scholarly journals Effect of Moderate Exercise Training on Peripheral Glucose Effectiveness, Insulin Sensitivity, and Endogenous Glucose Production in Healthy Humans Estimated by a Two-Compartment-Labeled Minimal Model

Diabetes ◽  
2004 ◽  
Vol 53 (2) ◽  
pp. 315-320 ◽  
Author(s):  
Y. Nishida ◽  
K. Tokuyama ◽  
S. Nagasaka ◽  
Y. Higaki ◽  
Y. Shirai ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Exercise Training ◽  
Minimal Model ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Moderate Exercise ◽  
Glucose Effectiveness ◽  
Healthy Humans ◽  
Endogenous Glucose ◽  
Moderate Exercise Training

SG, SI, and EGP of exercise-trained middle-aged men estimated by a two-compartment labeled minimal model

2002 ◽  
Vol 283 (4) ◽  
pp. E809-E816 ◽  
Author(s):  
Yuichiro Nishida ◽  
Kumpei Tokuyama ◽  
Shoichiro Nagasaka ◽  
Yasuki Higaki ◽  
Kanta Fujimi ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Minimal Model ◽  
Time Course ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Middle Aged ◽  
Intravenous Glucose ◽  
Glucose Effectiveness ◽  
Intravenous Glucose Tolerance Tests

To examine the effects of physical training on glucose effectiveness (SG), insulin sensitivity (SI), and endogenous glucose production (EGP) in middle-aged men, stable-labeled frequently sampled intravenous glucose tolerance tests (FSIGTT) were performed on 11 exercise-trained middle-aged men and 12 age-matched sedentary men. The time course of EGP during the FSIGTT was estimated by nonparametric stochastic deconvolution. Glucose uptake-specific indexes of glucose effectiveness (S[Formula: see text]*× 102: 0.81 ± 0.08 vs. 0.60 ± 0.05 dl · min−1· kg−1, P < 0.05) and insulin sensitivity [S[Formula: see text]*  × 104: 24.59 ± 2.98 vs. 11.89 ± 2.36 dl · min−1· (μU/ml)−1· kg−1, P < 0.01], which were analyzed using the two-compartment minimal model, were significantly greater in the trained group than in the sedentary group. Plasma clearance rate (PCR) of glucose was consistently greater in the trained men than in sedentary men throughout FSIGTT. Compared with sedentary controls, EGP of trained middle-aged men was higher before glucose load. The EGP of the two groups was similarly suppressed by ∼70% within 10 min, followed by an additional suppression after insulin infusion. EGP returned to basal level at ∼60 min in the trained men and at 100 min in the controls, followed by its overshoot, which was significantly greater in the trained men than in the controls. In addition, basal EGP was positively correlated with S[Formula: see text]*. The higher basal EGP and greater EGP overshoot in trained middle-aged men appear to compensate for the increased insulin-independent (S[Formula: see text]*) and -dependent (S[Formula: see text]*) glucose uptake to maintain glucose homeostasis.

scholarly journals Postprandial glucose fluxes and insulin sensitivity during exercise: A study in healthy individuals

2013 ◽  
Vol 305 (4) ◽  
pp. E557-E566 ◽  
Author(s):  
Michele Schiavon ◽  
Ling Hinshaw ◽  
Ashwini Mallad ◽  
Chiara Dalla Man ◽  
Giovanni Sparacino ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Healthy Subjects ◽  
Acute Exercise ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Fat Free Mass ◽  
Glucose Turnover ◽  
Sensitivity Index ◽  
Moderate Exercise ◽  
Insulin Sensitivity Index

Quantifying the effect size of acute exercise on insulin sensitivity (SIexercise) and simultaneous measurement of glucose disappearance (Rd), endogenous glucose production (EGP), and meal glucose appearance in the postprandial state has not been developed in humans. To do so, we studied 12 healthy subjects [5 men, age 37.1 ± 3.1 yr, body mass index 24.1 ± 1.1 kg/m2, fat-free mass (FFM) 50.9 ± 3.9 kg] during moderate exercise at 50% V̇o2max for 75 min, 120–195 min after a triple-tracer mixed meal consumed at time 0. Tracer infusion rates were adjusted to achieve constant tracer-to-tracee ratio and minimize non-steady-state errors. Glucose turnover was estimated by accounting for the nonstationary kinetics introduced by exercise. Insulin sensitivity index was calculated in each subject both in the absence [time ( t) = 0–120 min, SIrest] and presence ( t = 0–360 min, SIexercise) of physical activity. EGP at t = 0 min (13.4 ± 1.1 μM·kg FFM−1·min−1) fell at t = 120 min (2.4 ± 0.4 μM·kg FFM−1·min−1) and then rapidly rose almost eightfold at t = 180 min (18.2 ± 2.6 μM·kg FFM−1·min−1) before gradually falling at t = 360 min (10.6 ± 0.9 μM·kg FFM−1·min−1). Rd rapidly peaked at t = 120 min at the start of exercise (89.5 ± 11.6 μM·kg FFM−1·min−1) and then gradually declined at t = 195 min (26.4 ± 3.3 μM·kg FFM−1·min−1) before returning to baseline at t = 360 min. SIexercise was significantly higher than SIrest (21.6 ± 3.7 vs. 12.5 ± 2.0 10−4 dl·kg−1·min−1 per μU/ml, P < 0.0005). Glucose turnover was estimated for the first time during exercise with the triple-tracer technique. Our results, applying state-of-the-art techniques, show that moderate exercise almost doubles postprandial insulin sensitivity index in healthy subjects.

Insulin sensitivity and body composition in cirrhosis: changes after TIPS

2010 ◽  
Vol 299 (2) ◽  
pp. G486-G493 ◽  
Author(s):  
Peter Holland-Fischer ◽  
Michael Festersen Nielsen ◽  
Hendrik Vilstrup ◽  
Dennis Tønner-Nielsen ◽  
Anette Mengel ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Cell Mass ◽  
Area Under The Curve ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Endogenous Glucose

Insertion of a transjugular intrahepatic porto-systemic shunt (TIPS) increases body cell mass (BCM) in patients with liver cirrhosis. The responsible mechanism is unidentified, but may involve changes in insulin sensitivity and glucose metabolism. Eleven patients with liver cirrhosis were examined before and 6 mo after a TIPS procedure with bioimpedance analyses, 2-h oral glucose tolerance tests, and two-step hyperinsulinemic euglycemic clamp with tracer-determined endogenous glucose production. After TIPS, BCM increased by 4.8 kg [confidence interval (CI): 2.7–7.3]. Fasting (f)-insulin increased from 123 ± 81 to 193 ± 124 pmol/l ( P = 0.03), whereas f-glucose was unchanged (6.0 ± 0.8 vs. 6.2 ± 1.0 mmol/l). Glucose and insulin oral glucose tolerance test area under the curve increased by 14% (CI: 7–22%) and 53% (CI: 14–90%), respectively, P < 0.05. The C-peptide-to-insulin ratio decreased by 21% (CI: 8-35%, P = 0.01). Insulin sensitivity based on glucose infusion rate (4.69 ± 1.82 vs. 4.85 ± 2.37 mg·kg−1·min−1) and glucose tracer-based rate of disappearance were unchanged (5.01 ± 1.61 vs. 4.97 ± 2.13 mg·kg−1·min−1). Despite a further increase in peripheral hyperinsulinemia, f-endogenous glucose production did not change between study days (2.01 ± 0.42 vs. 2.42 ± 0.58 mg·kg−1·min−1) and was suppressed equally by insulin (1.1 ± 0.1 vs. 1.0 ± 0.1 mg·kg−1·min−1). Insulin clearance, growth hormone, cortisol, and glucagon levels were unchanged. BCM improvement did not correlate with the measured variables. After TIPS, BCM rose, despite enhanced hyperinsulinemia and aggravated glucose intolerance, but unchanged peripheral and hepatic insulin sensitivity. This apparent discrepancy may be ascribed to shunt-related decreased insulin exposure to the liver cells. However, the anabolic effect of TIPS seems not to be related to improvements in insulin sensitivity and remains mechanistically unexplained.

Endogenous glucose production, insulin sensitivity, and insulin secretion in normal glucose-tolerant Pima Indians with low birth weight

Metabolism ◽  
2004 ◽  
Vol 53 (7) ◽  
pp. 904-911 ◽  
Author(s):  
Norbert Stefan ◽  
Christian Weyer ◽  
Claire Levy-Marchal ◽  
Michael Stumvoll ◽  
William C Knowler ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Birth Weight ◽  
Insulin Sensitivity ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Pima Indians ◽  
Normal Glucose Tolerant ◽  
Normal Glucose ◽  
Glucose Tolerant ◽  
Endogenous Glucose

Effects of dexamethasone on hepatic glucose production and fructose metabolism in healthy humans

1997 ◽  
Vol 273 (2) ◽  
pp. E315-E320 ◽  
Author(s):  
P. Tounian ◽  
P. Schneiter ◽  
S. Henry ◽  
J. Delarue ◽  
L. Tappy
Keyword(s):  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Healthy Men ◽  
Fructose Metabolism ◽  
Healthy Humans ◽  
Hepatic Glucose ◽  
Endogenous Glucose ◽  
Total Glucose ◽  
Administration Rate

This study was designed to determine whether glucocorticoids alter autoregulation of glucose production and fructose metabolism. Two protocols with either dexamethasone (DEX) or placebo (Placebo) were performed in six healthy men during hourly ingestion of[13C]fructose (1.33 mmol.kg-1.h-1) for 3 h. In both protocols, endogenous glucose production (EGP) increased by 8 (Placebo) and 7% (DEX) after fructose, whereas gluconeogenesis from fructose represented 82 (Placebo) and 72% (DEX) of EGP. Fructose oxidation measured from breath 13CO2 was similar in both protocols [9.3 +/- 0.7 (Placebo) and 9.6 +/- 0.5 mumol.kg-1.min-1 (DEX)]. Nonoxidative carbohydrate disposal, calculated as fructose administration rate minus net carbohydrate oxidation rate after fructose ingestion measured by indirect calorimetry, was also similar in both protocols [5.8 +/- 0.8 (Placebo) and 5.9 +/- 2.0 mumol.kg-1.min-1 (DEX)]. We concluded that dexamethasone 1) does not alter the autoregulatory process that prevents a fructose-induced increase in gluconeogenesis from increasing total glucose production and 2) does not affect oxidative and nonoxidative pathways of fructose. This indicates that the insulin-regulated enzymes involved in these pathways are not affected in a major way by dexamethasone.

scholarly journals Effects of Growth Hormone and Free Fatty Acids on Insulin Sensitivity in Patients with Type 1 Diabetes

2009 ◽  
Vol 94 (9) ◽  
pp. 3297-3305 ◽  
Author(s):  
Burak Salgin ◽  
Maria L. Marcovecchio ◽  
Rachel M. Williams ◽  
Sarah J. Jackson ◽  
Leslie J. Bluck ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Growth Hormone ◽  
Type 1 Diabetes ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Endogenous Glucose

Context: Because GH stimulates lipolysis, an increase in circulating free fatty acid levels, as opposed to a direct effect of high GH levels, could underlie the development of insulin resistance in type 1 diabetes (T1D). Our aim was to explore the relative contributions of GH and free fatty acids to the development of insulin resistance in patients with T1D. Patients: Seven (four females, three males) nonobese patients with T1D aged 21–30 yr were studied on four occasions in random order. On each visit, overnight endogenous GH production was suppressed by octreotide. Three 1-h pulses of recombinant human GH (rhGH) or placebo were administered on two visits each. Acipimox, an antilipolytic drug, or a placebo were ingested every 4 h on two visits each. Stable glucose and glycerol isotopes were used to assess glucose and glycerol turnover. The overnight protocol was concluded by a two-step hyperinsulinemic euglycemic clamp on each visit. Main Outcome: rhGH administration led to increases in the insulin infusion rate required to maintain euglycemia overnight (P = 0.008), elevated basal endogenous glucose production (P = 0.007), decreased basal peripheral glucose uptake (P = 0.03), and reduced glucose uptake during step 1 of the clamp (P &lt; 0.0001). Coadministration of rhGH and acipimox reversed these effects and suppression of lipolysis in the absence of GH replacement led to further increases in insulin sensitivity. Results: GH pulses were associated with an increase in endogenous glucose production and decreased rates of peripheral glucose uptake, which was entirely reversed by acipimox. Therefore, GH-driven decreases in insulin sensitivity are mainly determined by the effect of GH on lipolysis. Growth hormone decreases insulin sensitivity through increases in free fatty acid levels.

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