Effects of fish oil on metabolic responses to oral fructose and glucose loads in healthy humans

1996 ◽  
Vol 270 (2) ◽  
pp. E353-E362 ◽  
Author(s):  
J. Delarue ◽  
C. Couet ◽  
R. Cohen ◽  
J. F. Brechot ◽  
J. M. Antoine ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fish Oil ◽  
Plasma Glucose ◽  
Specific Effect ◽  
Substrate Oxidation ◽  
Metabolic Responses ◽  
Glucose Disposal ◽  
Glucose Load ◽  
C Peptide ◽  
Healthy Humans

This study examines the effect of the substitution of 6 g/day of fish oil in a saturated diet on glucose and fructose metabolism in healthy humans. Five subjects were submitted to two 3-wk controlled-diet periods (polyunsaturated/saturated = 0.21). During one period, 6 g/day of fat used for dressing were replaced by 6 g/day of fish oil [1.1 g/day of 20:5 (n-3) fatty acids and 0.7 g/day of 22:6 (n-3) fatty acids]. At the end of each period the subjects ingested a 1 g/kg fructose or glucose load 2 days apart. Plasma glucose fluxes were traced with the use of deuterated glucose and [U-13C]glucose. Substrate oxidation was measured by indirect calorimetry. Fish oil induced a 4% increase in basal and postload glycemia and a 40% decrease in insulinemia, whereas plasma C-peptide remained unaffected. Glucose fluxes were unaffected by fish oil, but carbohydrate (CHO) oxidation was reduced (fructose: 55.5 +/- 4.1 vs. 62.9 +/- 3.6 g/6 h; glucose: 36.7 +/- 4.7 vs. 50.5 +/- 4.7 g/6 h; all P < 0.05). Lipid oxidation was increased 35% by fish oil after both CHO loads. Nonoxidative glucose disposal was increased by fish oil (fructose: 9.4 +/- 2.5 vs. 2.9 +/- 1.1 g/6 h; glucose: 28.3 +/- 5.1 vs. 14.4 +/- 4.7 g/6 h; all P < 0.05). Fish oil could affect glucose transport and decrease CHO oxidation through the decrease in insulinemia and/or a specific effect on glycolytic pathway.

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 Interaction of fish oil and a glucocorticoid on metabolic responses to an oral glucose load in healthy human subjects

2006 ◽  
Vol 95 (2) ◽  
pp. 267-272 ◽  
Author(s):  
Jacques Delarue ◽  
Chang-Hong Li ◽  
Richard Cohen ◽  
Charlotte Corporeau ◽  
Brigitte Simon
Keyword(s):  
Fish Oil ◽  
Plasma Glucose ◽  
Insulin Response ◽  
Substrate Oxidation ◽  
Oral Glucose ◽  
Oral Glucose Load ◽  
Glucose Load ◽  
Healthy Human ◽  
Chain Pufa ◽  
Long Chain

Compared with saturated fat, n-3 long-chain PUFA-rich fish oil improves insulin sensitivity in rats. We studied whether n-3 long-chain PUFA could prevent insulin resistance induced by dexamethasone (a glucocorticoid) in healthy human volunteers. A group of eight subjects was studied twice after a 2d dexamethasone treatment, before and after a 3-week supplementation with fish oil (providing daily doses of 1·1g 20:5n-3 and 0·7g 22:6n-3). The subjects were studied during the basal state and over the 6h following an oral glucose load (1g/kg). Plasma glucose fluxes were traced with [6,6-2H2]glucose and [13C]glucose (naturally 13C-enriched corn glucose). Substrate oxidation was obtained from indirect calorimetry. Following fish oil supplementation, plasma glucose fluxes and substrate oxidation were maintained despite a 17% reduction (P<0·05) in the area under the curve of plasma insulin response, suggesting an insulin-sensitizing effect.

Strategies for Hydration and Energy Provision during Soccer-Specific Exercise

2005 ◽  
Vol 15 (6) ◽  
pp. 625-640 ◽  
Author(s):  
N.D. Clarke ◽  
B. Drust ◽  
D.P.M. MacLaren ◽  
T. Reilly
Keyword(s):  
Fatty Acids ◽  
Plasma Glucose ◽  
Exercise Performance ◽  
Soccer Players ◽  
Metabolic Responses ◽  
Specific Exercise ◽  
Sports Drink ◽  
Specific Protocol ◽  
And Performance ◽  
Experimental Trials

The aim of the present study was to investigate the effect of manipulating the provision of sports drink during soccer-specific exercise on metabolism and performance. Soccer players (N = 12) performed a soccer-specific protocol on three occasions. On two, 7 mL/kg carbohydrate-electrolyte (CHOv) or placebo (PLA) solutions were ingested at 0 and 45 min. On a third, the same total volume of carbohydrate-electrolyte was consumed (CHOf) in smaller volumes at 0, 15, 30, 45, 60, and 75 min. Plasma glucose, glycerol, non-esterified free fatty acids (NEFA), cortisol, and CHO oxidation were not significantly different between CHOv and CHOf (P > 0.05). Sprint power was not significantly affected (P > 0.05) by the experimental trials. This study demonstrates when the total volume of carbohydrate consumed is equal, manipulating the timing and volume of ingestion elicits similar metabolic responses without affecting exercise performance.

Metabolic responses to intraduodenal glucose loading in insulin-infused diabetic dogs

1983 ◽  
Vol 245 (2) ◽  
pp. E200-E208
Author(s):  
R. W. Stevenson ◽  
H. Orskov ◽  
J. A. Parsons ◽  
K. G. Alberti
Keyword(s):  
Plasma Glucose ◽  
Insulin Infusion ◽  
Metabolic Responses ◽  
Immunoreactive Insulin ◽  
Glucose Load ◽  
Nonesterified Fatty Acids ◽  
Glucose Loading ◽  
Glucose Profiles ◽  
Diabetic Dogs ◽  
Intraportal Infusion

The hormonal and metabolic responses to an intraduodenal glucose load (0.5 g/kg) were first determined in eight normal dogs before diabetes (alloxan/streptozotocin) was induced and then comparison made of the responses to the glucose load when normal plasma glucose profiles were recreated by preprogrammed infusion of insulin via the portal or peripheral circulations. Basal intraportal and peripheral insulin infusions at 0.021 +/- 0.001 and 0.022 +/- 0.000 U . kg-1 . h-1, respectively, for 16 h to fasting diabetic dogs normalized peripheral plasma levels of glucose (5.5 +/- 0.3 and 5.6 +/- 0.6 mmol/liter, respectively), immunoreactive insulin (IRI) (11.5 +/- 1.2 and 16.4 +/- 1.6 microU/ml), glucagon (65 +/- 7 and 62 +/- 5 pg/ml), lactate (0.63 +/- 0.04 and 0.54 +/- 0.03 mmol/liter), and alanine (0.236 +/- 0.037 and 0.191 +/- 0.008 mmol/liter). However, peripheral but not intraportal infusion of insulin depressed levels of glycerol, nonesterified fatty acids (NEFA), and 3-hydroxybutyrate (0.074 +/- 0.006 vs. 0.109 +/- 0.013, P less than 0.01; 0.67 +/- 0.04 vs. 0.84 +/- 0.09, P less than 0.05; and 0.018 +/- 0.004 vs. 0.059 +/- 0.015 mmol/liter, P less than 0.01, respectively). With the preprogrammed insulin infusions used to normalize plasma glucose profiles to the intraduodenal glucose load, all hormonal and metabolic responses were normalized during intraportal infusion (IRI, 72.5 +/- 4.2 microU/ml; glucagon, 66 +/- 10 pg/ml; lactate, 1.06 +/- 0.10 mmol/liter; alanine, 0.251 +/- 0.042 mmol/liter; glycerol, 0.043 +/- 0.013 mmol/liter; NEFA, 0.24 +/- 0.03 mmol/liter; and 3-hydroxybutyrate, 0.012 +/- 0.007 mmol/liter) but marked hyperinsulinemia (103.2 +/- 6.1 microU/ml) and depressed glycerol, NEFA, and 3-hydroxybutyrate responses at 2 h (0.056 +/- 0.005, 0.52 +/- 0.10, and 0.019 +/- 0.010 mmol/liter, respectively) resulted during peripheral infusion. Therefore, only the portal route of insulin infusion achieved complete metabolic normalization during glucose loading in diabetic dogs.

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.

THE EFFECT OF RITODRINE ON CARBOHYDRATE AND LIPID METABOLISM IN NORMAL AND DIABETIC PREGNANT WOMEN

1979 ◽  
Vol 92 (4) ◽  
pp. 669-679 ◽  
Author(s):  
Suzan Lenz ◽  
Claus Kühl ◽  
Palle Wang ◽  
Lars Mølsted-Pedersen ◽  
Hans Orskov ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Pregnant Women ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Metabolic Effects ◽  
Plasma Sodium ◽  
C Peptide ◽  
Class A ◽  
Class B

ABSTRACT The metabolic effects of a one hour intravenous infusion of the β-2-receptor stimulating drug ritodrine were studied in seven normal pregnant women, three White class A pregnant diabetics and eight White class B-D pregnant diabetics. During ritodrine infusion all subjects in the three groups exhibited increases in plasma glucose (1.0, 1.6 and 2.1 mmol/l respectively), free fatty acids (360, 850 and 1150 μmol/l), lactate (0.43, 0.80 and 0.86 mmol/l) and β-hydroxybutyrate and decreases in standard bicarbonate. The rise in plasma glucose, free fatty acids and lactate was more pronounced in insulin treated diabetic. The rises in β-hydroxybutyrate and decreases in standard bicarbonate were of the same magnitude in all three groups. Plasma potassium fell in all subjects, whereas no detectable changes in plasma sodium were observed. The endocrine pancreatic function was assessed by measuring plasma insulin (White class A and normals), C-peptide (White class B-D) and glucagon (all subjects). Plasma insulin increased in normals (22 μIU/ml) and White class A diabetics (33 μIU/ml), whereas plasma C-peptide of the insulin treated patients (White class B-D) were below measurable concentrations. Plasma glucagon and cortisol concentrations were not influenced by ritodrine. The results suggest that the diabetogenic changes induced by ritodrine are augmented with the severity of diabetes but not ascribable to a diabetes-like change in the function of the endocrine pancreas.

scholarly journals Fish oil attenuates adrenergic overactivity without altering glucose metabolism during an oral glucose load in haemodialysis patients

2008 ◽  
Vol 99 (5) ◽  
pp. 1041-1047 ◽  
Author(s):  
Jacques Delarue ◽  
Marie-Paule Guillodo ◽  
Sophie Guillerm ◽  
Anthony Elbaz ◽  
Yanic Marty ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Fish Oil ◽  
Plasma Catecholamines ◽  
Substrate Oxidation ◽  
Whole Body ◽  
Plasma Norepinephrine ◽  
Oral Glucose ◽  
Glucose Load ◽  
Sensitizing Effect ◽  
Fish Oil Supplementation

Haemodialysis patients display an increased cardiac mortality, which may be partly related to increased sympathoadrenal activity and insulin resistance. Fish oil decreases adrenal activation induced by mental stress and has an insulin sensitizing effect in healthy subjects. Whole-body glucose metabolism after oral glucose was studied in eight haemodialysis patients before and after a 3-week oral fish oil supplementation (i.e. EPA + DHA at 1·8 g/d). Plasma glucose fluxes were traced by using [6,6-2H2]glucose infusion. Substrate oxidation was determined by using indirect calorimetry. Each patient was studied in the basal state and over the 6 h following absorption of a 1 g/kg glucose load. Energy expenditure in response to glucose re-increased over the last 2 h of the experiment (P < 0·05), which coincided with an increase in plasma catecholamines, especially epinephrine (P < 0·05), strongly suggesting a sympathoadrenal overactivity. Fish oil supplementation blunted both re-increase in thermogenic response and concomitant increase in plasma epinephrine, but not in plasma norepinephrine, over the last 2 h of the experiment. Fish oil did not alter either whole-body glucose metabolism or substrate oxidation. These data show that in haemodialysis patients, fish oil attenuates adrenal overactivity induced by oral glucose but does not modulate whole-body glucose metabolism and insulin sensitivity.

scholarly journals Plant- and Animal-Derived Omega-3 Polyunsaturated Fatty Acids Improve Glucose and Lipid Metabolism in Patients with Type 2 Diabetes and Dyslipidemia

2020 ◽  
Author(s):  
Hechun Liu ◽  
Feng Wang ◽  
Ying Li ◽  
Hui Xia ◽  
Da Pan ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Blood Glucose ◽  
Polyunsaturated Fatty Acids ◽  
Fish Oil ◽  
Density Lipoprotein ◽  
Omega 3 ◽  
Lipoprotein Subfractions ◽  
C Peptide ◽  
Hdl Subfractions

Objectives To determine the effects of omega-3 polyunsaturated fatty acids (&omega;-3 PUFA) from animal and plant sources on glucolipid metabolism and lipoprotein subfractions in type 2 diabetic patients with dyslipidemia. Methods Participants were recruited from the diabetes clinic at the Guanlin Hospital, Yixing City in Jiangsu province, China, from March 2017 through June 2017. Ninety participants were randomly assigned to take 3g/day fish oil (FO, containing EPA and DHA), 3g/day perilla oil (PO, containing ALA), or 3g/day blend oil containing fish oil and linseed oil (BO, containing EPA, DHA and ALA) for 3 months. The levels of serum glucose, glycated hemoglobin (HbA1c), C-peptide, triglyceride (TG), total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), non-HDL, apolipoprotein A1 (Apo A1), apolipoprotein B (Apo B), lipoprotein a (Lp(a)), and free fatty acids were determined at baseline and after the 3 months. In addition, four fatty acids in serum and red blood cells membranes (RBCm) were analyzed using gas chromatography-mass spectrometry. The Lipoprint System was used to determine the lipoprotein subfractions. Results All 90 participants completed the final 3-month follow-up at the end of the study. After three months of intervention, blood glucose and HbA1c levels in the PO group were significantly lower than those at the baseline (p &lt; 0.05). On the other hand, in the BO group, the HbA1c, non-HDL, Apo A1 and Lp(a) levels were significantly lower, while the C-peptide levels were significantly higher after intervention compared to the baseline (p &lt; 0.05). In the FO group, the HbA1c and TG levels were significantly lower after the intervention compared to the baseline (p &lt; 0.05). In addition, at the end of the study, there was significant increase in the levels of DPA and DHA in serum and RBCm of the FO group (p &lt; 0.05), while in the BO group, there was significant increase in the levels of EPA, DPA and DHA in RBCm (p &lt; 0.05). Finally, the FO group had the highest levels of large HDL subfractions compared to the BO and PO groups, but had the lowest levels of small HDL subfractions among the three groups. Conclusion For patients with diabetes, plant-derived &omega;-3 PUFAs are more effective at controlling blood glucose than animal-derived &omega;-3 PUFAs. However, animal-derived &omega;-3 PUFAs play a critical role in controlling blood lipids. Particularly, fish oil can effectively increase the beneficial large HDL subfractions and reduce the nonbeneficial small HDL subfractions. Both the animal- and plant-derived &omega; - 3 PUFAs have practical value in improving glucose and lipids metabolism in T2DM patients with dyslipidemia.

Effects of hyperglycemia on glucose metabolism before and after oral glucose ingestion in normal men

2006 ◽  
Vol 290 (6) ◽  
pp. E1198-E1204 ◽  
Author(s):  
Vincent Rigalleau ◽  
Marie-Christine Beauvieux ◽  
Jean-Louis Gallis ◽  
Henri Gin ◽  
Phillippe Schneiter ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Plasma Glucose ◽  
Glucose Disposal ◽  
Oral Glucose ◽  
Oral Glucose Load ◽  
Glucose Load ◽  
Glucose Ingestion ◽  
Before And After ◽  
Endogenous Glucose ◽  
Normal Men

The plasma glucose excursion may influence the metabolic responses after oral glucose ingestion. Although previous studies adressed the effects of hyperglycemia in conditions of hyperinsulinemia, it has not been evaluated whether the route of glucose administration (oral vs. intravenous) plays a role. Our aim was to determine the effects of moderately controlled hyperglycemia on glucose metabolism before and after oral glucose ingestion. Eight normal men underwent two oral glucose clamps at 6 and 10 mmol/l plasma glucose. Glucose turnover and cycling rates were measured by infusion of [2H7]glucose. The oral glucose load was labeled by d-[6,6-2H2]glucose to monitor exogenous glucose appearance, and respiratory exchanges were measured by indirect calorimetry. Sixty percent of the oral glucose load appeared in the systemic circulation during both the 6 and 10 mmol/l plasma glucose tests, although less endogenous glucose appeared during the 10 mmol/l tests before glucose ingestion ( P < 0.05). This inhibitory effect of hyperglycemia was not detectable after oral glucose ingestion, although glucose utilization was increased (+28%, P < 0.05) due to increased nonoxidative glucose disposal [10 vs. 6 mmol/l: +20%, not significant (NS) before oral glucose ingestion; +40%, P < 0.05 after oral glucose ingestion]. Glucose cycling rates were increased by hyperglycemia (+13% before oral glucose ingestion, P < 0.001; +31% after oral glucose ingestion, P < 0.05) and oral glucose ingestion during both the 6 (+10%, P < 0.05) and 10 mmol/l (+26%, P < 0.005) tests. A moderate hyperglycemia inhibits endogenous glucose production and contributes to glucose tolerance by enhancing nonoxidative glucose disposal. Hyperglycemia and oral glucose ingestion both stimulate glucose cycling.

The Effect of Encapsulated Soluble Fiber on Carbohydrate Metabolism during Exercise

1999 ◽  
Vol 9 (1) ◽  
pp. 13-23 ◽  
Author(s):  
Allen C. Parcell ◽  
Melinda L. Ray ◽  
Kristine A. Moss ◽  
Timothy M. Ruden ◽  
Rick L. Sharp ◽  
...  
Keyword(s):  
Carbohydrate Metabolism ◽  
Plasma Glucose ◽  
Muscle Glycogen ◽  
Guar Gum ◽  
Metabolic Responses ◽  
Oral Glucose ◽  
Oral Glucose Load ◽  
Glucose Load ◽  
Soluble Fiber ◽  
Glycogen Utilization

Previous investigations have reported that soluble fiber reduces the plasma glucose and insulin changes after an oral glucose load. To improve the payability of a soluble-fiber feeding, this study addressed how a combined, soluble fiber (delivered in capsule form) and a preexercise CHO feeding would affect metabolic responses during exercise. On 3 different days, participants ingested a placebo (CON), 75 g liquid CHO (GLU), or 75 g liquid CHO with 14.5 g encapsulated guar gum (FIB) 45 min before cycling for 60 min at 70% VO2peak. Peak concentrations of plasma glucose and insulin were similar and significantly greater than CON preexercise (p < .05). Similarities in carbohydrate reliance were observed in GLU and FIB. Muscle glycogen use did not differ significantly among trials. These results demonstrate that encapsulated soluble fiber delivered with a liquid CHO feeding does not affect plasma glucose, insulin, or muscle glycogen utilization during exercise.

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