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Maja Cigrovski Berkovic - One of the best experts on this subject based on the ideXlab platform.
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2484 pub association of gastrin levels and parameters of Glucoregulation in type 2 diabetes patients
Diabetes, 2019Co-Authors: Maja Cigrovski Berkovic, Davorka Herman Mahecic, Ines BiliccurcicAbstract:Background and Aims: Recent data suggest that co-administration of gastrin and GLP-1 improves glucose homeostasis and increase β-cell mass in a rodent model of diabetes, we hypothesized that higher baseline levels of endogenous gastrin prior treatment could be a predictor of beta cell function and Glucoregulation in newly diagnosed DMT2 patients. Patients and Methods: In this cross-sectional study 317 patients (116 males and 201 females) with new onset DMT2 were included. Patients treated with IPPs were excluded. Fasting plasma glucose (FPG), postprandial PG (PPG), HbA1c, fasting insulin, pancreatic B cell function (HOMA-B), insulin resistance index (HOMA-IR), c-peptide, CgA and gastrin levels were measured at the time of diagnosis, and after 6 months of follow-up. Results: Baseline Hba1c was 7,49±2,09%, average age of patients was 62.53 ±11.33 years. 65.7% of patients were overweight and obese. Parameters of Glucoregulation were not significantly correlated with gastrin (all p> 0.05), while there was moderate negative correlation with HOMA-B (HbA1c r=-.58, p Conclusion: At the time of DMT2 onset there was no association between baseline gastrin levels and parameters of Glucoregulation however after 6 months of follow-up increase in gastrin and CgA levels was observed along with the improvement of glycemic control indicating a possible relationship of gastrin levels and amelioration of beta cell function followed by metformin initiation as well as life style changes. Disclosure M. Cigrovski Berkovic: None. D. Herman Mahecic: None. I. Bilic-Curcic: None.
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gastrin a potential predictor of Glucoregulation in newly diagnosed type 2 diabetes patients
Diabetes, 2018Co-Authors: Maja Cigrovski Berkovic, Davorka Herman, Ines BiliccurcicAbstract:Background and Aims: Experimental data demonstrated that activation of GLP-1 and gastrin signaling induces beta cell neogenesis, resulting in a promotion of glucose-induced insulin secretion. In addition, treatment with proton pump inhibitors is associated with greater glycemic control in patients with type 2 diabetes (T2DM), particularly in those on insulin- or GLP-1-based therapy. The aim of this study was to assess gastrin as a potential predictor of beta cell function and Glucoregulation in newly diagnosed T2DM patients. Materials and Methods: In this cross sectional study 190 patients (64 males and 126 females) with new onset T2DM were included. Patients treated with IPPs were excluded. Fasting plasma glucose (FPG), postprandial PG, HbA1c, fasting insulin, pancreatic B cell function (HOMA-B), insulin resistance index (HOMA-IR), fasting c-peptide and gastrin levels were measured at the time of diagnosis. Results: Baseline HbA1c was 7.53±2.08%, average age of patients was 61.8±10.years and body mass index (BMI) was 31.25±5.73 kg/m2. Parameters of Glucoregulation were not significantly correlated with gastrin (all p>0.05), while there was moderate negative correlation with HOMA-B (HbA1c, FPG and PPG ; p 0.05) or HOMA-IR. Furthermore, no association was established between c-peptide, insulin levels and gastrin (p>0.05). Conclusion: Baseline gastrin levels are not sufficient to have a significant effect on Glucoregulation or HOMA-B and HOMA-IR in newly diagnosed T2DM, therefore it could be postulated that further stimulation of gastrin secretion (e.g., with IPPs or GLP-1 based therapy) is needed in order to influence beta cell function and glycemic control.
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BRIEF REPORT The Effects of Transition from Bedtime to Morning Glargine Administration in Patients with Poorly Regulated Type 1 Diabetes Mellitus: Croatian Pilot Study
2015Co-Authors: Marina Gradiser, Ines Bilic-curcic, Boris Djindjic, Maja Cigrovski BerkovicAbstract:The Author(s) 2015. This article is published with open access at Springerlink.com Introduction: The objective of this study was to compare differences in Glucoregulation, frequency of hypoglycemic episodes, glucose variability and lipid profiles of inpatients with poorly regulated type 1 diabetes mellitu
Ines Biliccurcic - One of the best experts on this subject based on the ideXlab platform.
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2484 pub association of gastrin levels and parameters of Glucoregulation in type 2 diabetes patients
Diabetes, 2019Co-Authors: Maja Cigrovski Berkovic, Davorka Herman Mahecic, Ines BiliccurcicAbstract:Background and Aims: Recent data suggest that co-administration of gastrin and GLP-1 improves glucose homeostasis and increase β-cell mass in a rodent model of diabetes, we hypothesized that higher baseline levels of endogenous gastrin prior treatment could be a predictor of beta cell function and Glucoregulation in newly diagnosed DMT2 patients. Patients and Methods: In this cross-sectional study 317 patients (116 males and 201 females) with new onset DMT2 were included. Patients treated with IPPs were excluded. Fasting plasma glucose (FPG), postprandial PG (PPG), HbA1c, fasting insulin, pancreatic B cell function (HOMA-B), insulin resistance index (HOMA-IR), c-peptide, CgA and gastrin levels were measured at the time of diagnosis, and after 6 months of follow-up. Results: Baseline Hba1c was 7,49±2,09%, average age of patients was 62.53 ±11.33 years. 65.7% of patients were overweight and obese. Parameters of Glucoregulation were not significantly correlated with gastrin (all p> 0.05), while there was moderate negative correlation with HOMA-B (HbA1c r=-.58, p Conclusion: At the time of DMT2 onset there was no association between baseline gastrin levels and parameters of Glucoregulation however after 6 months of follow-up increase in gastrin and CgA levels was observed along with the improvement of glycemic control indicating a possible relationship of gastrin levels and amelioration of beta cell function followed by metformin initiation as well as life style changes. Disclosure M. Cigrovski Berkovic: None. D. Herman Mahecic: None. I. Bilic-Curcic: None.
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gastrin a potential predictor of Glucoregulation in newly diagnosed type 2 diabetes patients
Diabetes, 2018Co-Authors: Maja Cigrovski Berkovic, Davorka Herman, Ines BiliccurcicAbstract:Background and Aims: Experimental data demonstrated that activation of GLP-1 and gastrin signaling induces beta cell neogenesis, resulting in a promotion of glucose-induced insulin secretion. In addition, treatment with proton pump inhibitors is associated with greater glycemic control in patients with type 2 diabetes (T2DM), particularly in those on insulin- or GLP-1-based therapy. The aim of this study was to assess gastrin as a potential predictor of beta cell function and Glucoregulation in newly diagnosed T2DM patients. Materials and Methods: In this cross sectional study 190 patients (64 males and 126 females) with new onset T2DM were included. Patients treated with IPPs were excluded. Fasting plasma glucose (FPG), postprandial PG, HbA1c, fasting insulin, pancreatic B cell function (HOMA-B), insulin resistance index (HOMA-IR), fasting c-peptide and gastrin levels were measured at the time of diagnosis. Results: Baseline HbA1c was 7.53±2.08%, average age of patients was 61.8±10.years and body mass index (BMI) was 31.25±5.73 kg/m2. Parameters of Glucoregulation were not significantly correlated with gastrin (all p>0.05), while there was moderate negative correlation with HOMA-B (HbA1c, FPG and PPG ; p 0.05) or HOMA-IR. Furthermore, no association was established between c-peptide, insulin levels and gastrin (p>0.05). Conclusion: Baseline gastrin levels are not sufficient to have a significant effect on Glucoregulation or HOMA-B and HOMA-IR in newly diagnosed T2DM, therefore it could be postulated that further stimulation of gastrin secretion (e.g., with IPPs or GLP-1 based therapy) is needed in order to influence beta cell function and glycemic control.
Naji N Abumrad - One of the best experts on this subject based on the ideXlab platform.
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effect of acute ethanol intoxication on Glucoregulation during prolonged insulin induced hypoglycemia
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 1994Co-Authors: Patricia E Molina, Kareem Jabbour, Phillip E Williams, Naji N AbumradAbstract:This study examined the interaction of acute ethanol administration on glucose homeostasis during insulin-induced hypoglycemia (IIH). Glucose kinetics and net hepatic balances of alanine, glycerol, and lactate were estimated in three groups of dogs: group I underwent 3 h of IIH; group II received a continuous ethanol infusion in addition to IIH; group III received ethanol for 3 h. In group I, IIH resulted in a sustained twofold increase in glucose rate of appearance (Ra) and net hepatic uptake (NHU) of glycerol and lactate but no change in NHU of alanine. In group II, glucose Ra rose transiently, NHU of alanine and glycerol increased two- and fivefold, respectively, whereas NHU of lactate dropped 60%. In group III, no alterations in plasma glucose levels, glucose Ra, and NHU of alanine and glycerol were observed, but NHU of lactate switched to a net output. These results demonstrate that ethanol alone or with IIH exclusively inhibited NHU of lactate, and this was responsible, in a stoichiometric fashion, for the failure of the delayed increase in glucose Ra during IIH.
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role of il 1α in central nervous system immunomodulation of Glucoregulation
Brain Research, 1993Co-Authors: Charles H Lang, Patricia E Molina, Khalil A Yousef, Patrick G Tepper, Naji N AbumradAbstract:Abstract Hyperglycemia is a hallmark of the stress response, and has been largely attributed to elevated plasma levels of catabolic hormones. Recently, various cytokines have been shown to be endogenously produced within the brain and may represent an important component of the central regulation of this metabolic response. Therefore, the aim of the present study was to determine whether the intracerebroventricular (i.c.v.) injection of one such peptide, interleukin (IL)-1, can produce hormonal and metabolic alterations comparable to those observed under stress conditions. An i.c.v. cannula and vascular catheters were placed in rats prior to the experiment. Whole body glucose flux was assessed in overnight fasted conscious unrestrained rats using [3-3H]glucose. A mild hyperglycemia was elicited 20 min after the i.c.v. injection of IL-1α (human recombinant, 100 ng) that was not detected in control rats. Glucose levels gradually increased and were 26% higher than control values during the last hour of the 3 h experimental period. The hyperglycemia resulted from a 44% increase in the rate of hepatic glucose output (HGO), which preceded a propertional rise in peripheral glucose utilization. No increase in metabolic clearance rate was observed, suggesting that the increased glucose uptake was the result of mass action. The increased glucose flux was associated with a transient hyperinsulinemia (+95%), and sustained elevations in the arterial concentrations of glucagon (56%) and corticosterone (175%). In contrast, glucose flux was not altered by intravenous administration of the same dose of IL-1α, or i.c.v. injection of IL-1β, or heat-inactivated IL-1α. Indomethacin (5 mg/kg, i.v.) blocked the hyperglycemia and increased HGO induced by i.c.v. injection of prostaglandin E2 (100 ng) produced comparable increases in glucose flux. These results indicate that IL-1α can act centrally to enhance whole body glucose metabolism, and that this response is probably mediated by prostaglandins.
David H Wasserman - One of the best experts on this subject based on the ideXlab platform.
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Glucoregulation during and after exercise in health and insulin dependent diabetes
Exercise and Sport Sciences Reviews, 2005Co-Authors: Raul C Camacho, Pietro Galassetti, Stephen N Davis, David H WassermanAbstract:An elegant control system prevents hypoglycemia despite dramatic increments in glucose usage by working muscle. Insulin excess disrupts this control system, leading to hypoglycemia. Recent hypoglycemic episodes blunt the glucoregulatory response to subsequent exercise, and exercise blunts the glucoregulatory response to subsequent insulin excess. These mechanisms of glucoregulatory failure may cause hypoglycemia in insulin-dependent diabetics during and after exercise.
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evidence that carotid bodies play an important role in Glucoregulation in vivo
Diabetes, 2000Co-Authors: Yoshiharu Koyama, Robert H. Coker, E E Stone, D B Lacy, Kareem Jabbour, Phillip E Williams, David H WassermanAbstract:The carotid bodies are sensitive to glucose in vitro and can be stimulated to cause hyperglycemia in vivo. The aim of this study was to determine if the carotid bodies are involved in basal Glucoregulation or the counterregulatory response to an insulin-induced decrement in arterial glucose in vivo. Dogs were surgically prepared >16 days before the experiment. The carotid bodies and their associated nerves were removed (carotid body resected [CBR]) or left intact (Sham), and infusion and sampling catheters were implanted. Removal of carotid bodies was verified by the absence of a ventilatory response to NaCN. Experiments were performed in 18-h fasted conscious dogs and consisted of a tracer ([3-3H]glucose) equilibration period (-120 to -40 min), a basal period (-40 to 0 min), and an insulin infusion (1 mU x kg(-1) x min(-1)) period (0-150 min) during which glucose was infused as needed to clamp at mildly hypoglycemic (65 mg/dl) or euglycemic (105 mg/dl) levels. Basal (8 microU/ml) and clamp (40 microU/ml) insulin levels were similar in both groups. Basal arterial glucagon was reduced in CBR compared with Sham (30 + 2 vs. 40 +/- 2 pg/ml) and remained reduced in CBR during hypoglycemia (peak levels of 36 +/- 3 vs. 52 +/- 7 pg/ml). Cortisol levels were not significantly different between the 2 groups in the basal state, but were reduced during the hypoglycemic clamp in CBR. Catecholamine levels were not significantly different between the 2 groups in the basal and hypoglycemic periods. The glucose infusion rate required to clamp glucose at 65 mg/dl was 2.5-fold greater in CBR compared with Sham (4.0 +/- 0.4 vs. 1.6 +/- 0.4 mg x kg(-1) x min(-1)). Basal endogenous glucose appearance (R(a)) was equal in CBR and Sham (2.5 +/- 0.1 vs. 2.5 +/- 0.2 mg x kg(-1) x min(-1)). During the hypoglycemic clamp, insulin suppressed R(a) in CBR but not Sham (1.1 +/- 0.2 vs. 2.5 +/- 0.2 mg x kg(-1) x min(-1) during the last 30 min of the clamp), reflecting impaired counterregulation. Glucose disappearance (R(d)) in the basal state was similar in CBR and Sham, whereas it was elevated in CBR during the hypoglycemic clamp (4.8 +/- 0.1 vs. 3.9 +/- 0.1 mg x kg(-1) x min(-1) during the last 30 min of the clamp). R(d) was also elevated in euglycemic clamp studies, indicating an effect of carotid body resection independent of hypoglycemia. There were no other measured systematic endocrine or metabolic effects of carotid body resection during euglycemic clamps. In conclusion, we found that the carotid bodies (or receptors anatomically close by) play an important role in the insulin-induced counterregulatory response to mild hypoglycemia.
Vladimir Trajkovic - One of the best experts on this subject based on the ideXlab platform.
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therapeutic improvement of Glucoregulation in newly diagnosed type 2 diabetes patients is associated with a reduction of il 17 levels
Immunobiology, 2013Co-Authors: Mirjana Sumaracdumanovic, Danka Jeremic, Aleksandar Pantovic, Kristina Janjetovic, Danica Stamenkovicpejkovic, Goran Cvijovic, Darko Stevanovic, Dragan Micic, Vladimir TrajkovicAbstract:Abstract We explored the effect of therapeutic Glucoregulation on the blood levels of proinflammatory T helper (Th)17 cytokines interleukin (IL)-17 and IL-23, and Th1 cytokines interferon (IFN)-γ and IL-12 in newly diagnosed type 2 diabetes patients. The investigated group consisted of 23 subjects (17 men and 6 women, age 26–64). The cytokine serum levels, glycated hemoglobin (HbA1c) as a marker of Glucoregulation, homeostasis model assessment index as a measure of insulin resistance (HOMA-IR), and body mass index (BMI) were determined before and after 12 weeks of therapy consisting of standard lifestyle modification and metformin (1000 mg b.i.d.). The levels of Th17 and Th1 cytokines before treatment did not correlate with age, BMI or HOMA-IR. The patients with poor Glucoregulation (HbA1c > 7%, n = 12), compared to those with good Glucoregulation (HbA1c ≤ 7%, n = 11), had higher serum levels of Th17 and Th1 cytokines, but only the differences in IL-17 (median 21.2 pg/ml vs. 4.8 pg/ml) and IFN-γ 5 (0.6 pg/ml vs. 27.7 pg/ml) reached statistical significance ( p = 0.003 and p = 0.012, respectively). The reduction of HbA1c values (from 8.6 to 5.9%, p = 0.000) observed upon treatment in patients with poor Glucoregulation was associated with a significant decrease in the concentration of IL-17 (from 21.2 to 12.9 pg/ml, p = 0.020), but not IFN-γ (50.6 vs. 52.3, p = 0.349). These data indicate that therapeutic improvement of Glucoregulation might contribute to a reduction of IL-17 levels in newly diagnosed type 2 diabetes patients.