OBJECTIVETo observe the structural and functional changes in islet beta cells in severely scalded rats, and to explore its relationship with dysfunction of glycometabolism.

METHODSSeventy-two Wistar rats were divided into scald (S) group and sham injury (SI) group according to the random number table, with 36 rats in each group. Rats in group S were inflicted with 50%TBSA full-thickness scald by a 12-s immersion of back and a 6-s immersion of abdomen in 94 °C hot water. Rats in group SI were sham injured through immersion of back and abdomen in 37 °C warm water. At post injury hour (PIH) 6 and on post injury day (PID) 3 and 7, plasma glucose level was measured for intraperitoneal glucose tolerance test (IPGTT) in 12 rats of each group, and the area under the curve (AUC) of plasma glucose level was calculated. After the IPGTT, pancreatic tissue was harvested and subjected to a double immunostaining for insulin and cell nuclei to determine the pancreatic insulin-positive area ratio, and the area and number of beta cells in the islets (referred to as "the three indicators in the islets"). Data were processed with the analysis of repeated measures and factorial designed analysis of variance, and LSD test was applied for paired comparison.

RESULTS(1) At PIH 6 and on PID 3, the overall plasma glucose levels of rats in group S before and after injection of glucose and at each time point were obviously higher than those of rats in group SI (with F values of main effects respectively 79.372 and 32.962, P values all below 0.001; with P values of paired comparison below 0.05 or 0.01). On PID 7, the overall plasma glucose levels in the two groups before and after injection of glucose and at each time point were close (with P values all above 0.05). (2) The overall AUC of plasma glucose levels of rats in group S was higher than that of rats in group SI (main effects: F = 337.87, P < 0.01). Compared with those of rats in group SI [(1019 ± 32), (1003 ± 72) mmol·min·L(-1)], the AUCs of plasma glucose levels of rats in group S were higher at PIH 6 and on PID 3 [(1501 ± 163), (1132 ± 67) mmol·min·L(-1), P values all below 0.001]. The AUCs of plasma glucose levels were close between two groups on PID 7 (P > 0.05). The AUCs of plasma glucose levels on PID 3 and 7 were both lower than that at PIH 6 in rats of group S (with P values all below 0.001). (3) The three indicators in the islets in rats of group S were all lower than those of rats in group SI (with F values of main effects respectively 135.17, 24.75 and 39.35, P values all below 0.01). There were no significant differences in the three indicators in the islets at PIH 6 between two groups (with P values all above 0.05). The three indicators in the islets of rats in group S on PID 3 and 7 [0.47 ± 0.05, 0.51 ± 0.07; (0.032 ± 0.008), (0.037 ± 0.008) mm(2); (303 ± 64), (341 ± 58) cells] were significantly lower than those of rats in group SI [0.63 ± 0.05, 0.64 ± 0.06; (0.043 ± 0.011), (0.044 ± 0.012) mm(2); (398 ± 112), (387 ± 90) cells; P < 0.05 or P < 0.01] and that at PIH 6 within group S (P < 0.05 or P < 0.01).

CONCLUSIONSThe number of beta cells is reduced, and the insulin secretion function of beta cells is decreased in the scalded rats, and they may constitute the cause of dysfunction of glycometabolism, mainly manifested as hyperglycemia.

Animals ; Blood Glucose ; metabolism ; Burns ; metabolism ; Insulin ; metabolism ; Insulin-Secreting Cells ; metabolism ; Male ; Rats ; Rats, Wistar

Adolescent ; Adult ; Fatty Liver ; metabolism ; Female ; Humans ; Insulin ; blood ; Insulin Resistance ; Leptin ; blood ; Male ; Middle Aged

Animals ; Colorectal Neoplasms ; blood ; etiology ; Humans ; Hyperinsulinism ; blood ; complications ; Insulin ; blood ; Insulin Resistance ; Insulin-Like Growth Factor Binding Proteins ; blood ; Insulin-Like Growth Factor I ; metabolism ; Metabolic Syndrome ; blood ; complications ; Receptor, IGF Type 1 ; blood ; Receptor, Insulin ; blood

Insulin resistance is a major risk factor for developing type 2 diabetes caused by the inability of insulin-target tissues to respond properly to insulin, and contributes to the morbidity of obesity. Insulin action involves a series of signaling cascades initiated by insulin binding to its receptor, eliciting receptor autophosphorylation and activation of the receptor tyrosine kinase, resulting in tyrosine phosphorylation of insulin receptor substrates (IRSs). Phosphorylation of IRSs leads to activation of phosphatidylinositol 3-kinase (PI3K) and, subsequently, to activation of Akt and its downstream mediator AS160, all of which are important steps for stimulating glucose transport induced by insulin. Although the mechanisms underlying insulin resistance are not completely understood in skeletal muscle, it is thought to result, at least in part, from impaired insulin-dependent PI3K activation and downstream signaling. This review focuses on the molecular basis of skeletal muscle insulin resistance in obesity and type 2 diabetes. In addition, the effects of insulin-sensitizing agent treatment and lifestyle intervention of human insulin-resistant subjects on insulin signaling cascade are discussed. Furthermore, the role of Rho-kinase, a newly identified regulator of insulin action in insulin control of metabolism, is addressed.
Blood Glucose/*metabolism ; Diabetes Mellitus, Type 2/*metabolism ; Humans ; Insulin/metabolism ; Insulin Resistance/*physiology ; Obesity, Abdominal/*metabolism ; Signal Transduction/physiology

OBJECTIVETo study the pattern of the alterations of blood glucose, insulin and insulin sensitivity after traumatic brain injury in rats, and verify the occurrence of insulin resistance after the injury.

METHODSBased on Feeney's model of brain injury, the blood glucose and insulin concentration of the dogs measured 30 min before and at 6, 12, 24, 48, 72 and 120 h after injury. BG60-120, GIR60-120, and insulin sensitivity index (ISI) reflecting the insulin sensitivity were measured at 6, 24, 48, and 72 hours following severe traumatic brain injury using euglycemic-hyperinsulinemic clamp.

RESULTSBoth the blood glucose and insulin concentration increased markedly in rats following moderate and severe brain injury. BG60-120 increased markedly, and GIR60-120 and ISI decreased significantly 6, 24, 48, and 72 h after severe brain trauma as compared with those of the sham operation group. Blood glucose concentration of rats following severe injury was positively correlated with insulin concentration and BG60-120 at the corresponding time points, but negatively with GIR60-120 and ISI.

CONCLUSIONBoth the blood glucose and insulin concentration increase markedly in rats following severe brain injury. Increased blood glucose even in the presence of high-level insulin is due to acute insulin resistance occurring after traumatic brain injury.

Animals ; Blood Glucose ; metabolism ; Brain Injuries ; blood ; complications ; physiopathology ; Hyperglycemia ; etiology ; Insulin ; blood ; Insulin Resistance ; Male ; Rats ; Rats, Wistar

The relationship between tyrosine phosphorylation (TP) and protein expression of insulin receptor (InsR) and insulin resistance (IR) in patients with gestational diabetes mellitus (GDM) was investigated. The InsR expression and TP in skeleton muscle tissue were determined by Western blotting and immunoprecipitation in women with GDM (GDM group, n=22), normal pregnant women (normal pregnancy group, n=22) and normal non-pregnant women (normal non-pregnant group, n=13). Fasting plasma glucose (FPG) and fasting insulin (FINS) were measured by oxidase assay and immunoradioassay. The results showed that the levels of FPG (5.61±0.78 mmol/L), FINS (15.42±5.13 mU/L) and Homeostasis model assessment-IR (HOMA-IR) (1.21±0.52) in GDM group were significantly higher than those in normal pregnancy group (4.43±0.46 mmol/L, 10.56±3.07 mU/L and 0.80±0.31 respectively) (P<0.01). The levels of FINS and HOMA-IR in normal pregnancy group were significantly higher than those in normal non-pregnant group (7.56±2.31 mU/L and 0.47±0.26 respectively) (P<0.01). There was no significant difference in the InsR expression level among the three groups (P>0.05). TP of InsR with insulin stimulation was significantly decreased in GDM group (0.20±0.05) as compared with normal pregnancy group (0.26±0.06) (P<0.01). TP of InsR with insulin stimulation in normal pregnancy group was lower than that in normal non-pregnant group (0.31±0.06) (P<0.01). TP of InsR with insulin stimulation was negatively related with HOMA-IR in GDM group (r=-0.525, P<0.01). There was no correlation between the protein expression of InsR and HOMA-IR in GDM group (r=-0.236, P>0.05). It was suggested that there is no significant correlation between the protein expression of InsR in skeletal muscle and IR in GDM, but changes in TP of InsR are associated with IR in GDM.
Adult ; Blood Glucose ; metabolism ; Blotting, Western ; Diabetes, Gestational ; blood ; metabolism ; Fasting ; blood ; Female ; Humans ; Insulin ; blood ; Insulin Resistance ; Muscle, Skeletal ; metabolism ; Phosphorylation ; Pregnancy ; Radioimmunoassay ; Receptor, Insulin ; metabolism ; Tyrosine ; metabolism

OBJECTIVETo explore the factors influencing insulin resistance in children with different nutritional status during pubertal development.

METHODSThree hundred children with simple obese aged 7 to 17 years, and 300 normal healthy children and 300 children with malnutrition, matched for age (+/- 3 months) and height (+/- 2 cm), were selected. Fasting serum levels of leptin, insulin, glucose, total cholesterol (TC), triglycerides (TG), low density lipoprotein-cholesterol (LDL-C) and high density lipoprotein-cholesterol (HDL-C) were measured for them.

RESULTSLevels of fasting serum insulin in obese children, except for boys at Tanner stage I and girls at Tanner stage II, were higher than those in normal and malnutrition children (P < 0.01). Average serum level of leptin in obese boys and girls at varied Tanner stages was higher than that in normal children, and higher in normal children than that in children with malnutrition (P<0.01). Serum level of TG in obese children [(1.53 +/- 0.13) mmol/L] was higher than that in normal ones [(1.12 +/- 0.10) mmol/L] and in children with malnutrition [(1.03 +/- 0.09) mmol/L]. There was no significant difference in levels of fasting blood glucose and other blood lipids between the three groups of children. Insulin sensitivity decreased with pubertal development and its index reversely correlated with Tanner stage and serum level of leptin (r=-0.27 and -0.36, respectively, P<0.01).

CONCLUSIONObesity (BMI), serum level of leptin and pubertal development were independent risk factors for insulin resistance in children aged 7 to 17 years.

Adolescent ; Body Mass Index ; Child ; Estradiol ; blood ; Growth Hormone ; metabolism ; Humans ; Insulin ; blood ; Insulin Resistance ; Leptin ; blood ; physiology ; Male ; Malnutrition ; blood ; Obesity ; blood ; physiopathology ; Puberty ; physiology ; Testosterone ; blood

Low birth weight is associated with insulin resistance and type 2 diabetes in adults. The fetal programming hypothesis has shown that insulin resistance and its associated metabolic disturbances result from a poor gestational environment, for which low birth weight is a surrogate. An at-home questionnaire survey was performed on 660 middle school students (12-15 years) in Seoul, Korea, and 152 cases were randomly selected based on their birth weight. Subjects were divided into three groups according to birth weight. We recorded their birth weight and measured their current anthropometric data, blood pressure, lipid profile, HOMA-IR, and HOMA-beta, and compared these parameters among the groups. The relation of birth weight to physiological characteristics in adolescence was examined. Systolic blood pressure, lipid profiles, and fasting plasma glucose, HOMA-beta were not significantly different among the groups, but diastolic blood pressure was lower in the third tertile. Insulin, C-peptide, and HOMA-IR were higher in the lower birth weight tertile. After adjustment for confounding factors, birth weight was inversely related to diastolic blood pressure, insulin, C-peptide, and HOMA-IR. We conclude that low birth weight may predict the risk of the insulin resistance and its progression over age, and that adequate gestational nutrition is therefore necessary to prevent low birth weight.
Male ; Korea/epidemiology ; Insulin-Secreting Cells/physiology ; *Insulin Resistance ; Insulin/blood ; Hyperinsulinism/epidemiology/etiology/metabolism ; Humans ; Female ; Child ; C-Peptide/blood ; Blood Pressure ; *Birth Weight ; Adolescent

OBJECTIVETo investigate the effects of intensive insulin therapy on insulin resistance(IR) and serum proteins after radical gastrectomy.

METHODSTwenty-two gastric cancer patients were randomly divided into the control (n=11) and intensive insulin therapy group (n=11), and underwent distal radical subtotal gastrectomy under epidural anesthesia. Fasting blood glucose (FBG), fasting insulin (FINS) and serum proteins were assayed preoperatively and at day 1, 3, 7 postoperatively. Insulin resistance index was calculated using homeostasis model assessment (HOMA). The length of hospital stay and postoperative complications were recorded respectively.

RESULTS(1)The levels of FBG, FINS, lnHOMA-IR (P<0.01,P<0.05) and the incidence of insulin resistance were remarkably decreased by intensive insulin therapy after the surgical procedure.(2)The levels of serum transferrin (TRF), prealbumin (PRE) and retinal binding protein (RBP) in the intensive insulin therapy group were significantly improved as compared to control group after operation(P<0.05). (3) The duration of fever, antibiotic use, passage of gas by anus, length of hospital stay and the occurrence of postoperative complications were also significantly lower than those in control group(P<0.01,P<0.05).

CONCLUSIONCompared to routine therapy, the intensive insulin therapy has more beneficial effects on the patients undergone distal radical subtotal gastrectomy in decreasing the insulin resistance, improving the status of nutrition and preventing postoperative complications.

Adult ; Aged ; Blood Glucose ; metabolism ; Blood Proteins ; metabolism ; Female ; Gastrectomy ; Humans ; Insulin ; metabolism ; therapeutic use ; Insulin Resistance ; Male ; Middle Aged ; Postoperative Complications ; Stomach Neoplasms ; drug therapy ; metabolism

Insulin-like growth factor (IGF) is closely associated with cardiovascular diseases. Low IGF-I level and high insulin-like growth factor binding protein-1 (IGFBP-1) level in serum can be used as a marker in predicting the long term morbidity and mortality of acute myocardial infarction (AMI). The article reviews the recent advances in IGFBP-1 in the prognosis of AMI.
Humans ; Insulin-Like Growth Factor Binding Protein 1 ; blood ; Insulin-Like Growth Factor I ; metabolism ; Myocardial Infarction ; blood ; Prognosis