Metabolic syndrome (MetS) is a cluster of metabolic abnormalities that include hypertension, altered glucose metabolism, dyslipidemia, and abdominal obesity and is strongly associated with an increased risk for diabetes and cardiovascular disease onset in obese adults and children. A progressively greater number of children and adolescents are being affected by this syndrome due to the constant increase in the prevalence of obesity. Like obesity, childhood MetS highly tracks to adulthood. The pathogenesis of MetS includes the interaction between obesity, insulin resistance, and inflammation. Early diagnosis and intervention are important in order to conduct lifestyle modification. In this article, we review the definition and pathophysiology of MetS, the importance of screening, and prevention and treatment options for MetS in childhood.
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Type 1 diabetes requires lifelong insulin therapy because insulin-secretion capability is diminished. Glycemic control and glucose monitoring are important to prevent type 1 diabetes complications. Diabetes technologies have developed rapidly; continuous glucose monitoring (CGM) and continuous subcutaneous insulin infusion (CSII) are now common and greatly aid glycemic control, especially in children and adolescents. The National Health Insurance Service has provided partial reimbursements for both CGM and CSII devices since 2019 and 2020, respectively; the devices are thus expected to become more popular. CGM reduces the frequency of hypoglycemia and the level of glycated hemoglobin. CSII affords more precise glycemic control than multi-dose insulin therapy. CSII showed reduced frequency of hypoglycemia and improved metabolic outcome without an increase in the body mass index z-score. Technological advancement of combined CGM and CSII will eventually serve as an artificial pancreas. The National Health Insurance Service should fund not only the devices but also education of patients and caregivers. In addition, healthcare providers must be continuously updated on new diabetes technologies.
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, Nadhum Abdulnabi Awad, Amel Hussein Mohammed We aimed to evaluate the effect of insulin resistance (IR) on serum Intelectin-1 and endocrinological hormones levels in obese and non-obese women with and without polycystic ovary syndrome (PCOS) in Basrah, Iraq.
From 124 women volunteers, 60 patients with primary and 64 patients with secondary, while 56 normal ovulatory women were taken as controls. Their fasting insulin hormone, intelectin-1, anti-Mullerian hormone, luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin (PRL), estradiol (E2) and testosterones (T) were determined by ELISA methods. BMI, glucose and quantitative insulin sensitivity check index as well as IR was determined by the homeostasis model assessment.
A significant changes (P<0.05) were seen in the level of homeostasis model assessment-IR, E2 and T. Levels of anti-Mullerian hormone, LH, LH/FSH ratio and prolactin were significantly (P<0.01) increased and level of intelectin-1 and E2/T ratio were significantly (P<0.01) decreased, while quantitative insulin sensitivity check index level was not significantly different (P>0.05) between the patients (1°PCOS and 2°PCOS) and control groups. On the other hand, our data reported that FSH level was significantly (P<0.05) lower in obese and higher in non-obese patients with PCOS as compared to control group.
Levels of intelectin-1 and endocrinological hormones have significantly associated with body mass index, IR and physical activity in patients and normal groups and the strategies that can modulate levels of these parameters would improve metabolic disarrangements in women with PCOS.
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, Jong Hak Kim, Hee Jung Baik, Minjin Lee, Youn Jin Kim The insulin-like growth factor binding proteins (IGFBP) regulate the bioavailability and bioactivity of insulin-like growth factor. We aimed to evaluate whether the IGFBP-3 level undergo major changes during perioperative periods according to the different kind of anesthetic agents.
Eighteen adults scheduled for elective total abdominal hysterectomy were enrolled. The patients were randomly assigned to have either propofol or isoflurane for maintenance of general anesthesia. A venous sample was taken for analysis of IGFBP-3 at the following time points: before induction, at the time of peritoneal closure, 1 hour after extubation at recovery room, and 2 and 5 postoperative days. The samples were analyzed by enzyme linked immunosolvent assay.
Demographic data were similar between groups. In the both groups, the IGFBP-3 concentration decreased after anesthesia induction, reaching a nadir at the time of peritoneal closure without a significant difference between groups. In analysis between groups, the IGFBP-3 concentration in the isoflurane group on the postoperative 5th day was recovered to preoperative value and significantly higher than that in the propofol group (P<0.05).
This is the first study to show that the anesthetics used for general anesthesia affect the IGFBP-3 level during perioperative periods. The decrease of IGFBP-3 level following anesthesia induction in the isoflurane group was recovered to preoperative value, whereas that observed in the propofol group was not recovered on the postoperative 5th day. Further study is needed to establish the definitive effect of general anesthetics on IGFBP-3 and provide a comprehensive interpretation.
, Han Ju Moon, Jin Seo Kim, Hong Il Kim, Cheol Hyeon Kim, Min Joo Kim Insulin autoimmune syndrome, a rare cause of endogenous hyperinsulinemic hypoglycemia, is characterized by insulin autoantibody, hyperinsulinemia and fasting hypoglycemia. It is well known that drugs containing a sulfhydryl group such as methimazole or α-mercaptopropionyl glycine can induce insulin autoimmune syndrome. However, insulin autoimmune syndrome caused by anti-tuberculosis treatment is very rare. We report a case of insulin autoimmune syndrome after anti-tuberculosis treatment with a review of the relevant literature.
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, Nan Ho Kyung The purpose of this study is to investigate the clinical efficacy and stabilityof human insulin therapy compared with conventional animal insulin therapy in respect ofadverse reactions, glycemic control, insulin requirement and subjective satisfaction.
To investigate the clinical efficacy and stability of human insulin therapy, weconducted this study in 55 university hospitals and goneral hospitals in Korea nationwide,for a period of 32 months from January 4, 1990 through December 31, 1992. The study wasset out to replace conventional animal insulin with human insulin(HumulinR) and observedadverse reactions, changes in blood glucose levels, HbA1C, insulin requirement and subjectivesatisfaction after replacement.
Results are given as fo11ows.
1) Blood glucose level, HbAlc, and insulin requirement were significantly decreased afterreplacement animal insulin with human insulin(p<0.05).
2) As for adverse reactions, hypoglycemia was observed more frequently and the incidenceof chills and local allergic reaction at the site of insulin injection were decreased after replacement animal insulin with human insulin.
3) As for subjective satisfaction of the patients, number of patients with subjective satisfactionwere significantly increased after replacement animal insulin with human insulin(p<0.O5).
These results suggest that human insulin is preferable to animal insulins interms of glycemic control, insulin requirement and subjecive clinical response.
The subcellular distribution of glucose transporter in rat hepatocytes was studied in the absence and presence of insulin by measuring glucose-sensitive cytochalasin B binding sites and immunoreactivities to antibodies specific to hepatocyte glucose transporter. Total hepatocyte membranes bound cytochalasin B at a class of glucose-sensitive sites with a Kd of l.6×l0-6M. and a Bt of 6.8 pmol/mg protein. The glucose-sensitive cytochalasin B binding sites were found in various subcellular membrane fractions with a relative abundance of 47% in a plasma membrane-nuclei-mitochondria-enriched fraction(PM/NM). 29% in a lysosome-enriched fraction(LYSO). 16% in a Golgi-enriched. high density microsomal fraction(HDM) and 8% in the low density microsome fraction(LDM). Relative abundances of two well known plasma membrane markers. 5'-nucleotidase and cell surface carbohydrate label, on the other hand, were found to he 48~50% in PM/NM. 41~43% in LYSO. 6~8% in HDM and l~2% in LDM.
Insulin treatment of intact hepatocytes did not induce any significant changes in the subcellular distributions of the glucose-sensitive. cytochalasin B binding activities, the immunoreactivities to the transporter specific antibodies, or the two cell surface membrane markers. These findings indicate that as much as 15% of the total hepatocyte glucose transporters occur in organelle(s) other than the pasma membrane, most likely representing an intracellular storage pool. which is not decreased by insulin. It is concluded that the rat hepatocyte lacks the insulin-mediated, glucose transporter translocation mechanism, thus would be a valuable experimental system in which one can study the celluar and molecular basis of this deficiency.
, Soo Kyung Lim, Ji young Chang, Eun kyo Jung, Youn-i Choi, Jee-Young Oh, Youngsun Hong, Yeon-Ah Sung, Hyejin Lee Gestational diabetes mellitus (GDM) affects 2%-4% of the all pregnant women, and it is a major risk factor for development of type 2 DM. We performed this cross-sectional study to determine whether there were defects in insulin secretory capacity or insulin sensitivity in women with previous GDM.
On 6-8 weeks after delivery, 75 g oral glucose tolerance test was performed in 36 women with previous GDM and 19 non-pregnant control women matched with age and weight. Intravenous glucose tolerance test was performed on 10-14 weeks after delivery. Insulin secretory capacity measured as the acute insulin response to glucose (AIRg) and insulin sensitivity as minimal model derived sensitivity index (SI) were obtained. AIRg×SI (β-cell disposition index) was used as an index of β-cell function.
Women with previous GDM were classified into normal glucose tolerance (postpartum-NGT, n=19) and impaired glucose tolerance (postpartum-IGT, n=17). Postpartum fasting glucose levels were significantly higher in postpartum-IGT compared to postpartum-NGT and control (P<0.05). AIRg×SI was significantly lower in postpartum-IGT compared to control (P<0.05). SI was lower in postpartum-NGT and postpartum-IGT compared to control, but the difference did not have the statistical significance. Frequency of parental history of type 2 diabetes was significantly greater in postpartum-IGT compared to postpartum-NGT (P<0.05).
Women with previous GDM showed impaired insulin secretion although their glucose tolerance states were restored to normal. It suggests impaired early insulin secretion may be a major pathophysiologic factor for development of type 2 DM, and this defect may be genetically determined.
, Hyejin Lee, Yeon-Ah Sung Insulin resistance is a major pathophysiology in polycystic ovary syndrome (PCOS), and assessment of insulin sensitivity is important. Various insulin sensitivity indices from fasting state or oral glucose tolerance test (OGTT) have been compared with euglycemic hyperinsulinemic clamp. We aimed to evaluate the usefulness of these indices in young Korean women with PCOS.
Euglycemic hyperinsulinemic clamp test and 75 g OGTT were performed in 290 women with PCOS. Insulin mediated glucose uptake (IMGU), the insulin sensitivity index from clamp, was compared with various insulin sensitivity indices such as composite insulin sensitivity index (ISIcomp), estimated metabolic clearance rate (MCRest) of glucose and estimated insulin sensitivity index (ISIest), area under the curve of glucose and insulin ratio (AUC-GIR), OGTT-derived Belfiore index, and oral glucose insulin sensitivity index (OGSI) by Kazama. Fasting state indices such as glucose insulin ratio (GIR), homeostasis model assessment for insulin resistance (HOMA-IR), fasting Belfiore index, and quantitative insulin sensitivity check index (QUICKI) were also compared with IMGU.
The correlation coefficients of ISIcomp, MCRest, ISIest, AUC-GIR, OGTT-Belfiore index, and OGSI with IMGU were all about 0.5 (Ps'<0.001) in PCOS women as a whole. The MCRest and ISIest were significantly correlated with IMGU in both obese (r=0.58 and 0.58, P<0.0001) and non-obese subjects (r=0.33 and 0.32, P<0.001). Fasting glucose and insulin-derived indices showed worse correlation with IMGU than OGTT-derived ones.
The MCRest and ISIest from OGTT might be the best replacement for the insulin sensitivity index from hyperinsulinemic euglycemic clamp independent of obesity.
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, Young Hyun Go, Ji Hee Lee Insulin stimulation of glucose transport in adipocytes results from the translocation of vesicles containing the GLUT4 glucose transporter from an intracellular pool to the plasma membrane. In mammalian cells a family of GTP-binding proteins has been implicated in the control of cellular trffic. Thus this study was planned to see whether G-proteins such as Rab, a small molecular mass G-protein and Gαh, a large molecular mass G-protein are involved in insulin induced GLUT4 translocation process.
Diabetic rats(Spraque-Dauley, 200-250g) were prepared by injection of streptozotocin(60mg/kg,IP) and treated with or without insulin(20U/rat) for 4 weeks. The purpose of the study is to elucidate a possible functional relationship between G-protein and the insulin-responsive GLUT4 translocation by immunoblotting method from the subcellular fractions of adipocytes of epididymal tissues.
As results Rab4 protein was coexisted in the membrane of GLUT4 immunoprecipitates of adipocyte total homogenates in normal rats, however Gαh, could not be detected. The amount of GLUT4 at plasma membrane(PM) obtained from insulin treated rats were increased by 21. 35% compared to that of streptozotocin diabetic rats. The increase of Rab4 at the same plasma membrane was negligible. On the other hand, the amounts of GLUT4 and Rab4 at low density microsome(LDM) were decreased by 7.82% and 9.25%, respectively.
These results show that Rab4 is co-localized with GLUT4 in an insulin-responsive intracellular compartment and Rab4 protein plays role in the action of insulin on the GLUT4 translocation but a large molecular G-protein, Gαh is not involved in the GLUT4 translocation process.
Insulin stimulates glucose transport in muscle cell and adipocyte via the rapid redistribution of GLUT4 glucose transporters from intracellular membrane compartments to the cell surface. The mechanism that insulin treggers the translocation of glucose transporters in not known yet whether it is due to the structural differences among glucose transporters or there is cell specific targetting/translocation apparatus insulin-sensitive cells.
This study was planned to examine this question by strdying insulin effect on the glucose transport rate at adipocyte and hepatocyte fused with GLUT1 vesicle, respecitively.
The results showed that treatment of 37nM insulin increased the transport rate of 3-0-methylglucose by 3.8-fold at adipocyte fused with GLUT1 but increased lnly by 1.2-fold at hepatocyte fused with GLUT1.
Therefore, it is suggested that insulin sensitive cell has a cell-specific targetting/translocation machinery which is triggered by insulin-insulin receptor interaction but insulin sensitivity may not dependent on isoform(structural)-specific manner.
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