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egp-endogenous-glucose-production

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Meeting Abstracts
Journal: Diabetes
Diabetes 2019;68(Supplement_1):246-OR
Published: 01 June 2019
...MARIAM ALATRACH; CHRISTINA AGYIN, IV; NITCHAKARN LAICHUTHAI; JOHN M. ADAMS, II; MUHAMMAD ABDUL-GHANI; CURTIS L. TRIPLITT; RALPH A. DEFRONZO; EUGENIO CERSOSIMO Aim: To examine the role of plasma glucose (GLU), insulin (INS) and glucagon (GG) changes in EGP stimulation during glucosuria (UGE...
Meeting Abstracts
Journal: Diabetes
Diabetes 2019;68(Supplement_1):1799-P
Published: 01 June 2019
... with diazoxide (DZX) reduces EGP in nondiabetic rodents and humans, but not in T2D. High fatty acids levels, typical of T2D, can increase endoplasmic reticulum (ER) stress and thereby impair glucose sensing by hypothalamic neurons. We thus hypothesized that lowering fatty acids with nicotinic acid (NA) could...
Meeting Abstracts
Journal: Diabetes
Diabetes 2018;67(Supplement_1):255-LB
Published: 01 July 2018
... acute and 7-day effects of SGLT inhibitors on EGP in rats by 13C-glucose tracer dilution method to identify a translational rodent model. Method: SD rats aged 7 weeks were assigned to 3 groups (n=6 each), vehicle, LX4211 (10 mg/kg) and canagliflozin (10 mg/kg). On day 1, rats were fasted...
Meeting Abstracts
Journal: Diabetes
Diabetes 2018;67(Supplement_1):1192-P
Published: 01 July 2018
... &***<0.001 *= DAPA & DAPA/SAXA vs. PCB; **=DAPA/SAXA vs. DAPA & PCB; ***=DAPA vs. DAPA/SAXA EGP=Endogenous Glucose Production; Ox: Oxidation Disclosure Y. Qin: None. J.M. Adams: None. R.A. Martinez: None. A. Di Pino: None. H. Al Jobori: None. A.M. Ali: None. C.L. Triplitt...
Images
Severe insulin resistance in <em>P465L/ob</em> mice. Normal <span class="search-highlight">glucose</span>...
Published: 01 October 2006
FIG. 4. Severe insulin resistance in P465L/ob mice. Normal glucose tolerance and insulin sensitivity in 3-month-old, chow-fed P465L/wt mice as shown by a glucose tolerance test (GTT) (intraperitoneal) (A) and hyperinsulinemic-euglycemic clamps (B and C) in P465L/wt (n = 10) and wt/wt (n = 10) mice. D: Glucose tolerance test (intraperitoneal). E: Insulin tolerance test (ITT) in P465L/wt and wt/wt mice fed a high-fat diet (HFD) for 16 weeks. F: Impaired response of P465L/ob mice to an insulin tolerance test (ITT) compared with ob/ob controls. Values are expressed as means ± SE. *P < 0.05 between P465L/ob and ob/ob. BGU, body glucose uptake; EGP, endogenous glucose production; GIR, glucose infusion rate; SkM, skeletal muscle FIG. 4. Severe insulin resistance in P465L/ob mice. Normal glucose tolerance and insulin sensitivity in 3-month-old, chow-fed P465L/wt mice as shown by a glucose tolerance test (GTT) (intraperitoneal) (A) and hyperinsulinemic-euglycemic clamps (B and C) in P465L/wt (n = 10) and wt/wt (n = 10) mice. D: Glucose tolerance test (intraperitoneal). E: Insulin tolerance test (ITT) in P465L/wt and wt/wt mice fed a high-fat diet (HFD) for 16 weeks. F: Impaired response of P465L/ob mice to an insulin tolerance test (ITT) compared with ob/ob controls. Values are expressed as means ± SE. *P < 0.05 between P465L/ob and ob/ob. BGU, body glucose uptake; EGP, endogenous glucose production; GIR, glucose infusion rate; SkM, skeletal muscle More
Images
Schematic showing effects of SGLT2i on α-cell function. SGLT2i have been pr...
Published: 13 April 2020
Figure 1 Schematic showing effects of SGLT2i on α-cell function. SGLT2i have been proposed to influence glucagon release through direct, paracrine, and indirect effects. Direct: Binding of SGLT2i might alter intracellular glucose and Na+ concentration, leading to changes in α-cell metabolism and membrane potential. Glucagon is decreased through poorly defined and complex mechanisms involving α-cell repolarization. Paracrine: Insulin binds to the insulin receptor on δ-cells to increase SGLT1/2 activity, leading to Ca2+ release from intracellular stores and stimulation of somatostatin release, which tonically inhibits glucagon secretion. SGLT2i block this effect by binding to either SGLT1 or SGLT2 on the δ-cell membrane, decreasing somatostatin secretion and releasing α-cells from tonic inhibition (but note that Saponaro et al. [ 11 ] did not detect presence of SGLT2 in δ-cells, unlike what has been reported by others [ 4 ]). Indirect: SGLT2i stimulate glycosuria, which lowers blood glucose levels. α-Cells respond to hypoglycemia by releasing glucagon, which increases endogenous glucose production. Heterogeneous: SGLT2/SLC5A2 expression is highly variable between donors and even islets of the same individuals. Some individuals/islets respond to SGLT2i, whereas others are less responsive, unresponsive, or even inhibited. If studies are underpowered, and depending on the samples examined (i.e., responsive, nonresponsive, or inhibited), effects of SGLT2i are likely to be reported as either: 1) positive, 2) negative, or 3) absent. EGP, endogenous glucose production; KATP channel, ATP-sensitive potassium channel; SST, somatostatin; Veh, vehicle. Adapted from Servier Medical Art under a CC BY3.0 license ( https://creativecommons.org/licenses/by/3.0/ ). Figure 1. Schematic showing effects of SGLT2i on α-cell function. SGLT2i have been proposed to influence glucagon release through direct, paracrine, and indirect effects. Direct: Binding of SGLT2i might alter intracellular glucose and Na+ concentration, leading to changes in α-cell metabolism and membrane potential. Glucagon is decreased through poorly defined and complex mechanisms involving α-cell repolarization. Paracrine: Insulin binds to the insulin receptor on δ-cells to increase SGLT1/2 activity, leading to Ca2+ release from intracellular stores and stimulation of somatostatin release, which tonically inhibits glucagon secretion. SGLT2i block this effect by binding to either SGLT1 or SGLT2 on the δ-cell membrane, decreasing somatostatin secretion and releasing α-cells from tonic inhibition (but note that Saponaro et al. [11] did not detect presence of SGLT2 in δ-cells, unlike what has been reported by others [4]). Indirect: SGLT2i stimulate glycosuria, which lowers blood glucose levels. α-Cells respond to hypoglycemia by releasing glucagon, which increases endogenous glucose production. Heterogeneous: SGLT2/SLC5A2 expression is highly variable between donors and even islets of the same individuals. Some individuals/islets respond to SGLT2i, whereas others are less responsive, unresponsive, or even inhibited. If studies are underpowered, and depending on the samples examined (i.e., responsive, nonresponsive, or inhibited), effects of SGLT2i are likely to be reported as either: 1) positive, 2) negative, or 3) absent. EGP, endogenous glucose production; KATP channel, ATP-sensitive potassium channel; SST, somatostatin; Veh, vehicle. Adapted from Servier Medical Art under a CC BY3.0 license (https://creativecommons.org/licenses/by/3.0/). More
Images
EPO treatment attenuates insulin resistance and <span class="search-highlight">glucose</span> intolerance during ...
Published: 14 June 2014
Figure 2 EPO treatment attenuates insulin resistance and glucose intolerance during DIO. WT C57BL/6 mice with obesity induced by HFD feeding for 12 weeks were treated with or without EPO (1,000 units/kg) every 48 h during the final 2 weeks of the study. Lean mice + saline were used as negative controls. A: For ITT, glucose levels were measured after intraperitoneal injection of 1 unit/kg insulin. B: For GTT, glucose levels were measured after intraperitoneal injection of 1 g/kg glucose. Fasting glucose levels (C), percentage hematocrit (D), serum glucose levels (E), and serum insulin levels (F) were measured. All measurements were performed at the end of week 12. Euglycemic–hyperinsulinemic clamps were performed in DIO mice fasted overnight after 2 weeks of EPO treatment (n = 5–8/group). G: GIR. H: Whole-body glucose fluxes, GIR, endogenous glucose production, and glucose disposal. I and J: Tissue 2-deoxyglucose update measured during clamp. Clamp plasma glucose levels were 209 + 39 and 157 + 13 mg/dL in saline- and EPO-treated mice, respectively. Clamp plasma insulin levels were 6.6 + 2.3 ng/mL in saline-treated mice and 5.8 + 0.8 ng/mL EPO-treated mice. Results are shown as mean ± SEM for n = 8 mice per group, representative of three independent experiments with similar results. *P < 0.05. BAT, brown adipose tissue; EGP, endogenous glucose production; Epi, epididymal; Ing, inguinal; Rd, glucose disposal. Figure 2. EPO treatment attenuates insulin resistance and glucose intolerance during DIO. WT C57BL/6 mice with obesity induced by HFD feeding for 12 weeks were treated with or without EPO (1,000 units/kg) every 48 h during the final 2 weeks of the study. Lean mice + saline were used as negative controls. A: For ITT, glucose levels were measured after intraperitoneal injection of 1 unit/kg insulin. B: For GTT, glucose levels were measured after intraperitoneal injection of 1 g/kg glucose. Fasting glucose levels (C), percentage hematocrit (D), serum glucose levels (E), and serum insulin levels (F) were measured. All measurements were performed at the end of week 12. Euglycemic–hyperinsulinemic clamps were performed in DIO mice fasted overnight after 2 weeks of EPO treatment (n = 5–8/group). G: GIR. H: Whole-body glucose fluxes, GIR, endogenous glucose production, and glucose disposal. I and J: Tissue 2-deoxyglucose update measured during clamp. Clamp plasma glucose levels were 209 + 39 and 157 + 13 mg/dL in saline- and EPO-treated mice, respectively. Clamp plasma insulin levels were 6.6 + 2.3 ng/mL in saline-treated mice and 5.8 + 0.8 ng/mL EPO-treated mice. Results are shown as mean ± SEM for n = 8 mice per group, representative of three independent experiments with similar results. *P < 0.05. BAT, brown adipose tissue; EGP, endogenous glucose production; Epi, epididymal; Ing, inguinal; Rd, glucose disposal. More
Images
EPO treatment attenuates insulin resistance and <span class="search-highlight">glucose</span> intolerance during ...
Published: 14 June 2014
Figure 2 EPO treatment attenuates insulin resistance and glucose intolerance during DIO. WT C57BL/6 mice with obesity induced by HFD feeding for 12 weeks were treated with or without EPO (1,000 units/kg) every 48 h during the final 2 weeks of the study. Lean mice + saline were used as negative controls. A: For ITT, glucose levels were measured after intraperitoneal injection of 1 unit/kg insulin. B: For GTT, glucose levels were measured after intraperitoneal injection of 1 g/kg glucose. Fasting glucose levels (C), percentage hematocrit (D), serum glucose levels (E), and serum insulin levels (F) were measured. All measurements were performed at the end of week 12. Euglycemic–hyperinsulinemic clamps were performed in DIO mice fasted overnight after 2 weeks of EPO treatment (n = 5–8/group). G: GIR. H: Whole-body glucose fluxes, GIR, endogenous glucose production, and glucose disposal. I and J: Tissue 2-deoxyglucose update measured during clamp. Clamp plasma glucose levels were 209 + 39 and 157 + 13 mg/dL in saline- and EPO-treated mice, respectively. Clamp plasma insulin levels were 6.6 + 2.3 ng/mL in saline-treated mice and 5.8 + 0.8 ng/mL EPO-treated mice. Results are shown as mean ± SEM for n = 8 mice per group, representative of three independent experiments with similar results. *P < 0.05. BAT, brown adipose tissue; EGP, endogenous glucose production; Epi, epididymal; Ing, inguinal; Rd, glucose disposal. Figure 2. EPO treatment attenuates insulin resistance and glucose intolerance during DIO. WT C57BL/6 mice with obesity induced by HFD feeding for 12 weeks were treated with or without EPO (1,000 units/kg) every 48 h during the final 2 weeks of the study. Lean mice + saline were used as negative controls. A: For ITT, glucose levels were measured after intraperitoneal injection of 1 unit/kg insulin. B: For GTT, glucose levels were measured after intraperitoneal injection of 1 g/kg glucose. Fasting glucose levels (C), percentage hematocrit (D), serum glucose levels (E), and serum insulin levels (F) were measured. All measurements were performed at the end of week 12. Euglycemic–hyperinsulinemic clamps were performed in DIO mice fasted overnight after 2 weeks of EPO treatment (n = 5–8/group). G: GIR. H: Whole-body glucose fluxes, GIR, endogenous glucose production, and glucose disposal. I and J: Tissue 2-deoxyglucose update measured during clamp. Clamp plasma glucose levels were 209 + 39 and 157 + 13 mg/dL in saline- and EPO-treated mice, respectively. Clamp plasma insulin levels were 6.6 + 2.3 ng/mL in saline-treated mice and 5.8 + 0.8 ng/mL EPO-treated mice. Results are shown as mean ± SEM for n = 8 mice per group, representative of three independent experiments with similar results. *P < 0.05. BAT, brown adipose tissue; EGP, endogenous glucose production; Epi, epididymal; Ing, inguinal; Rd, glucose disposal. More
Images
<em>A</em>–<em>F</em>: Hyperinsulinemic-euglycemic clamp in...
Published: 16 September 2011
FIG. 6. AF: Hyperinsulinemic-euglycemic clamp in wild-type (Wt) and A1AR−/− mice. Blood glucose (A), glucose infusion rate (GIR) (B), plasma glucose (C), plasma insulin (D), whole-body glucose fluxes (E), and tissue 2-DG (F) uptake were measured in 5-h–fasted, 18-week-old Wt (n = 16) and A1AR−/− (n = 14) littermate mice on a C57BL/6 background during a hyperinsulinemic-euglycemic clamp. CE: Basal parameters are the means ± SEM of data collected at −30 and −5 min (after a 90-min equilibration). At 0 min, mice were infused with insulin (4 mU/kg/min) and 20% glucose (variable rate) to maintain blood glucose concentrations at ~150 mg/dL. E: Clamp whole-body fluxes are the means ± SEM of data collected at 90–120 min. D: Clamp insulin was measured at 110 min. C: Bolus of 2-DG was administered at 80 min, and mice were killed at 120 min for tissue processing. BAT, brown adipose tissue; EGP, endogenous glucose production; Muscle, gastrocnemius muscle; RD, glucose disposal rate. *P < 0.05; **P < 0.01. FIG. 6. A–F: Hyperinsulinemic-euglycemic clamp in wild-type (Wt) and A1AR−/− mice. Blood glucose (A), glucose infusion rate (GIR) (B), plasma glucose (C), plasma insulin (D), whole-body glucose fluxes (E), and tissue 2-DG (F) uptake were measured in 5-h–fasted, 18-week-old Wt (n = 16) and A1AR−/− (n = 14) littermate mice on a C57BL/6 background during a hyperinsulinemic-euglycemic clamp. C–E: Basal parameters are the means ± SEM of data collected at −30 and −5 min (after a 90-min equilibration). At 0 min, mice were infused with insulin (4 mU/kg/min) and 20% glucose (variable rate) to maintain blood glucose concentrations at ~150 mg/dL. E: Clamp whole-body fluxes are the means ± SEM of data collected at 90–120 min. D: Clamp insulin was measured at 110 min. C: Bolus of 2-DG was administered at 80 min, and mice were killed at 120 min for tissue processing. BAT, brown adipose tissue; EGP, endogenous glucose production; Muscle, gastrocnemius muscle; RD, glucose disposal rate. *P < 0.05; **P < 0.01. More
Images
Effects on GIR, <span class="search-highlight">endogenous</span> <span class="search-highlight">glucose</span> <span class="search-highlight">production</span> (<span class="search-highlight">EGP</span>), and <span class="search-highlight">glucose</span> disappeara...
Published: 07 February 2017
Figure 2 Effects on GIR, endogenous glucose production (EGP), and glucose disappearance rate (Rd) in lean and overweight participants. Changes from the 20 min before spray application to the first predefined time period after spray, i.e., 100–120 min postspray (A, C, and E), and to the second predefined time period after spray, i.e., 190–210 min postspray (B, D, and F), in lean (left two bars) and overweight (right two bars) participants are indicated. A and B represent changes in GIR, C and D show changes in EGP, and E and F are changes in Rd. Means ± SEM. Differences between insulin and placebo spray were tested by pairwise two-tailed Student t tests. Figure 2. Effects on GIR, endogenous glucose production (EGP), and glucose disappearance rate (Rd) in lean and overweight participants. Changes from the 20 min before spray application to the first predefined time period after spray, i.e., 100–120 min postspray (A, C, and E), and to the second predefined time period after spray, i.e., 190–210 min postspray (B, D, and F), in lean (left two bars) and overweight (right two bars) participants are indicated. A and B represent changes in GIR, C and D show changes in EGP, and E and F are changes in Rd. Means ± SEM. Differences between insulin and placebo spray were tested by pairwise two-tailed Student t tests. More
Images
Impaired postabsorptive insulin-<span class="search-highlight">glucose</span> homeostasis and reduced whole-body ...
Published: 29 October 2020
Figure 2 Impaired postabsorptive insulin-glucose homeostasis and reduced whole-body and peripheral glucose disposal following intake of LCSFA-HFD but not following intake of MCSFA-HFD. A: randomized crossover study design with two intervention groups. B: HOMA-IR index in the basal state. C: Basal glucose Ra obtained in the fasted state prior to the clamp. D and E: GIR, expressed per kg body mass (BM). F: Glucose Ra during the last 20 min of the clamp. G: Glucose Rd during the clamp. H and I: Insulin-stimulated leg glucose uptake (expressed per kg leg mass [LM]). J and K: Basal and insulin-stimulated RER. L: ΔRER values, calculated as the increase in RER from basal to the end of the clamp. Oxidative glucose disposal (OGD) (M) and nonoxidative glucose disposal (NOGD) (N) during the clamp. Data in E, I, J, K, M, and N show average values from the last 60 min of the clamp. Bar graphs show means ± SEM with individual data plots. Two-way repeated-measures ANOVAs were applied to test for effect of group (MCSFA-HFD or LCSFA-HFD) and intervention or effect of insulin and intervention within each group. When ANOVA revealed interaction, this was indicated by intervention (int) × insulin. *P < 0.05, **P < 0.01, ***P < 0.001, effect of intervention (main effect in K and M). #P < 0.05, ###P < 0.001, effect of insulin (main effect in K). n = 8 in CON LCSFA-HFD and LCSFA-HFD; n = 9 in CON MCSFA-HFD and MCSFA-HFD. For the LCSFA-HFD group, data in E and I have previously been published ( 27 ). d, days; EGP, endogenous glucose production. Figure 2. Impaired postabsorptive insulin-glucose homeostasis and reduced whole-body and peripheral glucose disposal following intake of LCSFA-HFD but not following intake of MCSFA-HFD. A: randomized crossover study design with two intervention groups. B: HOMA-IR index in the basal state. C: Basal glucose Ra obtained in the fasted state prior to the clamp. D and E: GIR, expressed per kg body mass (BM). F: Glucose Ra during the last 20 min of the clamp. G: Glucose Rd during the clamp. H and I: Insulin-stimulated leg glucose uptake (expressed per kg leg mass [LM]). J and K: Basal and insulin-stimulated RER. L: ΔRER values, calculated as the increase in RER from basal to the end of the clamp. Oxidative glucose disposal (OGD) (M) and nonoxidative glucose disposal (NOGD) (N) during the clamp. Data in E, I, J, K, M, and N show average values from the last 60 min of the clamp. Bar graphs show means ± SEM with individual data plots. Two-way repeated-measures ANOVAs were applied to test for effect of group (MCSFA-HFD or LCSFA-HFD) and intervention or effect of insulin and intervention within each group. When ANOVA revealed interaction, this was indicated by intervention (int) × insulin. *P < 0.05, **P < 0.01, ***P < 0.001, effect of intervention (main effect in K and M). #P < 0.05, ###P < 0.001, effect of insulin (main effect in K). n = 8 in CON LCSFA-HFD and LCSFA-HFD; n = 9 in CON MCSFA-HFD and MCSFA-HFD. For the LCSFA-HFD group, data in E and I have previously been published (27). d, days; EGP, endogenous glucose production. More
Images
Effect of acute MB06322 administration (300 mg/kg) on <span class="search-highlight">endogenous</span> <span class="search-highlight">glucose</span> pr...
Published: 01 June 2006
FIG. 2. Effect of acute MB06322 administration (300 mg/kg) on endogenous glucose production (EGP) rates (A), the fractional contribution of gluconeogenesis and glycogenolysis to endogenous glucose production (B), and gluconeogenesis and glycogenolysis rates (C) in fasting conscious ∼10-week-old male ZDF rats. Endogenous glucose production was determined by standard tracer methodology, whereas the fractional contribution of gluconeogenesis and glycogenolysis to endogenous glucose production was determined by the deuterated water method, as described in research design and methods. Statistical analysis was not applied to the gluconeogenesis and glycogenolysis rates because they are the products of parameters (endogenous glucose production and fractional contributions of gluconeogenesis and glycogenolysis at 1:00 p.m.) measured in two different, but carefully matched, sets of animals (n = 6 per group). *P < 0.05 compared with vehicle (Student’s t test). FIG. 2. Effect of acute MB06322 administration (300 mg/kg) on endogenous glucose production (EGP) rates (A), the fractional contribution of gluconeogenesis and glycogenolysis to endogenous glucose production (B), and gluconeogenesis and glycogenolysis rates (C) in fasting conscious ∼10-week-old male ZDF rats. Endogenous glucose production was determined by standard tracer methodology, whereas the fractional contribution of gluconeogenesis and glycogenolysis to endogenous glucose production was determined by the deuterated water method, as described in research design and methods. Statistical analysis was not applied to the gluconeogenesis and glycogenolysis rates because they are the products of parameters (endogenous glucose production and fractional contributions of gluconeogenesis and glycogenolysis at 1:00 p.m.) measured in two different, but carefully matched, sets of animals (n = 6 per group). *P < 0.05 compared with vehicle (Student’s t test). More
Journal Articles
Journal: Diabetes
Diabetes 2003;52(1):133–137
Published: 01 January 2003
...Guenther Boden; Peter Cheung; Carol Homko To determine whether insulin induces acute changes in endogenous glucose production (EGP) via changes in gluconeogenesis (GNG), glycogenolysis (GL), or both, we measured GNG (with 2H2O) and GL (EGP-GNG) in nine patients with type 1...
Journal Articles
Journal: Diabetes
Diabetes 2004;53(7):1643–1648
Published: 01 July 2004
... the contraction-induced increase in endogenous glucose production (EGP). The cytokine interleukin (IL)-6 is released from skeletal muscle during contraction. Here we show that IL-6 contributes to the contraction-induced increase in EGP. Six men performed 2 h of bicycle exercise on three separate occasions...
Images
Changes in (<em>A</em>) <em>S</em><sub>i</sub>, (<em>B</em>...
Published: 03 December 2009
FIG. 3. Changes in (A) Si, (B) Rd, and (C) endogenous glucose production (EGP) as calculated from hyperinsulinemic EGCs prior to week 0 (▩) and after 14 weeks (■) of HFD. *Significantly different from corresponding week 0, P < 0.05 (paired t test). FIG. 3. Changes in (A) Si, (B) Rd, and (C) endogenous glucose production (EGP) as calculated from hyperinsulinemic EGCs prior to week 0 (▩) and after 14 weeks (■) of HFD. *Significantly different from corresponding week 0, P < 0.05 (paired t test). More
Journal Articles
Journal: Diabetes
Diabetes 2004;53(8):2042–2050
Published: 01 August 2004
...Rita Basu; Ananda Basu; C. Michael Johnson; W. Frederick Schwenk; Robert A. Rizza To determine whether the insulin dose-response curves for suppression of endogenous glucose production (EGP) and stimulation of splanchnic glucose uptake (SGU) differ in nondiabetic humans and are abnormal in type 2...
Meeting Abstracts
Journal: Diabetes
Diabetes 2000;49(6):969–974
Published: 01 June 2000
...J N Clore; J Stillman; H Sugerman Despite the effects of hyperinsulinemia and hyperglycemia, 2 factors known to inhibit endogenous glucose production (EGP) in nondiabetic subjects, increased EGP is a consistent feature of type 2 diabetes. Recent studies have suggested that increased glucose-6...
Journal Articles
Journal: Diabetes
Diabetes 2003;52(2):487–491
Published: 01 February 2003
...-3H]glucose) and glycogen synthesis by 31 and 40%, respectively (P < 0.01), almost completely abolished insulin suppression of endogenous glucose production (EGP) (13.6 vs. 10.0 μmol · kg−1 · min−1, NS), prevented the insulin induced increase in carbohydrate oxidation...
Meeting Abstracts
Journal: Diabetes
Diabetes 1999;48(5):1054–1060
Published: 01 May 1999
...S Nagasaka; K Tokuyama; I Kusaka; H Hayashi; K Rokkaku; T Nakamura; A Kawakami; M Higashiyama; S Ishikawa; T Saito Insulin sensitivity, glucose effectiveness, and endogenous glucose production (EGP) during stable-labeled, frequently sampled insulin-modified intravenous glucose tolerance test (FSIGT...
Meeting Abstracts
Journal: Diabetes
Diabetes 2000;49(5):701–707
Published: 01 May 2000
...M Roden; H Stingl; V Chandramouli; W C Schumann; A Hofer; B R Landau; P Nowotny; W Waldhäusl; G I Shulman Effects of free fatty acids (FFAs) on endogenous glucose production (EGP) and gluconeogenesis (GNG) were examined in healthy subjects (n = 6) during stepwise increased Intralipid/heparin...