Strenuous endurance training increases lipolysis and triglyceride-fatty acid cycling at rest

1993 ◽  
Vol 75 (1) ◽  
pp. 108-113 ◽  
Author(s):  
J. A. Romijn ◽  
S. Klein ◽  
E. F. Coyle ◽  
L. S. Sidossis ◽  
R. R. Wolfe
Keyword(s):  
Fatty Acid ◽  
Endurance Training ◽  
Plasma Concentrations ◽  
Whole Body ◽  
Acid Oxidation ◽  
Body Lipid ◽  
Control Subjects ◽  
Triglyceride Fatty Acid ◽  
Fatty Acid Release ◽  
Acid Release

Basal whole body lipid kinetics were evaluated in nine endurance-trained cyclists and 10 untrained healthy controls. The rate of appearance (Ra) of glycerol (an index of whole body lipolysis), the Ra of palmitate (an index of fatty acid release), and the rate of triglyceride-fatty acid cycling (reesterification of fatty acids released during lipolysis) were determined by infusing [2H5]glycerol and [2H2]palmitate in conjunction with indirect calorimetry. All subjects were studied while they were at rest after fasting overnight. Glycerol Ra and free fatty acid Ra in the athletes (7.33 +/- 0.68 and 14.88 +/- 1.35 mumol.kg-1 x min-1, respectively) were two- to threefold higher than the values in untrained control subjects (2.53 +/- 0.15 and 7.64 +/- 0.92 mumol.kg-1 x min-1, respectively; P < 0.02). The total rate of triglyceride-fatty acid cycling was approximately four-fold higher in the athletes (16.86 +/- 2.07 mumol.kg-1 x min-1) than in the control subjects (3.91 +/- 0.36 mumol.kg-1 x min-1). Plasma concentrations of insulin and catecholamines, hormones that regulate whole body lipid kinetics, were the same in both groups. We conclude that resting basal lipid kinetics are markedly increased in athletes involved in strenuous endurance training and that this enhances the potential for increasing fatty acid oxidation rapidly at the onset of exercise.

FAT/CD36 regulates PEPCK expression in adipose tissue

2013 ◽  
Vol 304 (5) ◽  
pp. C478-C484 ◽  
Author(s):  
Zhongxiao Wan ◽  
Sarthak Matravadia ◽  
Graham P. Holloway ◽  
David C. Wright
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Mrna Expression ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Fatty Acid Uptake ◽  
Acid Oxidation ◽  
Acid Uptake ◽  
Expression Of Genes ◽  
Fatty Acid Release ◽  
Acid Release

Fatty acid translocase (FAT)/CD36 has been extensively studied for its role in facilitating fatty acid uptake. Recent findings have also demonstrated that this protein regulates adipocyte lipolysis and may modulate fatty acid reesterification. As FAT/CD36 has been shown to control the expression of genes involved in fatty acid oxidation in adipocytes, we reasoned that this protein might also control the expression of enzymes involved in fatty acid reesterification. In adipose tissue from FAT/CD36 knockout (KO) mice, we found that glycerol and fatty acid release were reduced and this was associated with reductions in adipose triglyceride lipase. Decreases in lipolysis were paralleled by increases in the free fatty acid-to-glycerol ratio and reductions in primary and fractional rates of fatty acid reesterfication in cultured adipose tissue from FAT/CD36 KO mice. Reductions in reesterfication were associated with decreases in the mRNA expression and protein content of phosphoenolpyruvate carboxykinase (PEPCK). To determine if reductions in lipolysis could lead to decreases in PEPCK mRNA expression, we treated cultured mouse adipose tissue with the lipase inhibitor CAY10499 (2 μM) and found that this resulted in an ∼50% reduction in PEPCK mRNA expression. Treatment with hexarelin (10 μM, 12 h), a CD36 agonist, increased PEPCK mRNA expression independent of lipolysis. Collectively, our results provide novel evidence that FAT/CD36 regulates PEPCK in adipose tissue and that this could be secondary to reductions in lipolysis.

scholarly journals Biochemical actions of vasoactive peptide hormones. Time-synchronized activation of lipolysis and decreased fatty-acid release by bradykinin and angiotensin in the perfused rabbit kidney

1980 ◽  
Vol 192 (1) ◽  
pp. 127-131 ◽  
Author(s):  
M Schwartzman ◽  
A Raz
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Time Lag ◽  
Rabbit Kidney ◽  
Subsequent Decrease ◽  
Fatty Acid Release ◽  
Initial Activation ◽  
Acid Release ◽  
Sequential Processes ◽  
Vasoactive Peptide

Bradykinin and angiotensin administered to the isolated perfused rabbit kidney activate two sequential processes: (1) a selective release of the prostaglandin precursor arachidonate with concomitant partial conversion of the arachidonate into prostaglandin E2; (2) activation of a process that leads to decreased release of all fatty acids in the perfusate. There is a time lag of approx. 1 min between the initial activation of the arachidonate-specific deacylation reaction that is coupled to prostaglandin generation, and the subsequent decrease in the release of all fatty acids. This synchronized cycle provides for instant generation of required amounts of prostaglandins and at the same time serves to conserve cellular arachidonate.

scholarly journals Deletion of nuclear factor-κB p50 upregulates fatty acid utilization and contributes to an anti-obesity and high-endurance phenotype in mice

2015 ◽  
Vol 309 (6) ◽  
pp. E523-E533 ◽  
Author(s):  
Yoshihiko Minegishi ◽  
Satoshi Haramizu ◽  
Koichi Misawa ◽  
Akira Shimotoyodome ◽  
Tadashi Hase ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Nuclear Factor Κb ◽  
Whole Body ◽  
Acid Oxidation ◽  
Endurance Capacity ◽  
Peroxisome Proliferator ◽  
Primary Role ◽  
Nuclear Factor ◽  
Oxidation Activity ◽  
Fatty Acid Utilization

The transcription factor nuclear factor-κB (NF-κB) plays an important role in regulating physiological processes such as immunity and inflammation. In addition to this primary role, NF-κB interacts physically with peroxisome proliferator-activated receptors regulating lipid metabolism-related gene expression and inhibits their transcriptional activity. Therefore, inhibition of NF-κB may promote fatty acid utilization, which could ameliorate obesity and improve endurance capacity. To test this hypothesis, we attempted to elucidate the energy metabolic status of mice lacking the p50 subunit of NF-κB (p50 KO mice) from the tissue to whole body level. p50 KO mice showed a significantly lower respiratory quotient throughout the day than did wild-type (WT) mice; this decrease was associated with increased fatty acid oxidation activity in liver and gastrocnemius muscle of p50 KO mice. p50 KO mice that were fed a high-fat diet were also resistant to fat accumulation and adipose tissue inflammation. Furthermore, p50 KO mice showed a significantly longer maximum running time compared with WT mice, with a lower respiratory exchange ratio during exercise as well as higher residual muscle glycogen content and lower blood lactate levels after exercise. These results suggest that p50 deletion facilitates fatty acid catabolism, leading to an anti-obesity and high-endurance phenotype of mice and supporting the idea that NF-κB is an important regulator of energy metabolism.

Meal composition affects postprandial fatty acid oxidation

1993 ◽  
Vol 264 (6) ◽  
pp. R1065-R1070 ◽  
Author(s):  
D. M. Surina ◽  
W. Langhans ◽  
R. Pauli ◽  
C. Wenk
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Nutrient Utilization ◽  
Whole Body ◽  
Acid Oxidation ◽  
Plasma Ffa ◽  
Hepatic Fatty Acid Oxidation ◽  
Beta Hydroxybutyrate ◽  
Chain Fatty Acids

The influence of macronutrient content of a meal on postprandial fatty acid oxidation was investigated in 13 Caucasian males after consumption of a high-fat (HF) breakfast (33% carbohydrate, 52% fat, 15% protein) and after an equicaloric high-carbohydrate (HC) breakfast (78% carbohydrate, 6% fat, 15% protein). The HF breakfast contained short- and medium-chain fatty acids, as well as long-chain fatty acids. Respiratory quotient (RQ) and plasma beta-hydroxybutyrate (BHB) were measured during the 3 h after the meal as indicators of whole body substrate oxidation and hepatic fatty acid oxidation, respectively. Plasma levels of free fatty acids (FFA), triglycerides, glucose, insulin, and lactate were also determined because of their relationship to nutrient utilization. RQ was significantly lower and plasma BHB was higher after the HF breakfast than after the HC breakfast, implying that more fat is burned in general and specifically in the liver after an HF meal. As expected, plasma FFA and triglycerides were higher after the HF meal, and insulin and lactate were higher after the HC meal. In sum, oxidation of ingested fat occurred in response to a single HF meal.

Dose-dependent effect of insulin on plasma free fatty acid turnover and oxidation in humans

1990 ◽  
Vol 259 (5) ◽  
pp. E736-E750 ◽  
Author(s):  
R. C. Bonadonna ◽  
L. C. Groop ◽  
K. Zych ◽  
M. Shank ◽  
R. A. DeFronzo
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Lipid Oxidation ◽  
Plasma Insulin ◽  
Plasma Free Fatty Acid ◽  
Whole Body ◽  
Glucose Disposal ◽  
Body Lipid ◽  
Plasma Ffa ◽  
Dose Dependent

Methodology for measuring plasma free fatty acid (FFA) turnover/oxidation with [1–14C]palmitate was tested in normal subjects. In study 1, two different approaches (720-min tracer infusion without prime vs. 150-min infusion with NaH14CO3 prime) to achieve steady-state conditions of 14CO2 yielded equivalent rates of plasma FFA turnover/oxidation. In study 2, during staircase NaH14CO3 infusion, calculated rates of 14CO2 appearance agreed closely with NaH14CO3 infusion rates. In study 3, 300-min euglycemic insulin clamp documented that full biological effect of insulin on plasma FFA turnover/oxidation was established within 60–120 min. In study 4, plasma insulin concentration was raised to 14 +/- 2, 23 +/- 2, 38 +/- 2, 72 +/- 5, and 215 +/- 10 microU/ml. A dose-dependent insulin suppression of plasma FFA turnover/oxidation was observed. Plasma FFA concentration correlated positively with plasma FFA turnover/oxidation in basal and insulinized states. Total lipid oxidation (indirect calorimetry) was significantly higher than plasma FFA oxidation in the basal state, suggesting that intracellular lipid stores contributed to whole body lipid oxidation. Hepatic glucose production and total glucose disposal showed the expected dose-dependent suppression and stimulation, respectively, by insulin. In conclusion, insulin regulation of plasma FFA turnover/oxidation is maximally manifest at low physiological plasma insulin concentrations, and in the basal state a significant contribution to whole body lipid oxidation originates from lipid pool(s) that are different from plasma FFA.

Effects of treadmill exercise on fuel metabolism in hepatic cirrhosis

1991 ◽  
Vol 70 (1) ◽  
pp. 210-215 ◽  
Author(s):  
M. DeLissio ◽  
L. J. Goodyear ◽  
S. Fuller ◽  
E. L. Krawitt ◽  
J. T. Devlin
Keyword(s):  
Hepatic Cirrhosis ◽  
Treadmill Exercise ◽  
Energy Requirement ◽  
Plasma Concentrations ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Whole Body ◽  
Maximal Aerobic Capacity ◽  
Control Subjects ◽  
Fuel Metabolism

We studied whole body and regional fuel metabolism before, during, and after 90 min of treadmill exercise at 50% of maximal aerobic capacity (VO2max) in four subjects with hepatic cirrhosis and in four normal volunteers. Rates of endogenous glucose production (EGP) were measured using D-[6–3H]glucose infusions and fuel oxidation using indirect calorimetry. In the basal state, cirrhotic subjects had similar rates of EGP compared with controls. Forearm release of alanine and lactate was significantly greater in cirrhotic subjects (P less than 0.05), suggesting increased basal rates of gluconeogenesis. During exercise, EGP increased 2- to 2.5-fold in control subjects (P less than 0.01) but did not increase in cirrhotic subjects. Despite lower glucose concentrations in cirrhotic subjects, progressive hypoglycemia did not occur during exercise, probably because cirrhotic subjects demonstrated increased plasma concentrations of fat-derived substrates and derived a greater percentage of total energy requirement from fat oxidation than did controls (P less than 0.05) and because forearm muscle glucose extraction was significantly lower in cirrhotic subjects compared with controls (0.5 vs. 3.6%, respectively; P less than 0.05). During recovery, control subjects demonstrated significant increases in EGP rates compared with both the basal and exercise periods, but cirrhotic subjects showed no increase. In conclusion, cirrhotic subjects failed to demonstrate the normal increase in EGP during and after exercise. Significant hypoglycemia during exercise did not occur, possibly because of the increased availability of fat-derived fuels, which may spare the requirement for circulating glucose as an oxidative fuel for exercising muscle tissues.

Effect of adipocyte β3-adrenergic receptor activation on the type 2 diabetic MKR mice

2006 ◽  
Vol 290 (6) ◽  
pp. E1227-E1236 ◽  
Author(s):  
Hyunsook Kim ◽  
Patricia A. Pennisi ◽  
Oksana Gavrilova ◽  
Stephanie Pack ◽  
William Jou ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Receptor Activation ◽  
Whole Body ◽  
Acid Oxidation ◽  
Adrenergic Agonists ◽  
Nonobese Diabetic ◽  
Type 2 Diabetic

The antiobesity and antidiabetic effects of the β3-adrenergic agonists were investigated on nonobese type 2 diabetic MKR mice after injection with a β3-adrenergic agonist, CL-316243. An intact response to acute CL-316243 treatment was observed in MKR mice. Chronic intraperitoneal CL-316243 treatment of MKR mice reduced blood glucose and serum insulin levels. Hyperinsulinemic euglycemic clamps exhibited improvement of the whole body insulin sensitivity and glucose homeostasis concurrently with enhanced insulin action in liver and adipose tissue. Treating MKR mice with CL-316243 significantly lowered serum and hepatic lipid levels, in part due to increased whole body triglyceride clearance and fatty acid oxidation in adipocytes. A significant reduction in total body fat content and epididymal fat weight was observed along with enhanced metabolic rate in both wild-type and MKR mice after treatment. These data demonstrate that β3-adrenergic activation improves the diabetic state of nonobese diabetic MKR mice by potentiation of free fatty acid oxidation by adipose tissue, suggesting a potential therapeutic role for β3-adrenergic agonists in nonobese diabetic subjects.

Fatty acid kinetic responses to running above or below lactate threshold

1995 ◽  
Vol 79 (2) ◽  
pp. 439-447 ◽  
Author(s):  
J. A. Kanaley ◽  
C. D. Mottram ◽  
P. D. Scanlon ◽  
M. D. Jensen
Keyword(s):  
Fatty Acid ◽  
Endurance Training ◽  
Fatty Acid Oxidation ◽  
Indirect Calorimetry ◽  
Lactate Threshold ◽  
Exercise Group ◽  
Acid Oxidation ◽  
Running Exercise ◽  
Marathon Training ◽  
Energy Demands

During running exercise above the lactate threshold (LT), it is unknown whether free fatty acid (FFA) mobilization can meet the energy demands for fatty acid oxidation. This study was performed to determine whether FFA availability is reduced during running exercise above compared with below the LT and to assess whether the level of endurance training influences FFA mobilization. Twelve marathon runners and 12 moderately trained runners ran at a workload that was either above or below their individual LT. Fatty acid oxidation (indirect calorimetry) and FFA release ([1–14C]palmitate) were measured at baseline, throughout exercise, and at recovery. The plasma FFA rate of appearance increased during exercise in both groups; running above or below the LT, but the total FFA availability for 30 min of exercise was greater (P < 0.01) in the below LT group (marathon, 23 +/- 2 mmol; moderate, 21 +/- 2 mmol) than in the above LT group (18 +/- 3 and 13 +/- 3 mmol, respectively). Total fatty acid oxidation (indirect calorimetry) greatly exceeded circulating FFA availability, regardless of training or exercise group (P < 0.01). No statistically significant exercise intensity or training differences in fatty acid oxidation were found (above LT: marathon, 71 +/- 12, moderate, 64 +/- 17 mmol/30 min; below LT: marathon 91 +/- 12, moderate, 60 +/- 5 mmol/30 min). In conclusion, during exercise above or below LT, circulating FFA cannot meet the oxidative needs and intramuscular triglyceride stores must be utilized. Further marathon training does not enhance effective adipose tissue lipolysis during exercise compared with moderate endurance training.

Sign in / Sign up

Export Citation Format

Share Document