Effect of glycemia and nonesterified fatty acids on forearm glucose uptake in normal humans

1991 ◽  
Vol 261 (3) ◽  
pp. E304-E311 ◽  
Author(s):  
M. Walker ◽  
G. R. Fulcher ◽  
C. F. Sum ◽  
H. Orskov ◽  
K. G. Alberti
Keyword(s):  
Fatty Acid ◽  
Blood Glucose ◽  
Glucose Uptake ◽  
Whole Body ◽  
Glucose Disposal ◽  
Nonesterified Fatty Acid ◽  
Nonesterified Fatty Acids ◽  
Glucose Levels ◽  
And Control ◽  
Blood Glucose Concentrations

The purpose of this study was to examine the effect of physiological plasma nonesterified fatty acid (NEFA) levels on insulin-stimulated forearm and whole body glucose uptake and substrate oxidation during euglycemia and hyperglycemia. Seven healthy men received Intralipid and heparin for 210 min in two studies, with saline as control in two further studies. Insulin (0.05 U.kg-1.h-1) was infused from 60 min, and euglycemia was maintained during lipid (EL) and control (EC) studies, and hyperglycemia was maintained in the other studies (HL and HC). Forearm NEFA uptake was comparable in the lipid studies (+61 +/- 10 and +52 +/- 8 nmol.100 ml forearm-1.min-1, EL and HL) and was suppressed in the controls. With Intralipid, forearm glucose uptake decreased during euglycemia but not during hyperglycemia (+3.85 +/- 0.34 vs. +3.34 +/- 0.25 mumol.100 ml forearm-1.min-1, EC vs. EL, P less than 0.02), with comparable changes in whole body glucose uptake. Glucose oxidation and forearm alanine release decreased with Intralipid at both blood glucose levels, with no significant change in the rates of nonoxidative glucose disposal. These observations support the operation of the glucose-fatty acid cycle at physiological plasma NEFA levels at both blood glucose concentrations, but this was associated with a decrease in peripheral insulin sensitivity only during euglycemia.

Muscle net glucose uptake and glucose kinetics after endurance training in men

1999 ◽  
Vol 277 (1) ◽  
pp. E81-E92 ◽  
Author(s):  
B. C. Bergman ◽  
G. E. Butterfield ◽  
E. E. Wolfel ◽  
G. D. Lopaschuk ◽  
G. A. Casazza ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Glucose Uptake ◽  
Endurance Training ◽  
Power Output ◽  
Whole Body ◽  
Glucose Disposal ◽  
Moderate Intensity ◽  
Active Muscle ◽  
Glucose Kinetics ◽  
Glucose Flux

We evaluated the hypotheses that alterations in glucose disposal rate (Rd) due to endurance training are the result of changed net glucose uptake by active muscle and that blood glucose is shunted to working muscle during exercise requiring high relative power output. We studied leg net glucose uptake during 1 h of cycle ergometry at two intensities before training [45 and 65% of peak rate of oxygen consumption (V˙o 2 peak)] and after training [65% pretrainingV˙o 2 peak, same absolute workload (ABT), and 65% posttrainingV˙o 2 peak, same relative workload (RLT)]. Nine male subjects (178.1 ± 2.5 cm, 81.8 ± 3.3 kg, 27.4 ± 2.0 yr) were tested before and after 9 wk of cycle ergometer training, five times a week at 75%V˙o 2 peak. The power output that elicited 66.0 ± 1.1% ofV˙o 2 peak before training elicited 54.0 ± 1.7% after training. Whole body glucose Rd decreased posttraining at ABT (5.45 ± 0.31 mg ⋅ kg−1 ⋅ min−1at 65% pretraining to 4.36 ± 0.44 mg ⋅ kg−1 ⋅ min−1) but not at RLT (5.94 ± 0.47 mg ⋅ kg−1 ⋅ min−1). Net glucose uptake was attenuated posttraining at ABT (1.87 ± 0.42 mmol/min at 65% pretraining and 0.54 ± 0.33 mmol/min) but not at RLT (2.25 ± 0.81 mmol/min). The decrease in leg net glucose uptake at ABT was of similar magnitude as the drop in glucose Rd and thus could explain dampened glucose flux after training. Glycogen degradation also decreased posttraining at ABT but not RLT. Leg net glucose uptake accounted for 61% of blood glucose flux before training and 81% after training at the same relative (65%V˙o 2 peak) workload and only 38% after training at ABT. We conclude that 1) alterations in active muscle glucose uptake with training determine changes in whole body glucose kinetics; 2) muscle glucose uptake decreases for a given, moderate intensity task after training; and 3) hard exercise (65%V˙o 2 peak) promotes a glucose shunt from inactive tissues to active muscle.

Glucose-fatty acid interactions in prepubertal and pubertal children: effects of lipid infusion

1997 ◽  
Vol 272 (4) ◽  
pp. E523-E529 ◽  
Author(s):  
S. Arslanian ◽  
C. Suprasongsin
Keyword(s):  
Fatty Acid ◽  
Glucose Uptake ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Whole Body ◽  
Glucose Disposal ◽  
Healthy Children ◽  
Prepubertal Children ◽  
Tissue Sensitivity

This investigation examined whether puberty differs from prepuberty in regard to the effects of increased free fatty acid (FFA) on in vivo glucose metabolism. Nine prepubertal and 13 pubertal healthy children were studied. Each subject was studied twice, once with 0.9% sodium chloride solution (control study) and once with 20% Intralipid infusion in the basal state and during a 3-h hyperinsulinemic-euglycemic clamp, with [6,6-2H2]glucose tracer. During control studies, prepubertal children had lower basal fat oxidation and higher insulin-mediated glucose disposal than pubertal adolescents. During Intralipid infusion, basal glucose uptake increased in prepubertal children but did not change in pubertal adolescents. Insulin-stimulated whole body glucose disposal did not change in prepubertal children (control 77.6 +/- 8.9, Intralipid 84.5 +/- 13.3 micromol x kg(-1) x min(-1)) but decreased in pubertal adolescents (control 55.0 +/- 3.6, Intralipid 46.7 +/- 3.4 micromol x kg(-1) x min(-1), P = 0.01) despite comparable decrements in glucose oxidaion. We conclude that in prepubertal children lipids exert effects in the basal state by stimulating hepatic glucose production and glucose disposal, whereas in pubertal adolescents they induce peripheral tissue insulin resistance by decreasing insulin-stimulated glucose uptake. This differential response could be due to developmental-maturational changes in tissue sensitivity and/or specificity to the glucose-FFA interaction.

Physiological Levels of Plasma Non-Esterified Fatty Acids Impair Forearm Glucose Uptake in Normal Man

1990 ◽  
Vol 79 (2) ◽  
pp. 167-174 ◽  
Author(s):  
M. Walker ◽  
G. R. Fulcher ◽  
C. Catalano ◽  
G. Petranyi ◽  
H. Orskov ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Glucose Uptake ◽  
Fatty Acid Uptake ◽  
Whole Body ◽  
Saline Control ◽  
Acid Uptake ◽  
Lipid Infusion ◽  
Metabolite Exchange ◽  
Glucose Fatty Acid Cycle ◽  
And Control

1. The purpose of the present study was to maintain physiological plasma non-esterified fatty acid levels and to (i) examine their effect on skeletal muscle insulin-stimulated glucose uptake and metabolite exchange using the forearm technique, and (ii) evaluate their effect on whole-body glucose uptake and fuel oxidation. 2. Intralipid (10%) and heparin (Lipid) or saline (Control) was administered to eight healthy male subjects on separate occasions for 210 min. Insulin, glucagon and somatostatin were administered from 60 to 210 min in each study and euglycaemia was maintained. 3. Plasma non-esterified fatty acid levels plateaued at 420 ±50 μmol/l with the Lipid infusion but were completely suppressed during the Control clamp. Forearm non-esterified fatty acid uptake increased with the Lipid infusion (+ 50±10 nmol min−1 100 ml−1 of forearm) and was accompanied by a significant decrease in forearm glucose uptake (+ 3.23 ± 0.25 versus + 3.65 ± 0.35 μmol min−1 100 ml−1 of forearm, Lipid and Control, respectively; P < 0.05) and alanine release (–84±12 versus −113 ± 15 nmol min−1 100 ml−1 of forearm, Lipid and Control, respectively; P < 0.05). 4. Whole-body glucose uptake showed a comparable decrease with the Lipid infusion (6.36 ±0.81 versus 6.85±0.66 mg min−1 kg−1; P < 0.05) and was accompanied by an increase in lipid oxidation (0.33 ±0.08 versus 0.16 ±0.05 mg min−1 kg−1; P < 0.02) and a decrease in glucose oxidation (2.93 ±0.23 versus 3.30±0.20 mg min−1 kg−1; P < 0.05). 5. We conclude that the maintenance of physiological plasma non-esterified fatty acid levels is associated with a decrease in forearm and whole-body insulin-stimulated glucose uptake. The changes in substrate oxidation and forearm alanine exchange provide support for the operation of the glucose—fatty acid cycle.

scholarly journals Regulation of Postabsorptive and Postprandial Glucose Metabolism by Insulin-Dependent and Insulin-Independent Mechanisms: An Integrative Approach

Nutrients ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 159
Author(s):  
George D. Dimitriadis ◽  
Eirini Maratou ◽  
Aikaterini Kountouri ◽  
Mary Board ◽  
Vaia Lambadiari
Keyword(s):  
Skeletal Muscle ◽  
Blood Glucose ◽  
Glucose Homeostasis ◽  
Glucose Production ◽  
Postprandial Glucose ◽  
Mass Action ◽  
Glucose Disposal ◽  
Nonesterified Fatty Acids ◽  
Glucose Levels ◽  
Blood Glucose Levels

Glucose levels in blood must be constantly maintained within a tight physiological range to sustain anabolism. Insulin regulates glucose homeostasis via its effects on glucose production from the liver and kidneys and glucose disposal in peripheral tissues (mainly skeletal muscle). Blood levels of glucose are regulated simultaneously by insulin-mediated rates of glucose production from the liver (and kidneys) and removal from muscle; adipose tissue is a key partner in this scenario, providing nonesterified fatty acids (NEFA) as an alternative fuel for skeletal muscle and liver when blood glucose levels are depleted. During sleep at night, the gradual development of insulin resistance, due to growth hormone and cortisol surges, ensures that blood glucose levels will be maintained within normal levels by: (a) switching from glucose to NEFA oxidation in muscle; (b) modulating glucose production from the liver/kidneys. After meals, several mechanisms (sequence/composition of meals, gastric emptying/intestinal glucose absorption, gastrointestinal hormones, hyperglycemia mass action effects, insulin/glucagon secretion/action, de novo lipogenesis and glucose disposal) operate in concert for optimal regulation of postprandial glucose fluctuations. The contribution of the liver in postprandial glucose homeostasis is critical. The liver is preferentially used to dispose over 50% of the ingested glucose and restrict the acute increases of glucose and insulin in the bloodstream after meals, thus protecting the circulation and tissues from the adverse effects of marked hyperglycemia and hyperinsulinemia.

Neural control of glucose uptake by skeletal muscle after central administration of NMDA

1995 ◽  
Vol 268 (2) ◽  
pp. R492-R497 ◽  
Author(s):  
C. H. Lang ◽  
M. Ajmal ◽  
A. G. Baillie
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Glucose Uptake ◽  
Neural Control ◽  
Plasma Insulin ◽  
Regional Blood Flow ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Glucose Disposal ◽  
Central Administration

Intracerebroventricular injection of N-methyl-D-aspartate (NMDA) produces hyperglycemia and increases whole body glucose uptake. The purpose of the present study was to determine in rats which tissues are responsible for the elevated rate of glucose disposal. NMDA was injected intracerebroventricularly, and the glucose metabolic rate (Rg) was determined for individual tissues 20-60 min later using 2-deoxy-D-[U-14C]glucose. NMDA decreased Rg in skin, ileum, lung, and liver (30-35%) compared with time-matched control animals. In contrast, Rg in skeletal muscle and heart was increased 150-160%. This increased Rg was not due to an elevation in plasma insulin concentrations. In subsequent studies, the sciatic nerve in one leg was cut 4 h before injection of NMDA. NMDA increased Rg in the gastrocnemius (149%) and soleus (220%) in the innervated leg. However, Rg was not increased after NMDA in contralateral muscles from the denervated limb. Data from a third series of experiments indicated that the NMDA-induced increase in Rg by innervated muscle and its abolition in the denervated muscle were not due to changes in muscle blood flow. The results of the present study indicate that 1) central administration of NMDA increases whole body glucose uptake by preferentially stimulating glucose uptake by skeletal muscle, and 2) the enhanced glucose uptake by muscle is neurally mediated and independent of changes in either the plasma insulin concentration or regional blood flow.

scholarly journals Effect of exercise timing on elevated postprandial glucose levels

2017 ◽  
Vol 123 (2) ◽  
pp. 278-284 ◽  
Author(s):  
Yoichi Hatamoto ◽  
Ryoma Goya ◽  
Yosuke Yamada ◽  
Eichi Yoshimura ◽  
Sena Nishimura ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Effect Size ◽  
Exercise Intervention ◽  
Intermittent Exercise ◽  
Random Order ◽  
Postprandial Glucose ◽  
Glucose Levels ◽  
Exercise Timing ◽  
Daily Exercise ◽  
Blood Glucose Concentrations

There is no consensus regarding optimal exercise timing for reducing postprandial glucose (PPG). The purpose of the present study was to determine the most effective exercise timing. Eleven participants completed four different exercise patterns 1) no exercise; 2) preprandial exercise (jogging); 3) postprandial exercise; and 4) brief periodic exercise intervention (three sets of 1-min jogging + 30 s of rest, every 30 min, 20 times total) in a random order separated by a minimum of 5 days. Preprandial and postprandial exercise consisted of 20 sets of intermittent exercise (1 min of jogging + 30 s rest per set) repeated 3 times per day. Total daily exercise volume was identical for all three exercise patterns. Exercise intensities were 62.4 ± 12.9% V̇o2peak. Blood glucose concentrations were measured continuously throughout each trial for 24 h. After breakfast, peak blood glucose concentrations were lower with brief periodic exercise (99 ± 6 mg/dl) than those with preprandial and postprandial exercise (109 ± 10 and 115 ± 14 mg/dl, respectively, P < 0.05, effect size = 0.517). After lunch, peak glucose concentrations were lower with brief periodic exercise than those with postprandial exercise (97 ± 5 and 108 ± 8 mg/dl, P < 0.05, effect size = 0.484). After dinner, peak glucose concentrations did not significantly differ among exercise patterns. Areas under the curve over 24 h and 2 h postprandially did not differ among exercise patterns. These findings suggest that brief periodic exercise may be more effective than preprandial and postprandial exercise at attenuating PPG in young active individuals. NEW & NOTEWORTHY This was the first study to investigate the effect of different exercise timing (brief periodic vs. preprandial vs. postprandial exercise) on postprandial glucose (PPG) attenuation in active healthy men. We demonstrated that brief periodic exercise attenuated peak PPG levels more than preprandial and postprandial exercise, particularly in the morning. Additionally, PPG rebounded soon after discontinuing postprandial exercise. Thus, brief periodic exercise may be better than preprandial and postprandial exercise at attenuating PPG levels.

scholarly journals Interleukin-6 Increases Insulin-Stimulated Glucose Disposal in Humans and Glucose Uptake and Fatty Acid Oxidation In Vitro via AMP-Activated Protein Kinase

Diabetes ◽  
2006 ◽  
Vol 55 (10) ◽  
pp. 2688-2697 ◽  
Author(s):  
A. L. Carey ◽  
G. R. Steinberg ◽  
S. L. Macaulay ◽  
W. G. Thomas ◽  
A. G. Holmes ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Protein Kinase ◽  
Glucose Uptake ◽  
Fatty Acid Oxidation ◽  
Interleukin 6 ◽  
Glucose Disposal ◽  
Acid Oxidation ◽  
Amp Activated Protein Kinase

Antecubital Vein Cannula Position Impacts Assessment of Forearm Glucose Uptake During an Oral Glucose Challenge in Healthy Volunteers

2020 ◽  
Author(s):  
Cécile Bétry ◽  
Aline V. Nixon ◽  
Paul L. Greenhaff ◽  
Elizabeth J. Simpson
Keyword(s):  
Skeletal Muscle ◽  
Blood Glucose ◽  
Glucose Uptake ◽  
Venous Blood ◽  
Whole Body ◽  
Oral Glucose ◽  
Antecubital Vein ◽  
Glucose Challenge ◽  
The Impact

Abstract Introduction Skeletal muscle is a major site for whole-body glucose disposal, and determination of skeletal muscle glucose uptake is an important metabolic measurement, particularly in research focussed on interventions that impact muscle insulin sensitivity. Calculating arterial-venous difference in blood glucose can be used as an indirect measure for assessing glucose uptake. However, the possibility of multiple tissues contributing to the composition of venous blood, and the differential in glucose uptake kinetics between tissue types, suggests that sampling from different vein sites could influence the estimation of glucose uptake. This study aimed to determine the impact of venous cannula position on calculated forearm glucose uptake following an oral glucose challenge in resting and post-exercise states. Materials and Methods In 9 young, lean, males, the impact of sampling blood from two antecubital vein positions; the perforating vein (‘perforating’ visit) and, at the bifurcation of superficial and perforating veins (‘bifurcation’ visit), was assessed. Brachial artery blood flow and arterialised-venous and venous blood glucose concentrations were measured in 3 physiological states; resting-fasted, resting-fed, and fed following intermittent forearm muscle contraction (fed-exercise). Results Following glucose ingestion, forearm glucose uptake area under the curve was greater for the ‘perforating’ than for the ‘bifurcation’ visit in the resting-fed (5.92±1.56 vs. 3.69±1.35 mmol/60 min, P<0.01) and fed-exercise (17.38±7.73 vs. 11.40±7.31 mmol/75 min, P<0.05) states. Discussion Antecubital vein cannula position impacts calculated postprandial forearm glucose uptake. These findings have implications for longitudinal intervention studies where serial determination of forearm glucose uptake is required.

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