Effects of fatty acids on exercise plus insulin-induced glucose utilization in trained and sedentary subjects

2002 ◽  
Vol 282 (1) ◽  
pp. E125-E131 ◽  
Author(s):  
Oscar Matzinger ◽  
Philippe Schneiter ◽  
Luc Tappy
Keyword(s):  
Fatty Acids ◽  
Lipid Oxidation ◽  
Endurance Training ◽  
Glucose Utilization ◽  
Inhibitory Effect ◽  
Substrate Oxidation ◽  
Whole Body ◽  
Trained Subjects ◽  
Lipid Infusion ◽  
Sedentary Subjects

Fatty acids are known to decrease insulin-mediated glucose utilization in humans, both at rest and during exercise. To evaluate the effect of endurance training in this process, we infused lipids or saline in groups of sedentary and highly trained subjects. Whole body glucose utilization and substrate oxidation were monitored during a 2.5-h hyperinsulinemic clamp. During the last 30 min, a cycling exercise was superimposed. During hyperinsulinemia at rest, whole body glucose utilization and glucose oxidation were higher in trained subjects than in sedentary subjects. Compared with the control experiments with the antilipolytic agent acipimox, lipid infusion stimulated lipid oxidation to the same extent in trained as in sedentary subjects. It reduced whole body glucose utilization by 37% in trained and by 41% in sedentary subjects. During exercise, lipid infusion increased more lipid oxidation in trained than in sedentary subjects and reduced whole body glucose utilization by 43 ± 4% in trained and by 22 ± 4% in sedentary subjects ( P < 0.01). The present data indicate that lipid infusion has similar effects on lipid oxidation and whole body glucose utilization during hyperinsulinemia at rest in trained and sedentary subjects. During exercise, however, it increases more lipid oxidation and produces a more important reduction in glucose utilization in trained than in sedentary subjects. These results suggest that endurance training enhances the inhibitory effect of lipids on whole body glucose metabolism during exercise.

scholarly journals Albumin Knockout Mice Exhibit Reduced Plasma Free Fatty Acids but No Impairment in Whole Body Fat Oxidation

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 534-534
Author(s):  
Afsoun Abdollahi ◽  
Brianana N Dowden ◽  
Gregory C Henderson
Keyword(s):  
Fatty Acids ◽  
Serum Albumin ◽  
Free Fatty Acids ◽  
Body Fat ◽  
Knockout Mice ◽  
Substrate Oxidation ◽  
Whole Body ◽  
Wild Type ◽  
Plasma Free Fatty Acids ◽  
Plasma Ffa

Abstract Objectives To improve understanding of the control of lipid metabolism, we aimed to determine whether lack of serum albumin decreases plasma free fatty acids (FFA), hepatic triacylglycerol (TAG), and whole body substrate oxidation in albumin knockout mice compared to wild type mice. Methods Male and female homozygous albumin knockout mice and C57BL/6J wild type controls, each on the 5k52 diet which contains a moderate fat content, were studied at 6–8 weeks of age. Body composition was tested by magnetic resonance. Substrate oxidation was measured by indirect calorimetry over 24 hours in metabolic cages. Plasma and tissues were collected after a 5-hour fast. Plasma FFA was measured by liquid chromatography/mass spectrometry (LC/MS). Hepatic TAG was measured by a colorimetric kit. Results In albumin knockout mice compared to the wild type mice, plasma FFA (P &lt; 0.0001) and hepatic TAG content (P &lt; 0.0001) were each reduced, while body fat percentage was increased (P &lt; 0.01). In addition, female versus male showed higher hepatic TAG levels (P &lt; 0.01). These results indicate that the lack of serum albumin decreases plasma FFA and hepatic TAG accumulation. However, the average 24-hour oxygen consumption, metabolic rate, and respiratory quotient (RQ) were not altered in albumin knockout mice, indicating that total fuel oxidation and relative contribution of lipid to whole body metabolism was not significantly unaltered. Conclusions We propose that lack of albumin reduces plasma FFA which diminishes hepatic TAG content through changes in the lipid supply to the liver. The results indicate that tissue lipid accumulation can be altered by targeting albumin without substantially disrupting whole body substrate oxidation, suggesting that metabolic control of FFA trafficking toward sites of ectopic lipid deposition and toward oxidation can be regulated independently of one another. Funding Sources McKinley Educational Initiative and the Purdue University College of Health and Human Sciences

scholarly journals The effect of dietary fat and omega‐3 fatty acids on whole body lipid oxidation

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Cheryl Ainslie-Waldman ◽  
Lindsay R. Young ◽  
Mindy S. Kurzer ◽  
Susan K. Raatz ◽  
A. Saari Csallany
Keyword(s):  
Fatty Acids ◽  
Lipid Oxidation ◽  
Dietary Fat ◽  
Whole Body ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Body Lipid

Hyperglycemia stimulates carbohydrate oxidation in humans

1987 ◽  
Vol 253 (4) ◽  
pp. E376-E382 ◽  
Author(s):  
H. Yki-Jarvinen ◽  
C. Bogardus ◽  
B. V. Howard
Keyword(s):  
Fatty Acids ◽  
Lipid Oxidation ◽  
Substrate Oxidation ◽  
Carbohydrate Oxidation ◽  
Glucose Disposal ◽  
Absolute Rate ◽  
Total Rate ◽  
Oxidation Rates ◽  
Total Glucose ◽  
Glucose Availability

We examined whether hyperglycemia stimulates carbohydrate oxidation independent of insulin. Rates of total glucose disposal and substrate oxidation (indirect calorimetry) were measured at 4 insulin concentrations and at each level of insulin at 4 glucose concentrations in 88 separate studies in 22 normal volunteers. The insulin sensitivity of carbohydrate and lipid oxidation was independent of glycemia, but glucose, independent of insulin, increased the absolute rate of carbohydrate oxidation and decreased lipid oxidation. To compare the ability of glucose and insulin to stimulate carbohydrate oxidation, oxidation rates were examined at similar rates of total glucose disposal induced by hyperinsulinemia or hyperglycemia. At physiological matched rates of glucose disposal, insulin stimulated carbohydrate oxidation 2.4-fold more than glucose. The free fatty acids (FFA) were significantly lower in the presence of hyperinsulinemia than hyperglycemia. When compared at similar (supraphysiological) rates of total glucose disposal, where the FFA were completely suppressed, the rate of carbohydrate oxidation was related to the total rate of glucose disposal rather than the ambient glucose or insulin concentrations. We conclude that both glucose and insulin can increase carbohydrate oxidation in humans. We propose that the rate of carbohydrate oxidation is determined by FFA availability and by glucose availability independent of the FFA level in glucose-consuming tissues. Although FFA availability is almost solely determined by insulin, both glucose and insulin can increase carbohydrate oxidation by increasing glucose availability.

scholarly journals No effect of menstrual cycle phase on glucose kinetics and fuel oxidation during moderate-intensity exercise

2002 ◽  
Vol 282 (4) ◽  
pp. E752-E762 ◽  
Author(s):  
Tracy J. Horton ◽  
Emily K. Miller ◽  
Deborah Glueck ◽  
Kathleen Tench
Keyword(s):  
Menstrual Cycle ◽  
Glucose Utilization ◽  
Substrate Oxidation ◽  
Normal Weight ◽  
Whole Body ◽  
Moderate Intensity ◽  
Cycle Phase ◽  
Moderate Intensity Exercise ◽  
Fuel Oxidation ◽  
Significant Difference

Resting and exercise fuel metabolism was assessed in three different phases of the menstrual cycle, characterized by different levels of estrogen relative to progesterone: early follicular (EF, low estrogen and progesterone), midfollicular (MF, elevated estrogen, low progesterone), and midluteal (ML, elevated estrogen and progesterone). It was hypothesized that exercise glucose utilization and whole body carbohydrate oxidation would decrease sequentially from the EF to the MF to the ML phase. Normal-weight healthy females, experiencing a regular menstrual cycle, were recruited. Subjects were moderately active but not highly trained. Testing occurred after 3 days of diet control and after an overnight fast (12–13 h). Resting (2 h) and exercise (50% maximal O2 uptake, 90 min) measurements of whole body substrate oxidation, tracer-determined glucose flux, and substrate and hormone concentrations were made. No significant difference was observed in whole body fuel oxidation during exercise in the three phases (nonprotein respiratory exchange ratio: EF 0.84 ± 0.01, MF 0.85 ± 0.01, ML 0.85 ± 0.01) or in rates of glucose appearance or disappearance. There were, however, significantly higher glucose ( P < 0.05) and insulin ( P < 0.001) concentrations during the first 45 min of exercise in the ML phase vs. EF and MF phases. In conclusion, whole body substrate oxidation and glucose utilization did not vary significantly across the menstrual cycle in moderately active women, either at rest or during 90 min of moderate-intensity exercise. During the ML phase, however, this similar pattern of substrate utilization was associated with greater glucose and insulin concentrations. Both estrogen and progesterone are elevated during the ML phase of the menstrual cycle, suggesting that one or both of these sex steroids may play a role in this response.

scholarly journals Effects of dietary propionate on hepatic glucose production, whole-body glucose utilization, carbohydrate and lipid metabolism in normal rats

1995 ◽  
Vol 73 (2) ◽  
pp. 241-251 ◽  
Author(s):  
Josette Boillot ◽  
Catherine Alamowitch ◽  
Anne-Marie Berger ◽  
Jing Luo ◽  
Françoise Bruzzo ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Insulin Sensitivity ◽  
Glucose Utilization ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Whole Body ◽  
Dietary Fibres ◽  
Carbohydrate And Lipid Metabolism ◽  
Hepatic Glucose ◽  
Anaesthetized Rats

Increased intake of dietary fibres is associated with several beneficial effects on carbohydrate and lipid metabolism. The colonic fermentation of dietary fibres produces short-chain fatty acids (SCFA; acetate, propionate and butyrate). Some authors have suggested that SCFA could be partly responsible for the effects of dietary fibres. The purpose of the present study was to test the effects of one of the SCFA, propionate. The effects of moderate amounts of dietary propionate on insulin sensitivity and hepatic glucose production were studied in male Sprague-Dawley rats. Two groups of twenty-one adult rats were fed for 3 weeks on a diet containing 78 g propionate/kg (P) or 78 g/kg of a poorly fermentable cellulose (control group; C). Feed intake, body weight, fasting plasma glucose, insulin, free fatty acids, alanine, lactate, glycerol and β-hydroxybutyrate levels were measured weekly in anaesthetized rats. At the end of the feeding period basal hepatic glucose production (BHGP) was measured with a primed continuous infusion of [3−3H]glucose and the in vivo insulin sensitivity in rats was quantified by the euglycaemic-hyperinsulinaemic clamp technique (0.6 and 2 U/kg per h). At that time fasting plasma glucose measured in anaesthetized rats was significantly lower in group P than in group C: 7·7 (SE 0·2) v. 8.5 (SE 0·2) mmol/l respectively (P < 0·002); plasma insulin levels were not significantly different. Neither the BHGP (mg/min per kg; C 14·8 (SE 1·3), P 15·1 (SE 1·3); n 7, not significant) nor the basal metabolic clearance (ml/min per kg; 8·9 (SE 08) v. 9·9 (SE 1·1); not significant) were different between treatments. Hepatic glucose production and glucose utilization at the two insulin concentrations (approximately 500 and 1500 mU/l respectively, n 7) did not differ significantly between the two groups. These results show that dietary propionate chronically ingested by normal rats could decrease fasting glycaemia, but from our findings, no effect on hepatic glucose production and whole-body glucose utilization could be clearly demonstrated.

scholarly journals Effects of Euglycemic Hyperinsulinemia and Lipid Infusion on Circulating Cholecystokinin

2008 ◽  
Vol 93 (6) ◽  
pp. 2328-2333 ◽  
Author(s):  
M. O. Weickert ◽  
M. Möhlig ◽  
J. Spranger ◽  
C. Schöfl ◽  
C. V. Loeffelholz ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Blood Lipids ◽  
Intraclass Correlation ◽  
Biologically Active ◽  
Whole Body ◽  
Diabetic Patients ◽  
Complete Suppression ◽  
Lipid Infusion ◽  
Gut Hormone

Abstract Aims: Functions of the gut hormone cholecystokinin (CCK) include an important role in the regulation of gastric emptying, postprandial glucose homeostasis, and postmeal satiety. Postprandial CCK responses are significantly blunted in type 2 diabetic patients by unknown mechanisms. We hypothesized that hyperinsulinemia and lipid infusion influence circulating levels of biologically active CCK. Methods: Eleven healthy subjects were studied in a cross-over design after 10-h overnight fasts, using euglycemic-hyperinsulinemic clamps for 443 min, with an additional infusion of lipid-heparin (1.25 ml·min−1) or saline (1.25 ml·min−1) for the last 300 min after constant plasma glucose levels were achieved. Results: Euglycemic-hyperinsulinemia resulted in a sustained, up to 5-fold increase of plasma CCK (P &lt; 0.001). When adding lipid infusion instead of saline, CCK concentrations rapidly declined and returned to baseline levels (CCK300 min 1.1 ± 0.2 vs. 3.3 ± 0.3 pmol/liter, P &lt; 0.001). Partial intraclass correlation showed an independent correlation of plasma CCK with free fatty acids (ric = −0.377, P &lt; 0.001) but not with serum insulin (ric = 0.077, P = 0.32). Whole-body insulin sensitivity decreased in lipid-exposed subjects (M value 7.1 ± 0.7 vs. 5.6 ± 0.9 mg·kg·min−1, P = 0.017) but was not independently correlated with CCK (ric = 0.040, P = 0.61). Conclusions: We report novel findings showing that circulating CCK markedly increased in the euglycemic-hyperinsulinemic state, possibly as a result of near-complete suppression of circulating free fatty acids. Moreover, raising blood lipids even moderately by lipid infusion rapidly and significantly interfered with this effect, suggesting that a negative feedback mechanism of blood lipids on circulating CCK might exist.

scholarly journals Countering impaired glucose homeostasis during catch-up growth with essential polyunsaturated fatty acids: is there a major role for improved insulin sensitivity?

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Julie Calonne ◽  
Helena Marcelino ◽  
Christelle Veyrat-Durebex ◽  
Isabelle Scerri ◽  
Abdul G. Dulloo
Keyword(s):  
Fatty Acids ◽  
Insulin Sensitivity ◽  
Glucose Homeostasis ◽  
Skeletal Muscles ◽  
Glucose Utilization ◽  
Whole Body ◽  
High Fat ◽  
Adipose Tissue Depots ◽  
Body Level ◽  
Catch Up

Abstract Background/Objectives Catch-up growth, an important risk factor for later obesity and type 2 diabetes, is often characterized by a high rate of fat deposition associated with hyperinsulinemia and glucose intolerance. We tested here the hypothesis that refeeding on a high-fat diet rich in essential polyunsaturated fatty acids (ePUFA) improves glucose homeostasis primarily by enhancing insulin sensitivity in skeletal muscles and adipose tissues. Methods Rats were caloric restricted for 2 weeks followed by 1–2 weeks of isocaloric refeeding on either a low-fat (LF) diet, a high-fat (HF) diet based on animal fat and high in saturated and monounsaturated fatty acids (HF SMFA diet), or a HF diet based on vegetable oils (1:1 mixture of safflower and linseed oils) and rich in the essential fatty acids linoleic and α-linolenic acids (HF ePUFA diet). In addition to measuring body composition and a test of glucose tolerance, insulin sensitivity was assessed during hyperinsulinemic-euglycemic clamps at the whole-body level and in individual skeletal muscles and adipose tissue depots. Results Compared to animals refed the LF diet, those refed the HF-SMFA diet showed a higher rate of fat deposition, higher plasma insulin and glucose responses during the test of glucose tolerance, and markedly lower insulin-stimulated glucose utilization at the whole body level (by a-third to a-half) and in adipose tissue depots (by 2–5 folds) during insulin clamps. While refeeding on the ePUFA diet prevented the increases in fat mass and in plasma insulin and glucose, the results of insulin clamps revealed that insulin-stimulated glucose utilization was not increased in skeletal muscles and only marginally higher in adipose tissues and at the whole-body level. Conclusions These results suggest only a minor role for enhanced insulin sensitivity in the mechanisms by which diets high in ePUFA improves glucose homeostasis during catch-up growth.

scholarly journals Hypocalcin from Stannius corpuscles inhibits gill calcium uptake in trout

1988 ◽  
Vol 254 (6) ◽  
pp. R891-R896 ◽  
Author(s):  
F. P. Lafeber ◽  
G. Flik ◽  
S. E. Wendelaar Bonga ◽  
S. F. Perry
Keyword(s):  
Rainbow Trout ◽  
Calcium Uptake ◽  
Inhibitory Effect ◽  
Whole Body ◽  
Transepithelial Potential ◽  
Low Calcium ◽  
Stannius Corpuscles ◽  
Normal Calcium

Bidirectional whole body flux and branchial Ca2+ influx were measured in freshwater rainbow trout. Intra-arterial injections of homogenates of Stannius corpuscles (CS) as well as of a 54-kDa isolated product (hypocalcin) exerted an inhibitory effect on whole body Ca2+ influx, but did not effect Ca2+ efflux. Hypocalcin was more effective in reducing Ca2+ influx in trout acclimated to low-calcium freshwater than in fish from normal-calcium water. We conclude that the isolated product (hypocalcin) represents the hypocalcemic principle of the CS. Similar doses of hypocalcin caused quantitatively similar decreases in Ca2+ influx in vivo and in the isolated perfused head preparation. This indicates that the gills form the principle target for hypocalcin in trout. The branchial transepithelial potential did not change during hormone treatments. Possible mechanisms of hypocalcin action are suggested.

scholarly journals Evidence for the regulation of guinea-pig heart microsomal phosphatidylcholine-hydrolysing phospholipase A1 by guanosine 5′-[γ-thio]triphosphate

1992 ◽  
Vol 288 (3) ◽  
pp. 965-968 ◽  
Author(s):  
K Badiani ◽  
X Lu ◽  
G Arthur
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Guinea Pig ◽  
Molecular Species ◽  
Inhibitory Effect ◽  
Phospholipase A1 ◽  
Guinea Pig Heart ◽  
Substrate Specificities ◽  
Rate Of Hydrolysis ◽  
Hydrolysis Of

We have recently characterized lysophospholipase A2 activities in guinea-pig heart microsomes and postulated that these enzymes act sequentially with phospholipases A1 to release fatty acids selectively from phosphatidylcholine (PC) and phosphatidylethanolamine, thus providing an alternative route to the phospholipase A2 mode of release. In a further investigation of the postulated pathway, we have characterized the PC-hydrolysing phospholipase A1 in guinea-pig heart microsomes. Our results show that the enzyme may have a preference for substrates with C16:0 over C18:0 at the sn-1 position. In addition, although the enzyme cleaves the sn-1 fatty acid, the rate of hydrolysis of PC substrates with C16:0 at the sn-1 position was influenced by the nature of the fatty acid at the sn-2 position. The order of decreasing preference was C18:2 > C20:4 = C18:1 > C16:0. The hydrolyses of the molecular species were differentially affected by heating at 60 degrees C. An investigation into the effect of nucleotides on the activity of the enzyme showed that guanosine 5′-[gamma-thio]triphosphate (GTP[S]) inhibited the hydrolysis of PC by phospholipase A1 activity, whereas GTP, guanosine 5′-[beta-thio]diphosphate (GDP[S]), GDP, ATP and adenosine 5′-[gamma-thio]triphosphate (ATP[S]) did not affect the activity. The inhibitory effect of GTP[S] on phospholipase A1 activity was blocked by preincubation with GDP[S]. A differential effect of GTP[S] on the hydrolysis of different molecular species was also observed. Taken together, the results of this study suggest the presence of more than one phospholipase A1 in the microsomes with different substrate specificities, which act sequentially with lysophospholipase A2 to release linoleic or arachidonic acid selectively from PC under resting conditions. Upon stimulation and activation of the G-protein, the release of fatty acids would be inhibited.

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