tolerance test of mixed food was greater in subjects with fasting blood glucose < 7 mmol/L with respect to the subjects with fasting blood glucose ( 7 mmol/L (p= 0.012). Conclusions: The use of Nutrial I in the tolerance test of mixed food was useful in the assessment of the role of the β-cells in patients with recently diagnosed diabetes type 1. Low values of fasting blood glucose during this test are indirect markers of a residual function of (cells more preserved in type 1 diabetics of recent diagnosis(AU)
Subject(s)
Humans , Blood Glucose/physiology , Diabetes Mellitus, Type 1/diagnosis , Insulin Secretion/physiology , Epidemiology, Descriptive , Cross-Sectional StudiesABSTRACT
Islet βcell dysfunction is one of the important links in the development of type 2 diabetes (T2DM).The latest research shows that the main cause of the continuous β-cell dysfunction under metabolic stress is mainly the dedifferentiation of β-cells,and become endocrine progenitor -like cells with multiple differentiation potentials.Studies have found that the process of dedifferentiation of pancreatic islet βcells is reversible.This finding has provided possibilities and new ideas for preventing and reversing the progressive decline of βcell function and delaying the occurrence of T2DM.
ABSTRACT
Objective To investigate the effect of liraglutide combined with glargine insulin in treating the patients with newly diagnosed type 2 diabetes mellitus (T2DM).Methods Sixty-one cases of newly diagnosed T2DM in the endocrinology department of Affiliated Chaozhou Central Hospital of Southern Medical University,from August 2014 to December 2015 were selected and divided into two groups according to the random number table.The observation group (29 cases) was treated with liraglutide combined with glargine insulin and the control group (32 cases) was given the intensive insulin therapy.The curative effects before and after treatment were analyzed and compared between the two groups.Results The fast plasma glucose(FPG),postprandial 2 h blood glucose(PPG),glycosylated hemoglobin(HbA1c),fasting C peptide(FCP),postprandial 2 h C peptide(PCP),insulin resistance index(HOMA-IR),blood lipid indicators and body mass index after 12-week treatment were decreased in the treatment and follow up periods,while pancreatic β cell function index (HOMA-β) and HDL-C were increased,indicating that the two kinds of treatment method all were effective.The effect onset in the observation group was faster,the above indexes after 4-week treatment were significantly improved compared with before treatment.The above indexes after 4-,12-week treatment in the observation group were significantly superior to those in the control group,the difference was statistically significant(P<0.05).Conclusion Liraglutide combined with glargine insulin has better effect in the aspects of reducing blood glucose,regulating blood lipid,decreasing the body mass and islet function recovery than the intensive insulin treatment and is worthy of clinical promotion and application.
ABSTRACT
The aim of this study was to evaluate the anti-diabetic effects of the water extract of Lespedeza cuneata (LCW) using rat insulinoma (RIN) m5F cells and streptozotocin (STZ)-induced diabetic rats. The effect of LCW on the protection of pancreatic beta cells was assessed using MTT assay, and nitric oxide production was assessed using Griess reagent. STZ-induced diabetic rats were treated with 100 and 400 mg/kg body weight of LCW for 5 weeks. In results, LCW significantly protected cytokine-induced toxicity and NO production, and increased insulin secretion in RINm5F cells. LCW significantly decreased serum blood glucose, thiobarbituric acid reactive substances (TBARS), blood urea nitrogen (BUN) and advanced glycation end products (AGEs) levels, and renal fibronectin expression in STZ-induced diabetic rats. Also, LCW effectively improved BW loss in STZ-induced diabetic rats. Thus, our results suggest that LCW has a beneficial effect on cytokine-induced pancreatic beta cell damage and biomarkers of diabetic complication in hyperglycemic rats.
Subject(s)
Animals , Rats , Biomarkers , Blood Glucose , Blood Urea Nitrogen , Body Weight , Cytokines , Diabetes Complications , Fibronectins , Insulin , Insulin-Secreting Cells , Insulinoma , Lespedeza , Nitric Oxide , Streptozocin , Thiobarbituric Acid Reactive Substances , WaterABSTRACT
Pancreatic beta-cells have an important role in maintaining blood glucose homeostasis through insulin secretion. Therefore, decreased insulin secretion function induced by impaired beta-cell is one of the leading causes of diabetes mellitus. Accumulating data suggested that multiple factors such as age, body weight, smoking and alcohol intake may decrease beta-cell function. In addition, previous studies have reported that nutrient intake, such as carbohydrate, fat, vitamin and mineral intake, is associated with beta-cell function. The purpose of this study is to review the results regarding the association between nutrient intake and beta-cell function. We propose herein that nutrient intake helps prevent decreases in beta-cell function and preserves the optimal insulin secretion function.
Subject(s)
Blood Glucose , Body Weight , Diabetes Mellitus , Homeostasis , Insulin , Miners , Smoke , Smoking , VitaminsABSTRACT
ERS is a kind of universal existence in various cellular stress response.Recently, the research shows that ERS may affect bone metabolism balance from different ways.However, the specific mechanism is still not clear.The relationship between ERS and osteoporosis needs further research.This article will firstly introduce the pathways of ERS, then the relationship between the ERS and osteoporosis will be discussed from pancreatic beta cells, osteoblasts, osteoclasts and mesenchymal stem cells.Lastly, I will give perspectives on the future research on treatment of osteoporosis drug.
ABSTRACT
Activation of ß2 adrenergic receptors by catecholamine or catecholamine-mimetic substances may enhance insulin secretion. We herein investigated KCl- and nutrient-stimulated insulin secretion in pancreatic islets isolated from ß2 knockout (ß2KO) mice. ß2KO mice showed reduced body weight, fasting hypoglycaemia associate to a similar fasting insulinemia compared to control. ß2KO mice also showed reduced glucose tolerance despite the higher sensitivity to insulin. Glucose-induced insulin secretion was impaired in pancreatic islets isolated from ß2KO mice. Leucine-induced (20mM) insulin secretion was diminished in pancreatic islets isolated from ß 2KO mice when compared to control one. The depolarizing effect of KCl on insulin secretion was also impaired in pancreatic islets from ß2KO mice. These results suggested a possible role of ß2 adrenergic receptors on nutrient-induced insulin secretion.
A ativação dos receptores ß2-adrenérgicos por catecolaminas ou miméticos a catecolaminas podem aumentar a secreção de insulina. Nós investigamos a secreção de insulina estimulada por nutrients e KCl em ilhotas pancreáticas isoladas de camundongos com deleção dos receptores ß2-adrenérgicos (ß2KO). Camudongos ß2KO apresentaram reduzido peso corporal, hipoglicemia de jejum associada a semelhante concentração de insulina plasmática de jejum comparada ao grupo controle. Camundongos ß2KO apesar de apresentarem aumento da sensibilidade a insulina também apresentaram reduzida tolerância a glicose. A secreção de insulina induzida com glicose foi alterada em ilhotas pancreáticas isoladas de camundongos ß2KO. Secreção de insulina induzida por leucina (20mM) foi diminuída em ilhotas pancreáticas isoladas de camundongos ß2KO quando comparado ao controle. O efeito despolarizante do KCl sobre a secreção de insulina também foi alterado em ilhotas pancreáticas de camundongos ß2KO. Estes resultados sugerem um possível papel dos receptores ß2-adrenérgicos na secreção de insulina induzida por nutrientes.
Subject(s)
Mice , Glucose , Insulin-Secreting Cells , Leucine , Receptors, AdrenergicABSTRACT
The function of β-cells is closely correlated with the onset of type 2 diabetes mellitus.Currently the bariatric surgery has been considered to be the most effective therapy for ameliorating the complications and improving the prognosis of type 2 diabetes mellitus,while the mechanism remains unknown.The improvement of β-cells function following bariatric surgery might play important roles in the remission of type 2 diabetes mellitus.In this article,the relationship between the changes of related factors after bariatric surgery and the function of pancreatic β-cells is reviewed.
ABSTRACT
Pancreatic beta-cells are major cells responsible for glucose metabolism in the body. Hyperglycemia is known to be a primary factor in the induction of diabetes mellitus. Glutamate is also an excitatory neurotransmitter in diverse organs. Oxidative stress also plays a pivotal role in the development of diabetes mellitus. However, the effect of hyperglycemia in glutamate uptake in the pancreas is not clear. Furthermore, the relationship between high glucose-induced glutamate uptake and oxidative stress has not been investigated. Therefore, this study was conducted to investigate the effect of high glucose on glutamate uptake in pancreatic beta-cells. In the present study, 25 mM glucose stimulated the glutamate uptake in HIT-15 cells of hamster pancreatic beta-cells. The treatment of 25 mM glucose and 1 mM glutamate also decreased the cell viability in HIT-15 cells. In addition, the treatment of 25 mM glucose induced an increase of lipid peroxide formation. High glucose-induced increase of LPO formation was prevented by the treatment of antioxidants such as N-acetyl-L-cysteine and quercetin. Furthermore, high glucose-induced stimulation of glutamate uptake and decrease of cell viability were also blocked by the treatment of N-acetyl-L-cysteine and quercetin. In conclusion, high glucose stimulated glutamate uptake via oxidative stress in pancreatic beta-cells.
Subject(s)
Animals , Cricetinae , Acetylcysteine , Antioxidants , Cell Survival , Diabetes Mellitus , Glucose , Glutamic Acid , Hyperglycemia , Neurotransmitter Agents , Oxidative Stress , Pancreas , QuercetinABSTRACT
Objective To investigate the role of pancreatic β cell on pancreatic regeneration following experimental acute pancreatitis.Methods Eighty-seven SD male rats were randomly divided into four groups:control group ( n =15 ),STZ group ( n =24),L-Arg group ( n =24 ),STZ + Arg group ( n =24).60 mg/kg of STZ was administrated by intraperitoneal injection to induce the diabetes model.2.5 g/kg body weight of LArg was administrated by intraperitoneal injection to induce the acute pancreatitis model.The rats were sacrificed 1,3,5,7 d later and the serum levels of amylase and glucose were measured.Relative pancreatic weight (pancreatic weight/body weight) were measured.Pancreatic tissue underwent routine pathologic examination,and the percentage of area of necrosis and tissue transformation was calculated.The expression of Reg4 and insulin was performed by immunofluorescence.Results Serum level of glucose significantly increased after STZ injection.After L-Arg injection,serum level of amylase significantly increased,and there was pancreatic tissue edema,necrosis,infiltration of inflammatory cells,which suggested the successful model induction.The percentage of area of necrosis in STZ + L-Arg group was (71.6 ± 6.0) ％ at the 3rd day,which were significantly higher than (42.3 ± 4.0 ) ％ in L-Arg group; the percentage of area of transformation was (45.6 ± 5.4) ％,which were significantly lower than (78.5 ± 6.4) ％ in L-Arg group.Expression of Reg4 in pancreatic islets of STZ + L-Arg group was significantly lower than those in L-Arg group.Conclusions STZ impairs pancreatic β cells,aggravates pancreatic damage following L-arginine induced pancreatitis and inhibits pancreatic regeneration.
ABSTRACT
BACKGROUND: Blood glucose level continuously fluctuates within a certain range in the human body. In diabetes patients, the extent of such fluctuation is large, despite the strict control of blood glucose. Blood glucose fluctuation has been shown to mediate more adverse effects on vascular endothelial cells and diabetes complications than chronic hyperglycemia, which has been explained as due to oxidative stress. As few previous studies have reported the effects of chronic and intermittent hyperglycemia on the apoptosis and function of pancreatic beta cells, this study reported herein was performed to investigate such effects on these cells. METHODS: For chronic hyperglycemia, INS-1 cells were cultured for 5 days with changes of RPMI 1640 medium containing 33 mM glucose every 12 hours. For intermittent hyperglycemia, the medium containing 11 mM glucose was exchanged with the medium containing 33 mM glucose every 12 hours. Apoptosis was assessed by TUNEL assay Hoechst staining and cleaved caspase 3. Insulin secretory capacity was assessed, and the expression of Mn-SOD and Bcl-2 was measured by Western blotting. RESULTS: In comparison to the control group, INS-1 cells exposed to chronic hyperglycemia and intermittent hyperglycemia showed an increase in apoptosis. The apoptosis of INS-1 cells exposed to intermittent hyperglycemia increased significantly more than the apoptosis of INS-1 cells exposed to chronic hyperglycemia. In comparison to the control group, the insulin secretory capacity in the two hyperglycemic states was decreased, and more with intermittent hyperglycemia than with chronic hyperglycemia. The expression of Mn-SOD and Bcl-2 increased more with chronic hyperglycemia than with intermittent hyperglycemia. CONCLUSION: Intermittent hyperglycemia induced a higher degree of apoptosis and decreased the insulin secretory capacity more in pancreatic beta cells than chronic hyperglycemia. This activity may be mediated by the anti-oxidative enzyme Mn-SOD and the anti-apoptotic signal Bcl-2.
Subject(s)
Humans , Apoptosis , Blood Glucose , Blotting, Western , Caspase 3 , Diabetes Complications , Endothelial Cells , Glucose , Human Body , Hyperglycemia , In Situ Nick-End Labeling , Insulin , Insulin-Secreting Cells , Oxidative Stress , Superoxide DismutaseABSTRACT
11.1 mmol/L were treated by 2 weeks CSII.An intravenous glucose tolerance test(IVGTT) was performed before and after CSII.The levels of fasting plasma glucose(FPG),2 hours postprandial glucose(2hPG),glycosylated hemoglobin A1c(HbA1c),first-phase secretion of insulin,the mean area under the curve(AUC) of insulin,insulin sensitivity index(ISI),insulin resistance index(Homa IR) and insulin secretion index(Homa ?) were compared.Results The excellent control of FPG and 2hPG in 20 out of 21 patients were achieved stably in 2.8?1.6 days and 7.8?1.9 days by CSII.After the treatment,FPG,2h PG and HbA1c were significantly decreased(P
ABSTRACT
Objective To investigate the remission rate of the therapy of integrated TCM into intensive insulin treatment, and the relationship between each factor and the remission rate. The effect of TCM on improving ?-cell fimction and remission rate was also studied. Methods Forty-seven newly diagnosed type 2 diabetic patients were shortly treated with both continuous subcutaneous insulin infusion (CSII) and Chinese medicine. The remission rate was observed. The relationship between each factor and remission was analyzed by logistic regression. The ?-cell function of patients in remission group were evluated at the end of the treatment and during the period of follow-up. Results After treatment of (11.8?2.5)d, BMI and the ratio of the days of blood glucose reaching the standard and the total treatment days were the mainly factors affecting the remission. The remission rate at the end of treatment, one month after treatment and follow-up period (about six month) was 46.8%, 55.3%, 53.3% respectively. In following up, the remission rate in the Chinese medicine group and the control group was 66.7%, 44.4% respectively. Conclusions About half of newly diagnosed type 2 diabetic patients obtain clinical remission after the short-term intensive treatment of integrated insulin and Chinese medicine. Chinese medicine may have positive impaction on remission and extending honeymoon period.
ABSTRACT
Aim To probe the mechanism of the therapeutic effect of APS against DM rats by measuring the level of TNF-?,as well as observing the change of caspase-3 protein in pancreatic beta cells.Methods Thirty DM rats induced by STZ were randomly divided into three groups:DM group,APS low dosage group,APS high dosage group,and another 10 normal rats were taken as the control group.The drug was given for 6 weeks.The research included measuring the level of TNF-? in serum and the expression of caspase-3 protein in pancreatic beta cells.Results ① The level of TNF-? was higher in model group than that of the normal group(P
ABSTRACT
Objective:Anesthesia,surgery and cardiopulmonary bypass (CPB) are conventionally considered the major stress factors in the hormonal and metabolic responses to cardiac surgery.This study was to determine the influence of CPB on hormones,carbohydrate metabolism and insulin resistance.Methods:Blood samples were obtained from 19 patients at the following intervals:(1)before anesthesia(2)before CPB(3) 15 min after begining of CPB(4)5min after declamping of aorta(5)20min after CPB.Insulin,C-peptide,cortisol,growth hormone and blood glucose were measured.The ratio of insulin to glucose in blood(I/G) and insulin-sensitivity index [1/(I?G)] were obtained.Results:Insulin,growth hormone and cortisol were higher during and after CPB than that before CPB.Similar changes in levels of blood glucose,I/G and C-peptide were also observed,even though there was a significant decrease of insulin-sensitivity index.Conclusion:There are an obvious increase of concentrations in stress hormones and blood glucose and an aggravation of insulin resistance.All changes above do reflect the degree of surgical stress.The secretion of pancreatic beta cells is not suppressed during and after CPB.It is suggested that insulin supplement therapy may be beneficial to improve insulin resistance in the period of CPB.
ABSTRACT
13.1mmol/L were treated by 2 weeks short-term intensive insulin treatment. FBS, Fasting blood insulin(FINS), glycosylated hemoglobin A1c (HbA1c), 2 hours postprandial blood sugar(PBS 2), Homa ? and Homa IR were measured and compared between pre-treatment and post-treatment. Results After 2 weeks short-term intensive insulin treatment, the excellent control of FBS, PBS 2 in 23 out of 27 patients were achieved respectively in (5.6?2.3)days and (8.5?3.5)days. Homa ? significantly increased, and HbA1c and Homa IR decreased comared with pre-treatment. Conclusions The excellent glycemia control and improvement of ?-cell function can be induced by short-term intensive insulin treatment in newly diagnosed type 2 diabetic patients with severe hyperglycemia.
ABSTRACT
AIM:To study the function of pancreatic ? cells in the R6/2 transgenic mouse of Huntington's disease(HD),and to elucidate the pathogenetic mechanisms underlying diabetes mellitus in transgenic mice of HD. METHODS:By using the R6/2 transgenic mouse model of HD,fasting blood glucose and fasting insulin concentration in plasma of normal and HD mice were detected. Further,HE staining and immunofluorescence technique were used for morphometric analysis of islets in normal and HD mice. RESULTS:In contrast to normal mouse,R6/2 HD mouse showed hyperglycemia and hypoinsulinemia in fasting state. Pancreatic islets morphology showed that islets atrophied and cell number decreased in HD mouse. Poor functional index was observed in these mice,but insulin resistance index was normal. CONCLUSION:Impaired function of pancreatic cells may be the key factor contributing to the pathogenesis of diabetes in the R6/2 transgenic mouse model of HD.
ABSTRACT
Objective To examine the effect of tetraethylammonium (TEA, K~+ channel blocker) on pancreatic ?-cell apoptosis and explore the mechanism. Methods Mouse ? cells (NIT cells) were exposed to streptozotocin(STZ) to induce apoptosis, and TEA of different concentrations were applied along with STZ to prevent efflux of intracellular K~+. Cells were stained with annexin V, PI and rhodamine 123. Flow cytometer (FCM) was used to determine the percent of apoptotic or viable cells and the change of mitochondrial membrane potential. Culture media was collected to quantify the content of NO and ROS produced by NIT-cells. Cells were collected for detecting the activity of super oxide dismutase (SOD) in cells lysates. Results STZ induced apoptosis of NIT cells significantly (P