Comparison of thermogenic effect of fructose and glucose in normal humans

1986 ◽  
Vol 250 (6) ◽  
pp. E718-E724 ◽  
Author(s):  
L. Tappy ◽  
J. P. Randin ◽  
J. P. Felber ◽  
R. Chiolero ◽  
D. C. Simonson ◽  
...  
Keyword(s):  
Energy Expenditure ◽  
Lipid Oxidation ◽  
Plasma Insulin ◽  
Carbohydrate Oxidation ◽  
Insulin Concentration ◽  
Adrenergic Blockade ◽  
Plasma Insulin Concentration ◽  
Carbohydrate Ingestion ◽  
Glucose Ingestion ◽  
Adrenergic Nervous System

After nutrient ingestion there is an increase in energy expenditure that has been referred to as dietary-induced thermogenesis. In the present study we have employed indirect calorimetry to compare the increment in energy expenditure after the ingestion of 75 g of glucose or fructose in 17 healthy volunteers. During the 4 h after glucose ingestion the plasma insulin concentration increased by 33 +/- 4 microU/ml and this was associated with a significant increase in carbohydrate oxidation and decrement in lipid oxidation. Energy expenditure increased by 0.08 +/- 0.01 kcal/min. When fructose was ingested, the plasma insulin concentration increased by only 8 +/- 2 microU/ml vs. glucose. Nonetheless, the increments in carbohydrate oxidation and decrement in lipid oxidation were significantly greater than with glucose. The increment in energy expenditure was also greater with fructose. When the mean increment in plasma insulin concentration after fructose was reproduced using the insulin clamp technique, the increase in carbohydrate oxidation and decrement in lipid oxidation were markedly reduced compared with the fructose-ingestion study; energy expenditure failed to increase above basal levels. To examine the role of the adrenergic nervous system in fructose-induced thermogenesis, fructose ingestion was also performed during beta-adrenergic blockade with propranolol. The increase in energy expenditure during fructose plus propranolol was lower than with fructose ingestion alone. These results indicate that the stimulation of thermogenesis after carbohydrate ingestion is related to an augmentation of cellular metabolism and is not dependent on an increase in the plasma insulin concentration per se.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic blockade prevents endotoxin-induced increases in glucose metabolism

1988 ◽  
Vol 255 (5) ◽  
pp. E629-E635 ◽  
Author(s):  
D. M. Hargrove ◽  
G. J. Bagby ◽  
C. H. Lang ◽  
J. J. Spitzer
Keyword(s):  
Plasma Insulin ◽  
Lactate Concentration ◽  
Insulin Concentration ◽  
Adrenergic Blockade ◽  
Plasma Lactate ◽  
Glucose Kinetics ◽  
Plasma Insulin Concentration ◽  
Beta Adrenergic ◽  
Plasma Lactate Concentration ◽  
Adrenergic Antagonists

Combined alpha- and beta-adrenergic blockade was used to investigate the role of catecholamines in endotoxin-induced elevations in glucose kinetics. Glucose kinetics were measured before and for 4 h after the injection of endotoxin [100 micrograms/100 g body wt iv, 30% lethal dose (LD30) at 24 h]. Adrenergic blockade was achieved by the bolus injection of phentolamine and propranolol followed by their continuous infusion. Endotoxin-treated rats exhibited a transient hyperglycemia and sustained (greater than 4 h) increase in plasma lactate concentration, as well as elevated rates of glucose appearance (Ra, 83%), disappearance (Rd, 58%), recycling (160%), and metabolic clearance (23%). Adrenergic blockade prevented endotoxin-induced increases in plasma glucose concentration, Ra, Rd, and recycling but not glucose clearance. The increase in plasma lactate concentration was blunted by 35%. After 2 h, endotoxic animals infused with adrenergic antagonists developed hypoglycemia, which may have resulted from an increased plasma insulin concentration. The attenuation of elevated glucose turnover by adrenergic blockade in the endotoxin-treated animals was not due to a reduction in plasma glucagon level or differences in plasma insulin concentration. Administration of the alpha- or beta-adrenergic antagonists separately blunted but did not prevent endotoxin-induced changes in glucose kinetics, and therefore the efficacy of the adrenergic blockade could not be assigned to a single receptor class. These results indicate that catecholamines are important contributory factors to many of the early alterations in carbohydrate metabolism observed during endotoxemia.

Substrate metabolism when subjects are fed carbohydrate during exercise

1999 ◽  
Vol 276 (5) ◽  
pp. E828-E835 ◽  
Author(s):  
Jeffrey F. Horowitz ◽  
Ricardo Mora-Rodriguez ◽  
Lauri O. Byerley ◽  
Edward F. Coyle
Keyword(s):  
Plasma Insulin ◽  
Fat Oxidation ◽  
Insulin Concentration ◽  
Peak Oxygen Consumption ◽  
Moderate Intensity ◽  
Moderate Intensity Exercise ◽  
Plasma Insulin Concentration ◽  
Carbohydrate Ingestion ◽  
Low Intensity ◽  
Low Intensity Exercise

This study determined the effect of carbohydrate ingestion during exercise on the lipolytic rate, glucose disappearance from plasma (Rd Glc), and fat oxidation. Six moderately trained men cycled for 2 h on four separate occasions. During two trials, they were fed a high-glycemic carbohydrate meal during exercise at 30 min (0.8 g/kg), 60 min (0.4 g/kg), and 90 min (0.4 g/kg); once during low-intensity exercise [25% peak oxygen consumption (V˙o 2 peak)] and once during moderate-intensity exercise (68%V˙o 2 peak). During two additional trials, the subjects remained fasted (12–14 h) throughout exercise at each intensity. After 55 min of low-intensity exercise in fed subjects, hyperglycemia (30% increase) and a threefold elevation in plasma insulin concentration ( P < 0.05) were associated with a 22% suppression of lipolysis compared with when subjects were fasted (5.2 ± 0.5 vs. 6.7 ± 1.2 μmol ⋅ kg−1 ⋅ min−1, P < 0.05), but fat oxidation was not different from fasted levels at this time. Fat oxidation when subjects were fed carbohydrate was not reduced below fasting levels until 80–90 min of exercise, and lipolysis was in excess of fat oxidation at this time. The reduction in fat oxidation corresponded in time with the increase in Rd Glc. During moderate-intensity exercise, the very small elevation in plasma insulin concentration (∼3 μU/ml; P < 0.05) during the second hour of exercise when subjects were fed vs. when they were fasted slightly attenuated lipolysis ( P < 0.05) but did not increase Rd Glc or suppress fat oxidation. These findings indicate that despite a suppression of lipolysis after carbohydrate ingestion during exercise, the lipolytic rate remained in excess and thus did not limit fat oxidation. Under these conditions, a reduction in fat oxidation was associated in time with an increase in glucose uptake.

Normalization of carbohydrate-induced thermogenesis by fructose in insulin-resistant states

1988 ◽  
Vol 254 (2) ◽  
pp. E201-E207 ◽  
Author(s):  
D. C. Simonson ◽  
L. Tappy ◽  
E. Jequier ◽  
J. P. Felber ◽  
R. A. DeFronzo
Keyword(s):  
Energy Expenditure ◽  
Carbohydrate Oxidation ◽  
Cellular Mechanisms ◽  
Primary Defect ◽  
Plasma Insulin Concentration ◽  
Insulin Resistant ◽  
Obesity And Diabetes ◽  
Glucose Ingestion ◽  
Intracellular Metabolism ◽  
Insulin Dependent Diabetic

To examine whether defects in carbohydrate oxidation and thermogenesis in aging, obesity, and diabetes are secondary to impaired insulin action or to a primary defect in intracellular metabolism, we compared substrate oxidation and energy expenditure in 9 younger, 9 older, 9 obese, and 10 non-insulin-dependent diabetic subjects after the ingestion of 75 g of glucose or fructose (a monosaccharide whose transport into the cell and subsequent metabolism are independent of insulin). In young control subjects fructose produced a significantly greater increase in carbohydrate oxidation and energy expenditure than glucose despite significantly lower plasma glucose and insulin levels. In aged, obese, and diabetic individuals the increments in carbohydrate oxidation and energy expenditure after glucose ingestion were significantly imparied versus the younger controls. After fructose ingestion the increase in carbohydrate oxidation in the three insulin-resistant groups remained below that observed in the younger volunteers, whereas carbohydrate-induced thermogenesis was enhanced to levels that were comparable with those seen in the younger group. These data suggest that 1) the stimulation of thermogenesis after fructose ingestion is related to an augmentation of intracellular metabolism rather than an increase in the plasma insulin concentration per se, 2) the insulin resistance of aging, obesity, and diabetes is associated with a defect in intracellular carbohydrate oxidation, and 3) the cellular mechanisms involved in carbohydrate-induced thermogenesis are not primarily impaired in insulin-resistant states.

Lipolytic suppression following carbohydrate ingestion limits fat oxidation during exercise

1997 ◽  
Vol 273 (4) ◽  
pp. E768-E775 ◽  
Author(s):  
Jeffrey F. Horowitz ◽  
Ricardo Mora-Rodriguez ◽  
Lauri O. Byerley ◽  
Edward F. Coyle
Keyword(s):  
Oxygen Consumption ◽  
Plasma Insulin ◽  
Fat Oxidation ◽  
Insulin Concentration ◽  
Peak Oxygen Consumption ◽  
Whole Body ◽  
Plasma Insulin Concentration ◽  
Carbohydrate Ingestion ◽  
The Mean

This study determined if the suppression of lipolysis after preexercise carbohydrate ingestion reduces fat oxidation during exercise. Six healthy, active men cycled 60 min at 44 ± 2% peak oxygen consumption, exactly 1 h after ingesting 0.8 g/kg of glucose (Glc) or fructose (Fru) or after an overnight fast (Fast). The mean plasma insulin concentration during the 50 min before exercise was different among Fast, Fru, and Glc (8 ± 1, 17 ± 1, and 38 ± 5 μU/ml, respectively; P< 0.05). After 25 min of exercise, whole body lipolysis was 6.9 ± 0.2, 4.3 ± 0.3, and 3.2 ± 0.5 μmol ⋅ kg−1 ⋅ min−1and fat oxidation was 6.1 ± 0.2, 4.2 ± 0.5, and 3.1 ± 0.3 μmol ⋅ kg−1 ⋅ min−1during Fast, Fru, and Glc, respectively (all P < 0.05). During Fast, fat oxidation was less than lipolysis ( P < 0.05), whereas fat oxidation approximately equaled lipolysis during Fru and Glc. In an additional trial, the same subjects ingested glucose (0.8 g/kg) 1 h before exercise and lipolysis was simultaneously increased by infusing Intralipid and heparin throughout the resting and exercise periods (Glc+Lipid). This elevation of lipolysis during Glc+Lipid increased fat oxidation 30% above Glc (4.0 ± 0.4 vs. 3.1 ± 0.3 μmol ⋅ kg−1 ⋅ min−1; P < 0.05), confirming that lipolysis limited fat oxidation. In summary, small elevations in plasma insulin before exercise suppressed lipolysis during exercise to the point at which it equaled and appeared to limit fat oxidation.

Effects of prior exercise on the thermic effect of glucose and fructose

1991 ◽  
Vol 70 (4) ◽  
pp. 1463-1468 ◽  
Author(s):  
T. W. Balon ◽  
G. J. Welk
Keyword(s):  
Plasma Insulin ◽  
Plasma Concentrations ◽  
Insulin Concentration ◽  
Net Energy ◽  
O2 Consumption ◽  
Plasma Insulin Concentration ◽  
Prior Exercise ◽  
Glucose Ingestion ◽  
Thermic Effect

It has been previously observed that the thermic effect of a glucose load is potentiated by prior exercise. To determine whether this phenomenon is observed when different carbohydrates are used and to ascertain the role of insulin, the thermic effects of fructose and glucose were compared during control (rest) and postexercise trials. Six male subjects ingested 100 g fructose or glucose at rest or after recovery from 45 min of treadmill exercise at 70% of maximal O2 consumption. Measurements of O2 consumption, respiratory exchange ratio, and plasma concentrations of glucose, insulin, glycerol, and lactate were measured for 3 h postingestion. Although glucose and fructose increased net energy expenditure by 44 and 51 kcal, respectively, over baseline during control trials, exercise increased the thermic effect of both carbohydrate challenges an additional 20-25 kcal (P less than 0.05). Glucose ingestion was associated with large (P less than 0.05) increases in plasma insulin concentration during control and exercise trials, in contrast to fructose ingestion. Because fructose, which is primarily metabolized by liver, and glucose elicited a similar postexercise potentiation of thermogenesis, the results indicate that the thermogenic phenomenon is not limited to skeletal muscle. These results also demonstrate that carbohydrate-induced postexercise thermogenesis is not related to an incremental increase in plasma insulin concentration.

INHIBITORY EFFECT OF SOMATOSTATIN ON INSULIN SECRETION DURING α-ADRENERGIC BLOCKADE IN THREE DIFFERENT SPECIES

1979 ◽  
Vol 92 (1) ◽  
pp. 166-173 ◽  
Author(s):  
Johannes Järhult ◽  
Bo Ahrén ◽  
Ingmar Lundquist
Keyword(s):  
Insulin Secretion ◽  
B Cell ◽  
Insulin Release ◽  
Plasma Insulin ◽  
Inhibitory Effect ◽  
Insulin Concentration ◽  
Adrenergic Blockade ◽  
Plasma Insulin Concentration ◽  
Basal Plasma ◽  
Stimulation Of

ABSTRACT It has recently been suggested from experiments in dogs that somatostatin suppresses insulin release via a stimulation of the inhibitory α-adrenoceptors of the pancreatic B-cell. The effect of somatostatin on insulin secretion during α-adrenergic blockade with phentolamine was therefore studied in three different species; the rat, the cat and the mouse. It was found that somatostatin significantly depressed insulin release during α-adrenoceptor blockade in all three species. In the rat, infusion of somatostatin at a dose of 0.3 μg/kg/min decreased basal plasma insulin concentration by 92 %. In the presence of phentolamine, the same dose of somatostatin lowered plasma insulin by 85 %. In the cat, a similar infusion of somatostatin lowered basal plasma insulin concentration by 87 %, but its depressive effect during α-adrenergic blockade was comparatively less pronounced (68 %) than in the rat. In the mouse, a single iv injection of somatostatin induced a short-lasting depression of plasma insulin concentration during α-adrenergic blockade. From these results it seems unlikely that somatostatin should inhibit insulin release simply by stimulation of α-adrenoceptors on the B-cell. It cannot be ruled out, however, that a more complex interaction exists between somatostatin and the sympatho-adrenal system with regard to the control of insulin secretion.

scholarly journals 146 Nutritional Advances in Fetal and neonatal development: effect of fatty acid supplementation

2020 ◽  
Vol 98 (Supplement_3) ◽  
pp. 121-122
Author(s):  
Alejandro E Relling
Keyword(s):  
Small Intestine ◽  
Fatty Acid ◽  
Plasma Insulin ◽  
Linear Increase ◽  
Late Gestation ◽  
Insulin Concentration ◽  
Plasma Insulin Concentration ◽  
Pufa Supplementation ◽  
Epa And Dha ◽  
Offspring Growth

Abstract Data from a series of experiments demonstrates that maternal supply of polyunsaturated fatty acids, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), during late gestation affects offspring growth. The increase in growth is independent on the fatty acid supplemented during the growing or finishing phase of the offspring; but it is sex dependent. Dam PUFA supplementation increases wether growth. Supplementation with EPA and DHA to pregnant ewes and to their offspring after weaning showed a treatment interaction in mRNA concentration of hypothalamic neuropeptides associated with dry matter intake (DMI) regulation. A dose increased in EPA and DHA in pregnant ewe diets shows a linear increase in growth, but a quadratic change in DMI or feed efficiency; growth was associated with a linear increase in plasma glucose concentration and a linear decrease in plasma ghrelin concentration. In lambs born from ewes supplemented with different sources of FA during a glucose tolerance test; males’ plasma insulin concentration increased as FA unsaturation degree increased in the dam diet, the opposite happened with females’ plasma insulin concentration. Recent data from our lab showed that the supplementation with EPA and DHA during the last third of gestation to pregnant ewes increased liver and small intestine global DNA methylation and small intestine transporters for amino acids in the fetus. Despite EPA and DHA during late gestation increase growth in the offspring; when EPA and DHA were supplemented in early gestation, offspring growth was lesser that lambs born from ewes supplemented a saturated and monounsaturated lipid. The reason for the difference in results it is not clear. However, more studies focusing in some aspect of the biology will help to understand what specific fatty acid needs to be supplemented at different stages of gestation to improve offspring growth.

scholarly journals Fetal growth, glucose tolerance and plasma insulin concentration in rats given a marginal-zinc diet in the latter stages of pregnancy

1988 ◽  
Vol 59 (2) ◽  
pp. 315-322 ◽  
Author(s):  
Susan Southon ◽  
Susan J. Fairweather-Tait ◽  
Christine M. Williams
Keyword(s):  
Blood Glucose ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Insulin Concentration ◽  
Oral Glucose ◽  
Fetal Blood ◽  
Plasma Insulin Concentration ◽  
Pregnant Rats ◽  
Zn Content ◽  
Tail Blood

1. Wistar rats were fed on a control semi-synthetic diet throughout pregnancy, or a control diet in the first 2 weeks and a marginal-zinc diet in the 3rd week of pregnancy. On day 20, after an overnight fast, half the animals in each group were given glucose by gavage and the 0–30 min rise in blood glucose measured in tail blood. After 60 min blood was taken by cardiac puncture for glucose and insulin assay. Maternal pancreases were removed and the Zn contents measured. Fetuses from each litter were combined for wet/dry weights, protein and DNA determinations.2. Plasma insulin concentration was higher, and glucose concentration and pancreatic Zn content lower, in pregnantv. non-pregnant animals of similar age, fed on the same diet. Pancreatic Zn content was lowest in the marginal-Zn group of pregnant rats. Fetuses from mothers fed on the marginal-Zn diet during the last week of pregnancy were slightly heavier than controls and had a significantly higher protein: DNA ratio. The 0–30 min rise in blood glucose was significantly greater in the marginal-Zn animals.3. In a second experiment, pregnant rats were given similar diets to those used in the first study, but the marginal-Zn diet was given for a shorter period (days 15–19 of pregnancy). On day 19 the rats were meal-fed and on day 20, after an overnight fast, an oral glucose dose was administered. Tail-blood was taken at timed intervals up to 60 min post-dosing for glucose assay. Both maternal and fetal blood glucose and insulin concentration was measured 70 min post-dosing.4. Values for maternal and fetal blood glucose and plasma insulin, measured 70 min after the administration of a glucose dose, were similar in the two groups, but the initial rise in blood glucose concentration was again significantly higher in pregnant rats given the marginal-Zn diet towards term.5. It is suggested that the change in growth and composition, observed in fetuses from rats given a marginal-Zn diet in later pregnancy, is associated with altered maternal carbohydrate metabolism.

Carbohydrate ingestion before exercise: comparison of glucose, fructose, and sweet placebo

1981 ◽  
Vol 51 (4) ◽  
pp. 783-787 ◽  
Author(s):  
V. A. Koivisto ◽  
S. L. Karonen ◽  
E. A. Nikkila
Keyword(s):  
Plasma Glucose ◽  
Plasma Insulin ◽  
Cycle Ergometer ◽  
Vo2 Max ◽  
Vigorous Exercise ◽  
Carbohydrate Ingestion ◽  
Rapid Fall ◽  
Ergometer Exercise ◽  
Glucose Ingestion ◽  
Response To Exercise

To examine the effect of various carbohydrates on the metabolic and hormonal response to exercise, 75 g glucose, fructose, or placebo were given to nine well-trained males (VO2 max 60 +/- 1 ml . kg-1 . min-1) 45 min before cycle ergometer exercise performed at 75% VO2 max for 30 min. After glucose ingestion, the rise in plasma glucose was 3-fold (P less than 0.005) in plasma insulin 2.5-fold (P less than 0.01) greater than after fructose. During exercise, after glucose administration plasma glucose fell from 5.3 +/- 0.3 to 2.5 +/- 0.2 mmol/l (P less than 0.001) and after fructose from 4.5 +/- 0.1 to 3.9 +/- 0.3 mmol/l (P less than 0.05). The fall in plasma glucose was closely related to the preexercise levels of plasma insulin (r = 0.82, P less than 0.001) and glucose (r = 0.81, P less than 0.001). Both glucose and fructose ingestion decreased the FFA levels by 40–50% (P less than 0.005) and during exercise they remained 30–40% lower after carbohydrate than placebo administration (P less than 0.02). This study suggests that glucose ingestion prior to exercise results in hypoglycemia during vigorous exercise, this rapid fall in plasma glucose is mediated, at least in part, by hyperinsulinemia, and fructose ingestion is associated with a modest rise in plasma insulin and does not result in hypoglycemia during exercise.

scholarly journals The effect of acetoacetate on plasma insulin concentration

1971 ◽  
Vol 125 (2) ◽  
pp. 541-544 ◽  
Author(s):  
R. A. Hawkins ◽  
K. G. M. M. Alberti ◽  
C. R. S. Houghton ◽  
D. H. Williamson ◽  
H. A. Krebs
Keyword(s):  
Fatty Acids ◽  
Blood Glucose ◽  
Free Fatty Acids ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Blood Glucose Concentration ◽  
Diabetic Rats ◽  
Insulin Concentration ◽  
Plasma Insulin Concentration ◽  
Arterial Blood

1. Sodium acetoacetate was infused into the inferior vena cava of fed rats, 48h-starved rats, and fed streptozotocin-diabetic rats treated with insulin. Arterial blood was obtained from a femoral artery catheter. 2. Acetoacetate infusion caused a fall in blood glucose concentration in fed rats from 6.16 to 5.11mm in 1h, whereas no change occurred in starved or fed–diabetic rats. 3. Plasma free fatty acids decreased within 10min, from 0.82 to 0.64mequiv./l in fed rats, 1.16 to 0.79mequiv./l in starved rats and 0.83 to 0.65mequiv./l in fed–diabetic rats. 4. At 10min the plasma concentration rose from 20 to 49.9μunits/ml in fed unanaesthetized rats and from 6.4 to 18.5μunits/ml in starved rats. There was no change in insulin concentration in the diabetic rats. 5. Nembutal-anaesthetized fed rats had a more marked increase in plasma insulin concentration, from 30 to 101μunits/ml within 10min. 6. A fall in blood glucose concentration in fed rats and a decrease in free fatty acids in both fed and starved rats is to be expected as a consequence of the increase in plasma insulin. 7. The fall in the concentration of free fatty acids in diabetic rats may be due to a direct effect of ketone bodies on adipose tissue. A similar effect on free fatty acids could also be operative in normal fed or starved rats.

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