246-OR: Contribution of Plasma Glucose and Hormones to the Acute Compensatory Rise in Endogenous Glucose Production (EGP) during Glucosuria in T2D Patients

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 246-OR
Author(s):  
MARIAM ALATRACH ◽  
CHRISTINA AGYIN ◽  
NITCHAKARN LAICHUTHAI ◽  
JOHN M. ADAMS ◽  
MUHAMMAD ABDUL-GHANI ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Endogenous Glucose

Enteral infusion of glucose at rates approximating EGP enhances glucose disposal but does not cause hypoglycemia

2003 ◽  
Vol 285 (2) ◽  
pp. E280-E286 ◽  
Author(s):  
Farhad Zangeneh ◽  
Rita Basu ◽  
Pankaj Shah ◽  
Puneet Arora ◽  
Michael Camilleri ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Glucose Sensor ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Glucose Disposal ◽  
Wild Type ◽  
Glucose Disappearance ◽  
Endogenous Glucose ◽  
Glucose Plasma ◽  
Portal Infusion

Portal infusion of glucose at rates approximating endogenous glucose production (EGP) causes paradoxical hypoglycemia in wild-type but not GLUT2 null mice, implying activation of a specific portal glucose sensor. To determine whether this occurs in humans, glucose containing [3-3H]glucose was infused intraduodenally at rates of 3.1 mg · kg-1 · min-1 ( n = 5), 1.55 mg · kg-1 · min-1 ( n = 9), or 0/0.1 mg · kg-1 · min-1 ( n = 9) for 7 h in healthy nondiabetic subjects. [6,6-2H2]glucose was infused intravenously to enable simultaneous measurement of EGP, glucose disappearance, and the rate of appearance of the intraduodenally infused glucose. Plasma glucose concentrations fell ( P < 0.01) from 90 ± 1 to 84 ± 2 mg/dl during the 0/0.1 mg · kg-1 · min-1 id infusions but increased ( P < 0.001) to 104 ± 5 and 107 ± 3 mg/dl, respectively, during the 1.55 and 3.1 mg · kg-1 · min-1 id infusions. In contrast, insulin increased ( P < 0.05) during the 1.55 and 3.0 mg · kg-1 · min-1 infusions, reaching a peak of 10 ± 2 and 18 ± 5 μU/ml, respectively, by 2 h. Insulin concentrations then fell back to concentrations that no longer differed by study end (7 ± 1 vs. 8 ± 1 μU/ml). This resulted in comparable suppression of EGP by study end (0.84 ± 0.2 and 0.63 ± 0.1 mg · kg-1 · min-1). Glucose disappearance was higher ( P < 0.01) during the final hour of the 3.1 than 1.55 mg · kg-1 · min-1 id infusion (4.47 ± 0.2 vs. 2.6 ± 0.1 mg · kg-1 · min-1), likely because of the slightly, but not significantly, higher glucose and insulin concentrations. We conclude that, in contrast to mice, selective portal glucose delivery at rates approximating EGP does not cause hypoglycemia in humans.

Acute inhibition of lipolysis does not affect postprandial suppression of endogenous glucose production

2005 ◽  
Vol 289 (6) ◽  
pp. E941-E947 ◽  
Author(s):  
Peter E. Carey ◽  
Jean Gerrard ◽  
Gary W. Cline ◽  
Chiara Dalla Man ◽  
Philip T. English ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Glucose Homeostasis ◽  
Plasma Glucose ◽  
Peak Plasma ◽  
Serum Insulin ◽  
Glucose Production ◽  
Significant Negative Correlation ◽  
Endogenous Glucose Production ◽  
Liver Fat ◽  
Endogenous Glucose

To test the hypothesis that intrahepatic availability of fatty acid could modify the rate of suppression of endogenous glucose production (EGP), acipimox or placebo was administered before and during a test meal. We used a modified isotopic methodology to measure EGP in 11 healthy subjects, and 1H magnetic resonance spectroscopic measurement of hepatic triglyceride stores was also undertaken. Acipimox suppressed plasma free fatty acids markedly before the meal (0.05 ± 0.01 mmol/l at −10 min, P = 0) and throughout the postprandial period (0.03 ± 0.01 mmol/l at 150 min). Mean peak plasma glucose was significantly lower after the meal on acipimox days (8.9 ± 0.4 vs. 10.1 ± 0.5 mmol/l, P < 0.01), as was mean peak serum insulin (653.1 ± 99.9 vs. 909 ± 118 pmol/l, P < 0.01). Fasting EGP was similar (11.15 ± 0.58 μmol·kg−1·min−1 placebo vs. 11.17 ± 0.89 mg·kg−1·min−1 acipimox). The rate of suppression of EGP after the meal was almost identical on the 2 test days (4.36 ± 1.52 vs. 3.69 ± 1.21 μmol·kg−1·min−1 at 40 min). There was a significant negative correlation between the acipimox-induced decrease in peak plasma glucose and liver triglyceride content ( r = −0.827, P = 0.002), suggesting that, when levels of liver fat were low, inhibition of lipolysis was able to affect glucose homeostasis. Acute pharmacological sequestration of fatty acids in triglyceride stores improves postprandial glucose homeostasis without effect on the immediate postprandial suppression of EGP.

Improved tolerance to sequential glucose loading (Staub-Traugott effect): size and mechanisms

2009 ◽  
Vol 297 (2) ◽  
pp. E532-E537 ◽  
Author(s):  
Sandra Bonuccelli ◽  
Elza Muscelli ◽  
Amalia Gastaldelli ◽  
Elisabetta Barsotti ◽  
Brenno D. Astiarraga ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Plasma Glucose ◽  
Cell Function ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Fat Free Mass ◽  
Oral Glucose ◽  
Glucose Response ◽  
Glucose Loading ◽  
Endogenous Glucose

Improved glucose tolerance to sequential glucose loading (Staub-Traugott effect) is an important determinant of day-to-day glycemic exposure. Its mechanisms have not been clearly established. We recruited 17 healthy volunteers to receive two sequential oral glucose tolerance tests (OGTTs), at time 0 min and 180 min ( Study I). The protocol was repeated on a separate day ( Study II) except that plasma glucose was clamped at 8.3 mmol/l between 60 and 180 min. β-Cell function was analyzed by mathematical modeling of C-peptide concentrations. In a subgroup, glucose kinetics were measured by a triple-tracer technique (infusion of [6,6-2H2]glucose and labeling of the 2 glucose loads with [1-2H]glucose and [U-13C]glucose). In both Studies I and II, the plasma glucose response to the second OGTT equaled 84 ± 2% ( P = 0.003) of the response to the first OGTT. Absolute insulin secretion was lower (37.8 ± 4.3 vs. 42.8 ± 5.1 nmol/m2, P = 0.02), but glucose potentiation (i.e., higher secretion at the same glycemia) was stronger (1.08 ± 0.02- vs. 0.92 ± 0.02-fold, P = 0.006), the increment being higher in Study II (+36 ± 5%) than Study I (+19 ± 6%, P < 0.05). In pooled data, a higher glucose area during the first OGTT was associated with a higher potentiation during the second OGTT (rho=0.60, P = 0.002). Neither insulin clearance nor glucose clearance differed between loads, and appearance of glucose over 3 h totalled 60 ± 6 g for the first load and 52 ± 5 g for the second load ( P = not significant). Fasting endogenous glucose production [13.3 ± 0.6 μmol·min−1·kg fat-free mass (FFM)−1] averaged 6.0 ± 3.8 μmol·min−1·kg FFM−1 between 0 and 180 min and 1.7 ± 2.6 between 180 and 360 min ( P < 0.03). Glucose potentiation and stronger suppression of endogenous glucose release are the main mechanisms underlying the Staub-Traugott effect.

Glucose recycling and production in glycogenosis type I and III: stable isotope technique study

1989 ◽  
Vol 257 (3) ◽  
pp. E346-E353 ◽  
Author(s):  
B. Kalderon ◽  
S. H. Korman ◽  
A. Gutman ◽  
A. Lapidot
Keyword(s):  
Plasma Glucose ◽  
Storage Disease ◽  
Glucose Production ◽  
Glycogen Storage Disease Type ◽  
Glycogen Storage ◽  
Endogenous Glucose Production ◽  
Disease Type ◽  
Type I ◽  
Endogenous Glucose ◽  
Glucose Recycling

Glucose carbon recycling, endogenous glucose production, and glucose turnover rates were measured, by stable isotope methodology, in five patients with glycogen storage disease type I (GSD-I), two patients with glycogen storage disease type III (GSD-III), and three control children. A primed-constant infusion of D-[U-13C]glucose was administered nasogastrically to fasted subjects. The isotopic enrichments and 13C isotopomer distribution of plasma glucose were measured by chemical ionization gas chromatography mass spectroscopy. In response to increasing rates of glucose infusion, endogenous glucose production decreased, whereas the rate of glucose appearance or total glucose flux increased. Recycling of infused D-[U-13C]-glucose, calculated from changes in the isotopomer distribution of plasma [13C]glucose, was not detectable in GSD-I but reached 50% in GSD-III. In GSD-I the gluconeogenic pool was found to be highly labeled and recycled, whereas plasma glucose was diluted but not recycled. It is suggested that in GSD-I dilution of plasma glucose is due to release of glucose from branch points in glycogen. We propose that studies of the extent of glucose recycling and of isotopic enrichment of gluconeogenic precursors can be used as a noninvasive test for diagnosis of GSD-I and other defects in glucose production.

Suppression of glucose production by GLP-1 independent of islet hormones: a novel extrapancreatic effect

2003 ◽  
Vol 285 (4) ◽  
pp. E701-E707 ◽  
Author(s):  
Ronald L. Prigeon ◽  
Shaista Quddusi ◽  
Breay Paty ◽  
David A. D'Alessio
Keyword(s):  
Plasma Glucose ◽  
Hormone Secretion ◽  
Glucose Production ◽  
Preliminary Evidence ◽  
Endogenous Glucose Production ◽  
Glucose Disposal ◽  
Islet Hormones ◽  
Islet Hormone ◽  
Endogenous Glucose ◽  
Glucagon Like Peptide 1

Glucagon-like peptide-1 (GLP-1) is an intestinal hormone that stimulates insulin secretion and decreases glucagon release. It has been hypothesized that GLP-1 also reduces glycemia independent of its effect on islet hormones. Based on preliminary evidence that GLP-1 has independent actions on endogenous glucose production, we undertook a series of experiments that were optimized to address this question. The effect of GLP-1 on glucose appearance (Ra) and glucose disposal (Rd) was measured in eight men during a pancreatic clamp that was performed by infusing octreotide to suppress secretion of islet hormones, while insulin and glucagon were infused at rates adjusted to maintain blood glucose near fasting levels. After stabilization of plasma glucose and equilibration of [3H]glucose tracer, GLP-1 was given intravenously for 60 min. Concentrations of insulin, C-peptide, and glucagon were similar before and during the GLP-1 infusion (115 ± 14 vs. 113 ± 11 pM; 0.153 ± 0.029 vs. 0.156 ± 0.026 nM; and 64.7 ± 11.5 vs. 65.8 ± 13.8 ng/l, respectively). With the initiation of GLP-1, plasma glucose decreased in all eight subjects from steady-state levels of 4.8 ± 0.2 to a nadir of 4.1 ± 0.2 mM. This decrease in plasma glucose was accounted for by a significant 17% decrease in Ra, from 22.6 ± 2.8 to 19.1 ± 2.8 μmol · kg–1 · min–1 ( P < 0.04), with no significant change in Rd. These findings indicate that, under fasting conditions, GLP-1 decreases endogenous glucose production independent of its actions on islet hormone secretion.

scholarly journals 1216 ROLE OF PLASMA GLUCOSE IN THE REGULATION OF ENDOGENOUS GLUCOSE PRODUCTION IN THE HUMAN NEWBORN

1985 ◽  
Vol 19 (4) ◽  
pp. 313A-313A
Author(s):  
Satish C Kalhan ◽  
Anita Oliven ◽  
Katherine C King ◽  
Carlos Lucero
Keyword(s):  
Plasma Glucose ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Human Newborn ◽  
Endogenous Glucose

Intranasal insulin does not alter endogenous glucose production, but decreases liver fat and increases hepatic γATP in humans

2014 ◽  
Vol 9 (S 01) ◽  
Author(s):  
S Gancheva ◽  
C Koliaki ◽  
A Bierwagen ◽  
P Nowotny ◽  
A Nagel ◽  
...  
Keyword(s):  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Liver Fat ◽  
Intranasal Insulin ◽  
Endogenous Glucose

155-LB: The Increase in Endogenous Glucose Production with SGLT2 Inhibition Is Unchanged by Renal Denervation but Highly Correlates to Urinary Glucose Excretion

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 155-LB
Author(s):  
CAROLINA SOLIS-HERRERA ◽  
MARIAM ALATRACH ◽  
CHRISTINA AGYIN ◽  
HENRI HONKA ◽  
RUPAL PATEL ◽  
...  
Keyword(s):  
Renal Denervation ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Urinary Glucose Excretion ◽  
Urinary Glucose ◽  
Sglt2 Inhibition ◽  
Endogenous Glucose ◽  
Glucose Excretion

1832-P: Palmitic Acid Esters of Hydroxy Stearic Acids Reduce Endogenous Glucose Production through GPR43 Activation

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1832-P
Author(s):  
ANNA SANTORO ◽  
PENG ZHOU ◽  
YAN ZHU ◽  
ODILE D. PERONI ◽  
ANDREW T. NELSON ◽  
...  
Keyword(s):  
Palmitic Acid ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Endogenous Glucose ◽  
Acid Esters
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