scholarly journals Glucose effectiveness: Lessons from studies on insulin‐independent glucose clearance in mice

2020 ◽  
Author(s):  
Bo Ahrén ◽  
Giovanni Pacini
Keyword(s):  
Glucose Effectiveness ◽  
Glucose Clearance

scholarly journals Impaired basal glucose effectiveness but unaltered fasting glucose release and gluconeogenesis during short-term hypercortisolemia in healthy subjects

2004 ◽  
Vol 286 (1) ◽  
pp. E102-E110 ◽  
Author(s):  
Michael F. Nielsen ◽  
Andrea Caumo ◽  
Visvanathan Chandramouli ◽  
William C. Schumann ◽  
Claudio Cobelli ◽  
...  
Keyword(s):  
Healthy Subjects ◽  
Insulin Action ◽  
Cell Function ◽  
Glucose Production ◽  
Saline Infusion ◽  
Glucose Turnover ◽  
Short Term ◽  
Glucose Effectiveness ◽  
Glucose Release ◽  
Glucose Clearance

Excess cortisol has been demonstrated to impair hepatic and extrahepatic insulin action. To determine whether glucose effectiveness and, in terms of endogenous glucose release (EGR), gluconeogenesis, also are altered by hypercortisolemia, eight healthy subjects were studied after overnight infusion with hydrocortisone or saline. Glucose effectiveness was assessed by a combined somatostatin and insulin infusion protocol to maintain insulin concentration at basal level in the presence of prandial glucose infusions. Despite elevated insulin concentrations ( P < 0.05), hypercortisolemia resulted in higher glucose ( P < 0.05) and free fatty acid concentrations ( P < 0.05). Furthermore, basal insulin concentrations were higher during hydrocortisone than during saline infusion ( P < 0.01), indicating the presence of steroid-induced insulin resistance. Postabsorptive glucose production ( P = 0.64) and the fractional contribution of gluconeogenesis to EGR ( P = 0.33) did not differ on the two study days. During the prandial glucose infusion, the integrated glycemic response above baseline was higher in the presence of hydrocortisone than during saline infusion ( P < 0.05), implying a decrease in net glucose effectiveness (4.42 ± 0.52 vs. 6.65 ± 0.83 ml·kg-1·min-1; P < 0.05). To determine whether this defect is attributable to an impaired ability of glucose to suppress glucose production, to stimulate its own uptake, or both, glucose turnover and “hot” (labeled) indexes of glucose effectiveness (GE) were calculated. Hepatic GE was lower during cortisol than during saline infusion (2.39 ± 0.24 vs. 3.82 ± 0.51 ml·kg-1·min-1; P < 0.05), indicating a defect in the ability of glucose to restrain its own production. In addition, in the presence of excess cortisol, glucose disappearance was inappropriate for the prevailing glucose concentration, implying a decrease in glucose clearance ( P < 0.05). The decrease in glucose clearance was confirmed by the higher increment in [3-3H]glucose during hydrocortisone than during saline infusion ( P < 0.05), despite the administration of identical tracer infusion rates. In conclusion, short-term hypercortisolemia in healthy individuals with normal β-cell function decreases insulin action but does not alter rates of EGR and gluconeogenesis. In addition, cortisol impairs the ability of glucose to suppress its own production, which due to accumulation of glucose in the glucose space results in impaired peripheral glucose clearance. These results suggest that cortisol excess impairs glucose tolerance by decreasing both insulin action and glucose effectiveness.

Impaired Beta-Cell Compensation and Glucose Effectiveness in Insulin Resistant, Nondiabetic South Asians

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 251-LB
Author(s):  
CAROLINE SEDMAK ◽  
SHIVRAJ GREWAL ◽  
SHANAZ SIKDER ◽  
MICHAEL GLICKSMAN ◽  
REED G. MSZAR ◽  
...  
Keyword(s):  
Beta Cell ◽  
South Asians ◽  
Glucose Effectiveness ◽  
Insulin Resistant ◽  
Beta Cell Compensation

Nr4a1 and Nr4a3 Knock Out Mice Have Impaired Glucose Clearance and Beta-Cell Function under High-Fat Feeding

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2040-P
Author(s):  
COURTNEY J. SMITH ◽  
KYLE B. KENER ◽  
JEFFERY S. TESSEM
Keyword(s):  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
High Fat ◽  
Knock Out ◽  
Glucose Clearance ◽  
Knock Out Mice ◽  
Fat Feeding

Central KATP channels modulate glucose effectiveness in humans and rodents

2020 ◽  
Author(s):  
Ada Admin ◽  
Michelle Carey ◽  
Eric Lontchi-Yimagou ◽  
William Mitchell ◽  
Sarah Reda ◽  
...  
Keyword(s):  
Katp Channel ◽  
Glucose Production ◽  
Katp Channels ◽  
Endogenous Glucose Production ◽  
Elevated Plasma ◽  
Sprague Dawley ◽  
Glucose Effectiveness ◽  
Sprague Dawley Rats ◽  
The Central Nervous System

Hyperglycemia is a potent regulator of endogenous glucose production (EGP). Loss of this ‘glucose effectiveness’ is a major contributor to elevated plasma glucose concentrations in type 2 diabetes (T2D). ATP-sensitive potassium channels (K<sub>ATP</sub> channels) in the central nervous system (CNS) have been shown to regulate EGP in humans and rodents. We examined the contribution of central K<sub>ATP</sub> channels to glucose effectiveness. Under fixed hormonal conditions (‘pancreatic clamp’ studies), hyperglycemia suppressed EGP by ~50% in both non-diabetic humans and normal Sprague Dawley rats. By contrast, antagonism of K<sub>ATP</sub> channels with glyburide significantly reduced the EGP-lowering effect of hyperglycemia in both humans and rats. Furthermore, the effects of glyburide on EGP and gluconeogenic enzymes in rats were abolished by intracerebroventricular (ICV) administration of the KATP channel agonist diazoxide. These findings indicate that about half of EGP suppression by hyperglycemia is mediated by central K<sub>ATP</sub> channels. These central mechanisms may offer a novel therapeutic target for improving glycemic control in T2D.

1951-P: Glucose Effectiveness Fails to Compensate for Insulin Resistance after Fat Feeding in Dogs

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1951-P
Author(s):  
MARILYN ADER ◽  
CATHRYN M. KOLKA ◽  
RICHARD N. BERGMAN
Keyword(s):  
Insulin Resistance ◽  
Glucose Effectiveness ◽  
Fat Feeding

Reduced sampling protocols in estimation of insulin sensitivity and glucose effectiveness using the minimal model in NIDDM

Diabetes ◽  
1993 ◽  
Vol 42 (11) ◽  
pp. 1635-1641 ◽  
Author(s):  
P. A. Coates ◽  
R. L. Ollerton ◽  
S. D. Luzio ◽  
I. S. Ismail ◽  
D. R. Owens
Keyword(s):  
Insulin Sensitivity ◽  
Minimal Model ◽  
Glucose Effectiveness ◽  
Sampling Protocols

Insulin-independent acute restoration of euglycemia normalizes the impaired glucose clearance during exercise in diabetic dogs

Diabetes ◽  
1997 ◽  
Vol 46 (11) ◽  
pp. 1805-1812 ◽  
Author(s):  
S. J. Fisher ◽  
M. Lekas ◽  
Z. Q. Shi ◽  
D. Bilinski ◽  
G. Carvalho ◽  
...  
Keyword(s):  
Glucose Clearance ◽  
Diabetic Dogs

Effect of burn trauma on glucose turnover, oxidation, and recycling in guinea pigs.

1977 ◽  
Vol 233 (2) ◽  
pp. E80
Author(s):  
R R Wolfe ◽  
J F Burke
Keyword(s):  
Clearance Rate ◽  
Guinea Pigs ◽  
Glucose Oxidation ◽  
Burn Injury ◽  
Constant Infusion ◽  
Glucose Turnover ◽  
Glucose Kinetics ◽  
Burn Trauma ◽  
Glucose Clearance ◽  
Low Rate

The simultaneous primed-constant infusion of [6-3H]- and [U-14C]glucose was used to determine the effect of burn injury on glucose turnover, oxidation, and recycling in guinea pigs. Eleven burned animals survived more than 72 h (survivors), whereas five died between 60 and 72 h postburn. All of the controls (n = 9) survived more than 72 h. At 48 h postburn, glucose turnover in the burned survivors was elevated 40% above that in control animals. A greater portion of the burned survivors' turnover was due to recycling and less was directed towards oxidation. The nonsurvivors had both a significantly depressed rate of appearance of glucose and an increased glucose clearance rate. Consequently, they were profoundly hypoglycemic and had a low rate of glucose oxidation. The alterations in glucose kinetics and oxidation apparent after burn did not reflect an inability of burned animals to oxidize exogenously infused glucose, however, because of 2-h infusion of 55 mumol/kg-min of unlabeled glucose doubled glucose oxidation in the burned survivors and tripled it in the nonsurvivors.

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