Home About us Contact | |||
Plasma Insulin Levels (plasma + insulin_level)
Selected AbstractsThe effect of capsaicin on blood glucose, plasma insulin levels and insulin binding in dog modelsPHYTOTHERAPY RESEARCH, Issue 5 2001I. Tolan Abstract Capsicum frutescens has been used to treat diabetes mellitus by traditional healers in Jamaica. This study was designed to identify any hypoglycaemic principle(s) and to determine the mechanism of action. Purification experiments employing thin layer chromatography (TLC) and high performance liquid chromatography (HPLC) led to the extraction of the active principle, capsaicin. Capsaicin caused a decrease in blood glucose levels of 4.91,±,0.52 (n,=,6),mmol/dL versus 6.40,±,0.13,mmol/dL (n,=,6) for the control (p,<,0.05) at the 2.5,h time interval when the oral glucose tolerance test (OGTT) was performed on dogs treated with capsaicin and compared with the control. Plasma insulin levels measured at the 2.5,h time interval showed that there was an increase in plasma insulin levels of 5.78,±,0.76,µIU/mL (n,=,6) for the capsaicin treated dogs versus 3.70,±,0.43,µIU/mL (n,=,10) for the control (p,<,0.05). Insulin receptor studies, using a modification of the method of Gambhir et al. done on monocytes obtained from blood at the 2.5,h time interval showed that there was a decrease in the percentage receptor binding for the capsaicin treated dogs when compared with the control. Insulin affinity results showed that there was a decrease of 2.4,×,10,4 in monocytes for the capsaicin treated dogs versus 8.77,×,10,4 for the control (p,<,0.05). Also, insulin receptor calculations showed a decrease in number, 2.63,×,108,±,5.73,×,107, compared with 8.77,×,108,±,1.47,×,108 for the control. In conclusion it can be stated that capsaicin is responsible for the hypoglycaemic episodes seen in the dogs and that it also causes an increase in insulin secretion which leads to a reduction of insulin binding on the insulin receptors. Copyright © 2001 John Wiley & Sons, Ltd. [source] Continuous Subcutaneous Glucose Monitoring System in diabetic mothers during labour and postnatal glucose adaptation of their infantsDIABETIC MEDICINE, Issue 4 2008E. Stenninger Abstract Aims To assess a new technique for continuous monitoring of glucose concentration during labour in diabetic mothers. A second objective was to study maternal glucose levels in relation to postnatal glucose adaptation and the need for intravenous (IV) glucose treatment in the newborn infant. Methods Fifteen pregnant women with insulin-treated diabetes mellitus participated in this prospective pilot study. To measure their glucose control during labour we used the Continuous Subcutaneous Glucose Monitoring System (CGMS; Medtronic, Minneapolis, MN, USA) to calculate the mean glucose concentration and the area under the curve (AUC) in the last 120 min before delivery. All infants of these women were transferred to the neonatal care unit for early oral feeding and blood glucose measurements up to 14 h after delivery. Infants received IV glucose if blood glucose values were repeatedly < 2.2 mmol/l. Results All women coped well with the CGMS monitoring. AUC 0,120 min before delivery, mean glucose concentration 0,120 min before delivery and cord plasma insulin level were all significantly associated with the need for IV glucose in the newborn children. Conclusions In this study we found an association between maternal glucose concentrations during labour and postnatal glucose adaptation and need for IV glucose treatment in the infants. Online monitoring of glucose levels during delivery might help us to achieve maternal normoglycaemia and further reduce the risk of postnatal hypoglycaemia in the offspring. [source] Antidiabetic activity of flavone from Ipomoea Batatas leaf in non-insulin dependent diabetic ratsINTERNATIONAL JOURNAL OF FOOD SCIENCE & TECHNOLOGY, Issue 1 2007Rui Zhao Summary The effects of flavone extracted from Ipomoea batatas leaf (FIBL) on body weight, blood glucose, serum lipid profiles, serum insulin and free radicals in rats with non-insulin dependent diabetes mellitus (NIDDM) were studied. FIBL treatment (25, 50, 100 mg kg,1) for 2 weeks resulted in a significant decrease in the concentration of plasma triglyceride (TG), plasma cholesterol (TC) and weight in NIDDM rats. Furthermore, FIBL markedly decreased fasting plasma insulin level, blood glucose (FBG) level, low-density lipoprotein cholesterol (LDL-C), and malondialdehyde (MDA) levels and significantly increased the Insulin Sensitive Index (ISI) and superoxide dismutase (SOD) level in NIDDM rats. In addition, flavone extracted from I. batatas leaf did not show any physical or behavioural signs of toxicity. More significantly, our data demonstrate the FIBL at the dose of 50 mg kg,1 body weight exhibited the optimal effect. The above results suggest that flavone extracted from I. batatas leaf could control blood glucose and modulate the metabolism of glucose and blood lipid, and decrease outputs of lipid peroxidation and scavenge the free radicals in non-insulin dependent diabetic rats. [source] Active immunization against (Pro3)GIP improves metabolic status in high-fat-fed miceDIABETES OBESITY & METABOLISM, Issue 9 2010I. A. Montgomery Aim: Ablation of gastric inhibitory polypeptide (GIP) receptor signalling can prevent many of the metabolic abnormalities associated with dietary-induced obesity-diabetes. The present study was designed to assess the ability of active immunization against (Pro3)GIP to counter metabolic dysfunction associated with diet-induced obesity in high-fat-fed mice. Methods: Normal male Swiss NIH mice were injected (s.c.) once every 14 days for 98 days with complexed (Pro3)GIP peptide, with transfer to a high-fat diet on day 21. Results: Active immunization against (Pro3)GIP resulted in circulating GIP antibody production and significantly (p < 0.05 p < 0.01) reduced circulating blood glucose concentrations compared to high-fat control mice from day 84 onwards. Glucose levels were not significantly different from lean controls. The glycaemic response to i.p. glucose was correspondingly improved (p < 0.01) in (Pro3)GIP-immunized mice. Furthermore, circulating and glucose-stimulated plasma insulin levels were significantly (p < 0.01 to p < 0.001) depressed compared to high-fat control mice. Liver triglyceride, pancreatic insulin and circulating LDL-cholesterol levels were also significantly reduced in (Pro3)GIP-immunized mice. These changes were independent of any effects on food intake or body weight. The glucose-lowering effect of native GIP was annulled in (Pro3)GIP-immunized mice consistent with the induction of biologically effective GIP-specific neutralizing antibodies. Conclusion: These results suggest that immunoneutralization of GIP represents an effective means of countering the disruption of metabolic processes induced by high-fat feeding. [source] Moxonidine improves glycaemic control in mildly hypertensive, overweight patients: a comparison with metforminDIABETES OBESITY & METABOLISM, Issue 4 2006Irina Chazova Aim:, To compare the effects of moxonidine and metformin on glycaemic control in patients with impaired glucose tolerance and signs of the metabolic syndrome. Methods:, A multicentre, prospective, randomized, open-label study design was adopted with blinded endpoint evaluation. Patients ,40 years old, with impaired glucose tolerance (or diabetes mellitus treated with diet alone) and a body mass index (BMI) of at least 27 kg/m2 were treated twice daily with moxonidine 0.2 mg or metformin 500 mg for 16 weeks. Oral glucose tolerance test (OGTT) was performed at baseline and end-of-study; plasma insulin and plasma glucose levels were measured at 0, 60, 120 and 180 min after administration. Results:, With regard to effects on insulin [mean area under the curve (AUC) for insulin], the primary efficacy endpoint of the study, both drugs did not show equivalence. On the contrary, in the per protocol (PP) population, moxonidine statistically significantly (p = 0.025) decreased the AUC for insulin from baseline in the PP population; for metformin, the treatment effect on insulin was a small, net increase resulting in a statistically significant between-group difference of 16.2% (95% CI = 0.1,35.0). The change in mean insulin AUC was most marked in the subgroup of patients with higher sympathetic activity (heart rate >80 bpm). Mean fasting plasma glucose (FPG) levels and HbA1c levels were largely unchanged by moxonidine treatment but significantly decreased by metformin treatment. The difference between the groups was 14.7% (p = 0.0523) in the intent-to-treat (ITT) sample. By study end, both treatments had significantly increased the Matsuda Insulin Sensitivity Index (ISI) from baseline to a comparable extent: moxonidine by reducing plasma insulin after a glucose challenge, metformin by reducing FPG. BMI fell significantly in both groups and blood pressure normalized; both drugs were well tolerated. Conclusions:, Moxonidine improved insulin sensitivity in response to glucose challenge in patients with evidence of metabolic syndrome. This improvement resulted from a reduction in plasma insulin levels and was most marked in patients with high sympathetic drive at baseline. By enhancing insulin sensitivity, moxonidine treatment may help prevent the development of diabetes and thereby ameliorate the risk for cardiovascular disease. [source] Activation of the PI3K/Akt signal transduction pathway and increased levels of insulin receptor in protein repair-deficient miceAGING CELL, Issue 1 2005Christine Farrar Summary Protein l -isoaspartate (d -aspartate) O -methyltransferase is an enzyme that catalyses the repair of isoaspartyl damage in proteins. Mice lacking this enzyme (Pcmt1,/, mice) have a progressive increase in brain size compared with wild-type mice (Pcmt1+/+ mice), a phenotype that can be associated with alterations in the PI3K/Akt signal transduction pathway. Here we show that components of this pathway, including Akt, GSK3, and PDK-1, are more highly phosphorylated in the brains of Pcmt1,/, mice, particularly in cells of the hippocampus, in comparison with Pcmt1+/+ mice. Examination of upstream elements of this pathway in the hippocampus revealed that Pcmt1,/, mice have increased activation of insulin-like growth factor-I (IGF-I) receptor and/or insulin receptor. Western blot analysis revealed an approximate 200% increase in insulin receptor protein levels and an approximate 50% increase in IGF-I receptor protein levels in the hippocampus of Pcmt1,/, mice. Higher levels of the insulin receptor protein were also found in other regions of the adult brain and in whole tissue extracts of brain, liver, heart and testes of both juvenile and adult Pcmt1,/, mice. There were no significant differences in plasma insulin levels for adult Pcmt1,/, mice during glucose tolerance tests. However, they did show higher peak levels of blood glucose, suggesting a mild impairment in glucose tolerance. We propose that Pcmt1,/, mice have altered regulation of the insulin pathway, possibly as a compensatory response to altered glucose uptake or metabolism or as an adaptive response to a general accumulation of isoaspartyl protein damage in the brain and other tissues. [source] Impaired Glucose Tolerance in the R6/1 Transgenic Mouse Model of Huntington's DiseaseJOURNAL OF NEUROENDOCRINOLOGY, Issue 2 2008K. Josefsen Previous reports have highlighted a possible link between Huntington's disease (HD) and diabetes mellitus (DM), but the association has not been characterised in detail. A transgenic mouse model for HD, the R6/2 mouse, also develops diabetes. In the present study, we examined the R6/1 mouse, which carries a shorter CAG repeat than the R6/2 mouse, and found that, although not diabetic, the mice showed several signs of impaired glucose tolerance. First, following i.p. glucose injection, the blood glucose concentration was approximately 30% higher in young R6/1 mice (10 weeks) compared to wild-type mice (P = 0.004). In older mice (38 weeks), glucose tolerance was further impaired in both R6/1 and wild-type animals. Second, during glucose challenge, the R6/1 mice reached higher plasma insulin levels than wild-type mice, but the peripheral insulin sensitivity was normal as measured by injection of human or mouse insulin or when evaluated by the quantitative insulin sensitivity check index (QUICKI). Third, the beta cell volume was 17% and 39% smaller at 10 and 38 weeks of age, respectively, compared to age-matched wild-type littermates and the reduction was not caused by apoptosis at either age. Finally, we demonstrated the presence of the HD gene product, huntingtin (htt), in both alpha- and beta-cells in R6/1 islets of Langerhans. Since pancreatic beta cells and neurons share several common traits, clarification of the mechanism associating neurodegenerative diseases with diabetes might improve our understanding of the pathogenic events leading to both groups of diseases. [source] Antidiabetic properties of the alcoholic extract of Sphaeranthus indicus in streptozotocin-nicotinamide diabetic ratsJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 7 2008Kirti S. Prabhu We have investigated the possible antihyperglycaemic effects of Sphaeranthus indicus extract in rats rendered diabetic by nicotinamide (120 mgkg,1 i.p.) and streptozotocin (STZ) (60 mgkg,1 i.p). Fasting plasma glucose levels, serum insulin levels, serum lipid profiles, magnesium levels, glycosylated haemoglobin, changes in body weight and liver glycogen levels were evaluated in normal and diabetic rats. Oral administration of S. indicus for 15 days resulted in significant decrease in blood glucose levels and increases in hepatic glycogen and plasma insulin levels. Fasting normal rats treated with the alcoholic extract of S. indicus showed significant improvement in oral glucose tolerance test. Glibenclamide was used as a reference standard. The findings demonstrate that the alcoholic S. indicus extract may be useful in the treatment of diabetes. [source] Insulin-related metabolism following hematopoietic stem cell transplantation in childhoodPEDIATRIC DIABETES, Issue 2 2009Ronit Elhasid Objectives:, To assess insulin-related metabolism following hematopoietic stem cell transplantation (HSCT) in childhood. Study design:, Thirty-four patients who underwent HSCT were compared with 21 patients with similar diseases who were not transplanted. Median follow-up was 3.6 yr after HSCT. Anthropometric parameters, fasting plasma glucose and insulin levels, hemoglobin A1c (HbA1c) and lipid profile were measured and compared. Results:, HbA1c was significantly higher (p = 0.001) in the study group. Two (5.8%) patients in the study group developed type 2 diabetes mellitus. Among thalassemic patients, significantly lower insulin resistance indices (p = 0.05) and fasting plasma insulin levels (p = 0.033) were found in the study group compared with the control group. Conclusions:, Attentive follow-up of insulin-related metabolism following HSCT in children is needed. The significance of the higher HbA1c values in the study group remains to be evaluated in a larger cohort of patients. [source] The effect of capsaicin on blood glucose, plasma insulin levels and insulin binding in dog modelsPHYTOTHERAPY RESEARCH, Issue 5 2001I. Tolan Abstract Capsicum frutescens has been used to treat diabetes mellitus by traditional healers in Jamaica. This study was designed to identify any hypoglycaemic principle(s) and to determine the mechanism of action. Purification experiments employing thin layer chromatography (TLC) and high performance liquid chromatography (HPLC) led to the extraction of the active principle, capsaicin. Capsaicin caused a decrease in blood glucose levels of 4.91,±,0.52 (n,=,6),mmol/dL versus 6.40,±,0.13,mmol/dL (n,=,6) for the control (p,<,0.05) at the 2.5,h time interval when the oral glucose tolerance test (OGTT) was performed on dogs treated with capsaicin and compared with the control. Plasma insulin levels measured at the 2.5,h time interval showed that there was an increase in plasma insulin levels of 5.78,±,0.76,µIU/mL (n,=,6) for the capsaicin treated dogs versus 3.70,±,0.43,µIU/mL (n,=,10) for the control (p,<,0.05). Insulin receptor studies, using a modification of the method of Gambhir et al. done on monocytes obtained from blood at the 2.5,h time interval showed that there was a decrease in the percentage receptor binding for the capsaicin treated dogs when compared with the control. Insulin affinity results showed that there was a decrease of 2.4,×,10,4 in monocytes for the capsaicin treated dogs versus 8.77,×,10,4 for the control (p,<,0.05). Also, insulin receptor calculations showed a decrease in number, 2.63,×,108,±,5.73,×,107, compared with 8.77,×,108,±,1.47,×,108 for the control. In conclusion it can be stated that capsaicin is responsible for the hypoglycaemic episodes seen in the dogs and that it also causes an increase in insulin secretion which leads to a reduction of insulin binding on the insulin receptors. Copyright © 2001 John Wiley & Sons, Ltd. [source] (Pro3)GIP[mPEG]: novel, long-acting, mPEGylated antagonist of gastric inhibitory polypeptide for obesity-diabetes (diabesity) therapyBRITISH JOURNAL OF PHARMACOLOGY, Issue 5 2008P L McClean Background and purpose: Antagonism of the gastric inhibitory polypeptide (GIP) receptor with daily injection of proline-3 gastric inhibitory polypeptide ((Pro3)GIP) can reverse or prevent many of the metabolic abnormalities associated with diet-induced obesity-diabetes (diabesity). This study has examined the ability of a novel and longer-acting form of (Pro3)GIP, (Pro3)GIP mini-polyethylene glycol ((Pro3)GIP[mPEG]), to counter diet-induced diabesity in mice, using a daily and intermittent dosing regime. Experimental approach: We studied the actions of (Pro3)GIP[mPEG] at the GIP receptor in vitro and in vivo in both dietary and genetic diabesity. Key results: (Pro3)GIP[mPEG] was completely resistant to degradation by dipeptidyl peptidase IV. (Pro3)GIP[mPEG] inhibited GIP-induced cAMP and insulin production in vitro. A greater and prolonged antagonism of GIP-induced glucose-lowering action was followed (Pro3)GIP[mPEG] administration, compared with (Pro3)GIP. In contrast with (Pro3)GIP, mice injected once every 3 days for 48 days with (Pro3)GIP[mPEG] displayed reduced body weight gain and hyperinsulinemia with improved glucose tolerance and insulin secretory responses, compared with high-fat-fed controls. Daily i.p. injection of (Pro3)GIP, (Pro3)GIP[mPEG] or (Pro3)GIP b.i.d. for 21 days also decreased body weight, circulating plasma insulin levels and improved glucose tolerance, compared with high-fat controls. Plasma triglycerides were decreased by (Pro3)GIP[mPEG] and (Pro3)GIP b.i.d. treatment groups. The observed changes were accompanied by enhancement of insulin sensitivity in all treatment regimes. (Pro3)GIP[mPEG] was also effective over 16 days treatment of genetically obese-diabetic ob/ob mice. Conclusions and implications: These data demonstrate the utility of GIP receptor antagonism for the treatment of diabesity and the potential offered by (Pro3)GIP[mPEG] as a long-acting stable GIP receptor antagonist. British Journal of Pharmacology (2008) 155, 690,701; doi:10.1038/bjp.2008.317; published online 11 August 2008 [source] Effects of T4 replacement therapy on glucose metabolism in subjects with subclinical (SH) and overt hypothyroidism (OH)CLINICAL ENDOCRINOLOGY, Issue 6 2008Ammon Handisurya Summary Objective To evaluate ,-cell function and insulin sensitivity in subjects with overt (OH) and subclinical hypothyroidism (SH) before and after T4 replacement therapy. Background Disturbances in glucose metabolism have been observed in hypothyroid states. However, the clinical significance and potential reversibility of these alterations by T4 replacement therapy remain to be elucidated especially in patients with SH. Design and patients Parameters of glucose metabolism have been investigated in subjects with OH (n = 12) and SH (n = 11). Insulin sensitivity has been assessed by the euglycaemic,hyperinsulinaemic clamp technique and ,-cell function by mathematical modelling of data derived from an oral glucose tolerance test. Results Fasting and dynamic glycaemia as assessed by the AUCGlucose remained unaltered following substitution therapy (P > 0·05). Insulin sensitivity significantly improved only in subjects with OH (P < 0·05). Fasting insulin and proinsulin concentrations increased proportionally in both groups (P < 0·05) with the proinsulin : insulin ratio remaining unchanged (P > 0·05). Total insulin secretion was higher in OH before initiation of therapy (P < 0·05). In both groups, dynamic parameters including total insulin secretion, hepatic insulin extraction and the adaptation index were significantly attenuated (P < 0·05) after restoration of thyroid function, whereas the disposition index and the basal insulin secretion rate remained unaltered (P > 0·05). Conclusion In summary, SH and OH are characterized by attenuated basal plasma insulin levels and increased glucose-induced insulin secretion. T4 replacement therapy partially ameliorates the insulin secretion profile and reduces the demand on pancreatic ,-cells after glucose challenge to an extent that exceeds any effect attributable to the improvement in insulin sensitivity. [source] |