scholarly journals Glycemic index of a meal fed before exercise alters substrate use and glucose flux in exercising horses

2002 ◽  
Vol 92 (1) ◽  
pp. 117-128 ◽  
Author(s):  
Eduard Jose-Cunilleras ◽  
Kenneth W. Hinchcliff ◽  
Richard A. Sams ◽  
Steven T. Devor ◽  
Jon K. Linderman
Keyword(s):  
Fatty Acid ◽  
Lipid Oxidation ◽  
Plasma Glucose ◽  
Serum Insulin ◽  
Carbohydrate Oxidation ◽  
Nonesterified Fatty Acid ◽  
Soluble Carbohydrate ◽  
Lower Plasma Glucose ◽  
Rate Of Oxygen Consumption ◽  
Serum Glycerol

In a randomized, balanced, crossover study each of six fit, adult horses ran on a treadmill at 50% of maximal rate of oxygen consumption for 60 min after being denied access to food for 18 h and then 1) fed corn (51.4 kJ/kg digestible energy), or 2) fed an isocaloric amount of alfalfa 2–3 h before exercise, or 3) not fed before exercise. Feeding corn, compared with fasting, resulted in higher plasma glucose and serum insulin and lower serum nonesterified fatty acid concentrations before exercise ( P < 0.05) and in lower plasma glucose, serum glycerol, and serum nonesterified fatty acid concentrations and higher skeletal muscle utilization of blood-borne glucose during exercise ( P < 0.05). Feeding corn, compared with feeding alfalfa, resulted in higher carbohydrate oxidation and lower lipid oxidation during exercise ( P < 0.05). Feeding a soluble carbohydrate-rich meal (corn) to horses before exercise results in increased muscle utilization of blood-borne glucose and carbohydrate oxidation and in decreased lipid oxidation compared with a meal of insoluble carbohydrate (alfalfa) or not feeding. Carbohydrate feedings did not produce a sparing of muscle glycogen compared with fasting.

Plasma leptin responses to fasting in Pima Indians.

1997 ◽  
Vol 273 (3) ◽  
pp. E644 ◽  
Author(s):  
R E Pratley ◽  
M Nicolson ◽  
C Bogardus ◽  
E Ravussin
Keyword(s):  
Fatty Acid ◽  
Energy Balance ◽  
Metabolic Rate ◽  
Plasma Glucose ◽  
Test Meal ◽  
Nonesterified Fatty Acid ◽  
Pima Indians ◽  
Short Term ◽  
Nonesterified Fatty Acids ◽  
Plasma Leptin

Leptin is believed to play a role in the regulation of energy balance, but little is known about factors influencing plasma leptin concentrations. To determine the effect of short-term changes in energy balance, we measured plasma leptin concentrations as well as plasma glucose, insulin, triglyceride, nonesterified fatty acid concentrations, and metabolic rate in response to a standard test meal followed by a 24-h fast in 21 healthy Pima Indians. Plasma leptin concentrations decreased by 8% (P < 0.05) 2-4 h after the test meal. They returned to baseline 6-12 h after the subjects ate, then subsequently decreased, and, by the end of the fast, were an average of 37% below baseline (P < 0.0001). Changes in plasma leptin concentrations did not correlate with changes in plasma glucose, insulin, triglyceride, or nonesterified fatty acid concentrations or with changes in metabolic rate. The results of this study indicate that plasma leptin concentrations decrease in response to short-term energy restriction. These changes were not due to changes in glucose, insulin, triglycerides, or nonesterified fatty acids, nor did they relate to changes in metabolic rate. The decrease in plasma leptin concentrations with fasting may be an important homeostatic response to an energy deficit, stimulating food intake and thus restoring energy balance.

Mechanism, temporal patterns, and magnitudes of the metabolic responses to the KATP channel agonist diazoxide

2005 ◽  
Vol 288 (1) ◽  
pp. E80-E85 ◽  
Author(s):  
Bharathi Raju ◽  
Philip E. Cryer
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Fatty Acid ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Temporal Patterns ◽  
Metabolic Responses ◽  
Nonesterified Fatty Acid ◽  
Nonesterified Fatty Acids ◽  
C Peptide

To assess the mechanism, temporal patterns, and magnitudes of the metabolic responses to the ATP-dependent potassium channel agonist diazoxide, neuroendocrine and metabolic responses to intravenous diazoxide (saline, 1.0 and 2.0 mg/kg) and oral diazoxide (placebo, 4.0 and 6.0 mg/kg) were assessed in healthy young adults. Intravenous diazoxide produced rapid, but transient, decrements ( P = 0.0023) in plasma insulin (e.g., nadirs of 2.8 ± 0.5 and 1.8 ± 0.3 μU/ml compared with 7.0 ± 1.0 μU/ml after saline at 4.0–7.5 min) and C-peptide ( P = 0.0228) associated with dose-related increments in plasma glucose ( P = 0.0044) and serum nonesterified fatty acids ( P < 0.0001). After oral diazoxide, plasma insulin appeared to decline, as did C-peptide, again associated with dose-related increments in plasma glucose ( P < 0.0001) and serum nonesterified fatty acids ( P = 0.0141). Plasma glucagon, as well as cortisol and growth hormone, was not altered. Plasma epinephrine increased ( P = 0.0215) slightly only after intravenous diazoxide. There were dose-related increments in plasma norepinephrine ( P = 0.0038 and P = 0.0005, respectively), undoubtedly reflecting a compensatory sympathetic neural response to vasodilation produced by diazoxide, but these would not raise plasma glucose or serum nonesterified fatty acid levels. Thus selective suppression of insulin secretion, without stimulation of glucagon secretion, raised plasma glucose and serum nonesterified fatty acid concentrations. These findings define the temporal patterns and magnitudes of the metabolic responses to diazoxide and underscore the primacy of regulated insulin secretion in the physiological regulation of postabsorptive carbohydrate and lipid metabolism.

scholarly journals β-Adrenergic and Atrial Natriuretic Peptide Interactions on Human Cardiovascular and Metabolic Regulation

2006 ◽  
Vol 91 (12) ◽  
pp. 5069-5075 ◽  
Author(s):  
Andreas L. Birkenfeld ◽  
Michael Boschmann ◽  
Cedric Moro ◽  
Frauke Adams ◽  
Karsten Heusser ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Atrial Natriuretic Peptide ◽  
Lipid Oxidation ◽  
Natriuretic Peptide ◽  
Adrenergic Receptor ◽  
Metabolic Regulation ◽  
Venous Blood ◽  
Nonesterified Fatty Acid ◽  
Lipid Mobilization ◽  
Atrial Natriuretic

Abstract Context: Atrial natriuretic peptide (ANP) has well-known cardiovascular effects and modifies lipid and carbohydrate metabolism in humans. Objective: The objective of the study was to determine the metabolic and cardiovascular interaction of β-adrenergic receptors and ANP. Design: This was a crossover study, conducted 2004–2005. Setting: The study was conducted at an academic clinical research center. Patients: Patients included 10 healthy young male subjects (body mass index 24 ± 1 kg/m2). Intervention: We infused iv incremental ANP doses (6.25, 12.5, and 25 ng/kg·min) with and without propranolol (0.20 mg/kg in divided doses followed by 0.033 mg/kg·h infusion). Metabolism was monitored through venous blood sampling, im, and sc microdialysis and indirect calorimetry. Cardiovascular changes were monitored by continuous electrocardiogram and beat-by-beat blood pressure recordings. Main Outcome Measures: Venous nonesterified fatty acid, glycerol, glucose, and insulin; and microdialysate glucose, glycerol, lactate, and pyruvate were measured. Results: ANP increased heart rate dose dependently. β-Adrenergic receptor blockade abolished the response. ANP elicited a dose-dependent increase in serum nonesterified fatty acid and glycerol concentrations. The response was not suppressed with propranolol. Venous glucose and insulin concentrations increased with ANP, both without or with propranolol. ANP induced lipid mobilization in sc adipose tissue. In skeletal muscle, microdialysate lactate increased, whereas the lactate to pyruvate ratio decreased, both with and without propranolol. Higher ANP doses increased lipid oxidation, whereas energy expenditure remained unchanged. Propranolol tended to attenuate the increase in lipid oxidation. Conclusions: Selected cardiovascular ANP effects are at least partly mediated by β-adrenergic receptor stimulation. ANP-induced changes in lipid mobilization and glycolysis are mediated by another mechanism, presumably stimulation of natriuretic peptide receptors, whereas substrate oxidation might be modulated through adrenergic mechanisms.

scholarly journals High-fat Overfeeding Does Not Exacerbate Rapid Changes in Forearm Glucose and Fatty Acid Balance During Immobilization

2019 ◽  
Vol 105 (1) ◽  
pp. 276-289 ◽  
Author(s):  
Marlou L Dirks ◽  
Benjamin T Wall ◽  
Britt Otten ◽  
Ana M Cruz ◽  
Mandy V Dunlop ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
High Fat Diet ◽  
Serum Insulin ◽  
Physiological Adaptation ◽  
Nonesterified Fatty Acid ◽  
Model Assessment ◽  
High Fat ◽  
Cast Immobilization ◽  
Induce Insulin Resistance

Abstract Context Physical inactivity and high-fat overfeeding have been shown to independently induce insulin resistance. Objective Establish the contribution of muscle disuse and lipid availability to the development of inactivity-induced insulin resistance. Design, Setting, Participants, and Interventions 20 healthy males underwent 7 days of forearm cast immobilization combined with a fully controlled eucaloric diet (n = 10, age 23 ± 2 yr, body mass index [BMI] 23.8 ± 1.0 kg·m-2) or a high-fat diet (HFD) providing 50% excess energy from fat (high-fat diet, n = 10, age 23 ± 2 yr, BMI 22.4 ± 0.8 kg·m-2). Main Outcome Measures Prior to casting and following 2 and 7 days of immobilization, forearm glucose uptake (FGU) and nonesterified fatty acid (NEFA) balance were assessed using the arterialized venous–deep venous (AV-V) forearm balance method following ingestion of a mixed macronutrient drink. Results 7 days of HFD increased body weight by 0.9 ± 0.2 kg (P = 0.002), but did not alter fasting, arterialized whole-blood glucose and serum insulin concentrations or the associated homeostatic model assessment of insulin resistance or Matsuda indices. Two and 7 days of forearm immobilization led to a 40 ± 7% and 52 ± 7% decrease in FGU, respectively (P &lt; 0.001), with no difference between day 2 and 7 and no effect of HFD. Forearm NEFA balance tended to increase following 2 and 7 days of immobilization (P = 0.095). Conclusions Forearm immobilization leads to a rapid and substantial decrease in FGU, which is accompanied by an increase in forearm NEFA balance but is not exacerbated by excess dietary fat intake. Altogether, our data suggest that disuse-induced insulin resistance of glucose metabolism occurs as a physiological adaptation in response to the removal of muscle contraction.

scholarly journals Fish-oil supplementation reduces stimulation of plasma glucose fluxes during exercise in untrained males

2003 ◽  
Vol 90 (4) ◽  
pp. 777-786 ◽  
Author(s):  
Jacques Delarue ◽  
Francois Labarthe ◽  
Richard Cohen
Keyword(s):  
Fish Oil ◽  
Lipid Oxidation ◽  
Olive Oil ◽  
Plasma Glucose ◽  
Clearance Rate ◽  
Carbohydrate Oxidation ◽  
Metabolic Clearance ◽  
Metabolic Clearance Rate ◽  
Fish Oil Supplementation ◽  
Stimulation Of

The present study examined the effects of a 3-week fish-oil supplementation (6 g/d) on the rate of plasma glucose disappearance (Rd glucose), hepatic glucose production (HGP), carbohydrate oxidation and lipid oxidation during exercise. Six untrained males (23±1 years; 67·6±2·7kg) performed two 90min cycling exercise sessions at 60% of maximal O2 output separated by 20 d. During the 20 d before the first test, they ingested 6g olive oil/d, then 6g fish oil/d during the 20 d before the second test. Plasma glucose fluxes and lipolysis were traced using 6,6-[2H2]glucose and 1,1,2,3,3-[2H5]glycerol respectively. Substrates oxidation was obtained from indirect calorimetry. At rest HGP and the Rd glucose were similar after olive oil and fish oil (1.83 (se 0·05) v. 1·67 (se 0·11) mg/kg per min). During exercise, fish oil reduced the stimulation of both the Rd glucose (5·06 (se 0·23) v. 6·37 (se 0·12) mg/kg per min; P<0·05) and HGP (4·88 (se 0·24) v. 5·91 (se 0·21) mg/kg per min; P<0·05). Fish oil also reduced glucose metabolic clearance rate (6·93 (se 0·29) v. 8·30 (se 0·57) ml/min). Carbohydrate oxidation tended to be less stimulated by exercise after fish oil than after olive oil (12·09 (se 0·60) v. 13·86 (se 1·11) mg/kg per min; NS). Lipid oxidation tended to be more stimulated by exercise after fish oil (7·34 (se 0·45) v. 6·85 (se 0·17) mg/kg per min; NS). Glycaemia, lactataemia, insulinaemia and glucagonaemia were similarly affected by exercise after fish oil and olive oil. Lipolysis at rest was similar after fish oil and olive oil (2·92 (se 0·42) v. 2·94 (se 0·28) μmol/kg per min) and similarly stimulated by exercise (6·42 (se 0·75) v. 6·77 (se 0·72) μmol/kg per min). It is concluded that fish oil reduced the Rd glucose by 26% by reducing glucose metabolic clearance rate, possibly by facilitating fat oxidation, and reduced HGP by 21%, possibly by a feedback mechanism.

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