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The Effect of Buffering High Acid Load Meal with Sodium Bicarbonate on Postprandial Glucose Metabolism in Humans-A Randomized Placebo-Controlled Study.

ABSTRACT: Background: High dietary acid load relates to increased risk of type 2 diabetes in epidemiological studies. We aimed to investigate whether buffering a high acid load meal with an alkalizing treatment changes glucose metabolism post meal. Methods: Non-diabetic participants (n = 32) were randomized to receive either 1680 mg NaHCO? or placebo, followed by a high acid load meal in a double-blind placebo-controlled crossover (1-4 weeks apart) study. Thirty (20 men) participants completed the study. Venous blood pH, serum bicarbonate, blood glucose, serum insulin, C-peptide, non-esterified fatty acid (NEFA), and plasma glucagon-like peptide-1 (GLP-1) concentrations were measured at baseline (fasting) and at 15-30 min intervals for 3 h post meal. Results: The treatment was well tolerated. Venous blood pH declined in the first 15 min post meal with the placebo (p = 0.001), but not with NaHCO? (p = 0.86) and remained decreased with the placebo for 3 h (pinteraction = 0.04). On average over the 3 h blood pH iAUC was greater with NaHCO? compared with placebo (p = 0.02). However, postprandial glucose, insulin, C-peptide, NEFA and GLP-1 were not different between treatments (pinteraction ? 0.07). Conclusions: An alkalizing medication administered pre-meal has no acute effect on glycaemia and insulin response in healthy individuals. Long-term interventions in at-risk populations are necessary to investigate the effect of sustained alkalization on glucose metabolism.

SUBMITTER: Kozan P

PROVIDER: S-EPMC5579654 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature

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The Effect of Buffering High Acid Load Meal with Sodium Bicarbonate on Postprandial Glucose Metabolism in Humans-A Randomized Placebo-Controlled Study.

Kozan Pinar P Blythe Jackson C JC Greenfield Jerry R JR Samocha-Bonet Dorit D

Nutrients 20170811 8

Background: High dietary acid load relates to increased risk of type 2 diabetes in epidemiological studies. We aimed to investigate whether buffering a high acid load meal with an alkalizing treatment changes glucose metabolism post meal. Methods: Non-diabetic participants (n = 32) were randomized to receive either 1680 mg NaHCO₃ or placebo, followed by a high acid load meal in a double-blind placebo-controlled crossover (1-4 weeks apart) study. Thirty (20 men) participants ...[more]

PMID: 28800090

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Project description:Introduction: Fatty acids are a major nutrient in dietary fat, some of which are ligands of long-chain fatty acid receptors, including G-protein-coupled receptor (GPR) 40 and GPR120. Pretreatment with GPR40 agonists enhanced the secretion of insulin in response to elevating blood glucose levels after glucose load in a diabetes model, but pretreatment with GPR120 agonist did not ameliorate postprandial hyperglycemia. This study examined whether oral administration of linoleic acid (LA), a GPR40 and GPR120 agonist, immediately before glucose load would affect the elevation of postprandial blood glucose levels in rats. Methods: Male rats and rats with type 1 diabetes administered streptozocin were orally administered LA, trilinolein, α-linolenic acid (α-LA), oleic acid, TAK-875, or TUG-891 immediately before glucose load. Blood glucose levels were measured before, then 15, 30, 60 and 120 min after glucose load. CACO-2 cells were used to measure the uptake of [14C] α-MDG for 30 min with or without LA. Gastric content from rats administered LA was collected 15 and 30 min after glucose load, and blood samples were collected for measurement of glucagon-like peptide 1 (GLP-1) and cholecystokinin concentrations. Results: The elevation of postprandial blood glucose levels was slowed by LA but not by trilinolein in rats without promotion of insulin secretion, and this effect was also observed in rats with type 1 diabetes. The uptake of α-MDG, an SGLT-specific substrate, was, however, not inhibited by LA. Gastric emptying was slowed by LA 15 min after glucose load, and GLP-1, but not cholecystokinin, level was elevated by LA 15 min after glucose load. TUG-891, a GPR120 agonist, ameliorated postprandial hyperglycemia but TAK-875, a GPR40 agonist, did not. Pretreatment with AH7614, a GPR120 antagonist, partially canceled the improvement of postprandial hyperglycemia induced by LA. α-LA, which has high affinity with GPR120 as well as LA, slowed the elevation of postprandial blood glucose levels, but oleic acid, which has lower affinity with GPR120 than LA, did not. Conclusion: Oral administration of LA immediately after glucose load ameliorated postprandial hyperglycemia due to slowing of gastric emptying via promotion of GLP-1 secretion. The mechanisms may be associated with GPR120 pathway.

Project description:BackgroundHigh postprandial glucose excursions may increase risk for disease. Individuals have widely varying glucose responses to different meals, and precision nutrition approaches often seek to personalize diets to minimize postprandial glycemic responses as measured by continuous glucose monitors (CGMs). However, it is unknown whether different CGM devices result in concordant meal rankings according to postprandial glycemic excursions.ObjectiveWe explored whether meal rankings according to postprandial glycemic excursions differ between 2 simultaneously worn CGMs.MethodsWe collected 27,489 simultaneous measurements from Dexcom G4 Platinum and Abbott Freestyle Libre Pro CGMs during 28 inpatient days in 16 adults without diabetes. Simultaneous glucose measurements obtained for 2 h following 760 ad libitum meals were used to compare within-subject meal rankings between the CGM devices according to their incremental glucose response.ResultsPostprandial responses to ad libitum meals were highly variable, with the Abbott and Dexcom systems resulting in within-subject incremental mean ± SD glucose CVs of 91.7 ± 1.9% and 94.2 ± 2.7%, respectively. Within-subject meal rankings for incremental glycemic responses were relatively discordant between CGMs, with a mean Kendall rank correlation coefficient of 0.43 ± 0.05. Meals in the bottom compared with those in the top half of incremental glycemic responses ranked by Abbott resulted in 50 ± 10% (P = 0.0002) less glycemic reduction as measured by Dexcom, and vice versa. The missing glycemic reduction by eating meals ranked according to the discordant CGM was inversely correlated with each subject's Kendall rank correlation coefficient (r = -0.95; P < 0.0001).ConclusionsPrecision nutrition approaches that use CGMs to personalize meal recommendations for minimizing glycemic excursions may be premature given the discordance of within-subject meal rankings between simultaneous CGM devices. More research is needed to clarify the source of this imprecision. This trial was registered at clinicaltrials.gov as NCT03407053.

Project description:Background: The potential impact of prior meal composition on the postprandial glycemic response and glycemic index (GI) and glycemic load (GL) value determinations remains unclear.Objective: We determined the effect of meals that varied in macronutrient composition on the glycemic response and determination of GI and GL values of a subsequent standard test food.Design: Twenty healthy participants underwent 6 test sessions within 12 wk. The subjects received each of 3 isocaloric breakfast meals (i.e., high carbohydrate, high fat, or high protein) on separate days in a random order, which was followed by a standard set of challenges (i.e., white bread and a glucose drink) that were tested on separate days in a random order 4 h thereafter. Each challenge provided 50 g available carbohydrate. Arterialized venous blood was sampled throughout the 2-h postchallenge period. GI, GL, and insulin index (II) values were calculated with the use of the incremental area under the curve (AUCi) method, and serum lipids were determined with the use of standard assays.Results: The consumption of the high-protein breakfast before the white-bread challenge attenuated the rise in the postprandial serum glucose response (P < 0.0001) and resulted in lower glucose AUCi (P < 0.0001), GI (P = 0.0096), and GL (P = 0.0101) values than did the high-carbohydrate and high-fat breakfasts. The high-protein breakfast resulted in a lower insulin AUCi (P = 0.0146) for white bread than did the high-fat breakfast and a lower II value (P = 0.0285) than did the high-carbohydrate breakfast. The 3 breakfasts resulted in similar serum lipid responses to the white-bread challenge.Conclusions: These data indicate that the macronutrient composition of the prior meal influences the glycemic response and the determination of GI and GL values for white bread. Future studies are needed to determine whether the background food macronutrient composition influences mean dietary GI and GL values that are calculated for eating patterns, which may alter the interpretation of the associations between these values and chronic disease risk. This trial was registered at clinicaltrials.gov as NCT01023646.

Project description:Background: The potential confounding effect of different amounts and proportions of macronutrients across eating patterns on meal or dietary glycemic index (GI) and glycemic load (GL) value determinations has remained partially unaddressed.Objective: The study aimed to determine the effects of different amounts of macronutrients and fiber on measured meal GI and GL values.Design: Four studies were conducted during which participants [n = 20-22; women: 50%; age: 50-80 y; body mass index (in kg/m2): 25-30)] received food challenges containing different amounts of the variable nutrient in a random order. Added to the standard 50 g available carbohydrate from white bread was 12.5, 25, or 50 g carbohydrate; 12.5, 25, or 50 g protein; and 5.6, 11.1, or 22.2 g fat from rice cereal, tuna, and unsalted butter, respectively, and 4.8 or 9.6 g fiber from oat cereal. Arterialized venous blood was sampled for 2 h, and measured meal GI and GL and insulin index (II) values were calculated by using the incremental area under the curve (AUCi) method.Results: Adding carbohydrate to the standard white-bread challenge increased glucose AUCi (P < 0.0001), measured meal GI (P = 0.0066), and mean GL (P < 0.0001). Adding protein (50 g only) decreased glucose AUCi (P = 0.0026), measured meal GI (P = 0.0139), and meal GL (P = 0.0140). Adding fat or fiber had no significant effect on these variables. Adding carbohydrate (50 g), protein (50 g), and fat (11.1 g) increased the insulin AUCi or II; fiber had no effect.Conclusions: These data indicate that uncertainty in the determination of meal GI and GL values is introduced when carbohydrate-containing foods are consumed concurrently with protein (equal amount of carbohydrate challenge) but not with carbohydrate-, fat-, or fiber-containing foods. Future studies are needed to evaluate whether this uncertainty also influences the prediction of average dietary GI and GL values for eating patterns. This trial was registered at clinicaltrials.gov as NCT01023646.

Dataset Information

The Effect of Buffering High Acid Load Meal with Sodium Bicarbonate on Postprandial Glucose Metabolism in Humans-A Randomized Placebo-Controlled Study.

Publications

The Effect of Buffering High Acid Load Meal with Sodium Bicarbonate on Postprandial Glucose Metabolism in Humans-A Randomized Placebo-Controlled Study.

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