Co-ingestion of whey protein hydrolysate with milk minerals rich in calcium potently stimulates glucagon-like peptide-1 secretion: an RCT in healthy adults

Chen, Yung-Chih; Smith, Harry; Hengist, Aaron; Chrzanowski-Smith, Oliver; Mikkelsen, Ulla Ramer; Carroll, Harriet; Betts, James A.; Thompson, Dylan; Saunders, John; Gonzalez, Javier T.

doi:10.1007/s00394-019-02092-4

Cited by 18 publications

(29 citation statements)

References 40 publications

(65 reference statements)

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“…In a series of acute experiments, Chen et al ( 35 ) provided further evidence of a synergy between calcium and protein. In the first study, preloads (matched for calcium content—1000 mg) consisted of 4380 mg calcium citrate, 3745 mg milk minerals high in calcium, and 2050 mg milk minerals high in calcium with 50 g whey protein hydrolysate.…”

Section: Current Status Of Knowledgementioning

confidence: 97%

“…Previously, carbohydrate, fat, and protein ingestion, as well as SCFAs produced by the gut microbiota, have been found to independently stimulate GLP-1 release ( 31–33 ). Emerging evidence suggests that the synergy of protein and calcium could also act as a potent secretagogue of GLP-1 ( 34 , 35 ). In the most recent human study ( 35 ), this synergy produced some of the highest reported concentrations of GLP-1 following physiological ingestion to date.…”

Section: Introductionmentioning

confidence: 99%

“…Emerging evidence suggests that the synergy of protein and calcium could also act as a potent secretagogue of GLP-1 ( 34 , 35 ). In the most recent human study ( 35 ), this synergy produced some of the highest reported concentrations of GLP-1 following physiological ingestion to date. This is particularly interesting given that calcium does not provide energy, and therefore GLP-1 release is relatively greater despite no additional energy provision.…”

Section: Introductionmentioning

confidence: 99%

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Protein- and Calcium-Mediated GLP-1 Secretion: A Narrative Review

Watkins

Koumanov

Gonzalez

2021

Advances in Nutrition

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Glucagon-like peptide 1 (GLP-1) is an incretin hormone produced in the intestine that is secreted in response to nutrient exposure. GLP-1 potentiates glucose-dependent insulin secretion from the pancreatic β cells and promotes satiety. These important actions on glucose metabolism and appetite have led to widespread interest in GLP-1 receptor agonism. Typically, this involves pharmacological GLP-1 mimetics or targeted inhibition of dipeptidyl peptidase-IV, the enzyme responsible for GLP-1 degradation. However, nutritional strategies provide a widely available, cost-effective alternative to pharmacological strategies for enhancing hormone release. Recent advances in nutritional research have implicated the combined ingestion of protein and calcium with enhanced endogenous GLP-1 release, which is likely due to activation of receptors with high affinity and/or sensitivity for amino acids and calcium. Specifically targeting these receptors could enhance gut hormone secretion, thus providing a new therapeutic option. This narrative review provides an overview of the latest research on protein- and calcium-mediated GLP-1 release with an emphasis on human data, and a perspective on potential mechanisms that link potent GLP-1 release to the co-ingestion of protein and calcium. In light of these recent findings, potential future research directions are also presented.

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Section: Current Status Of Knowledgementioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Protein- and Calcium-Mediated GLP-1 Secretion: A Narrative Review

Watkins

Koumanov

Gonzalez

2021

Advances in Nutrition

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“…Nonetheless, lower circulating glucagon-like peptide-1 may be a risk factor for type 2 diabetes (Lastya et al, 2014), thus if our data are showing a causal relationship, it could mean that those with a sweet tooth have lower type 2 diabetes risk, and this speculatively may be further enhanced by consuming a low sugar (non-sweet) breakfast. The magnitude of change was ~1.4 time higher, which is approximately half of what would be expected in the fasted to postprandial state (Chen et al, 2020). Despite the elevated glucagon-like peptide-1 concentration in those with a sweet tooth after PLAIN, insulin did not increase preto post-intervention.…”

Section: Resultsmentioning

confidence: 71%

Effect of plain versus sugar‐sweetened breakfast on energy balance and metabolic health: A secondary data analysis stratified by participant-defined sweet preference

Carroll¹

2020

Preprint

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Background: Variability in sweet preference between people is well established, with those who have a high preference colloquially identified as having a sweet tooth. Although characteristics have been described demonstrating key differences between those with and without a sweet tooth (such as differences in body mass index), it is less clear whether sweet preference moderates appetite and health responses to stimuli of different sweetness levels.Objective: To explore appetite and health responses to a sugar-sweetened (SWEET) and unsweetened (PLAIN) porridge-based breakfast, according to whether participants identified as having a sweet tooth or not. Methods: Secondary data analysis of a previously published randomised crossover trial in which n = 29 participants consumed an isocaloric PLAIN (~8 g sugar) and SWEET (~32 g sugar) porridge-based breakfast for three weeks each. Fasted pre- and post-intervention measures included blood biomarkers of health and appetite hormones, anthropometrics and metabolic rate, and a series of questionnaires assessing psychological appetite/approach to food. During each three week intervention, four days of lifestyle monitoring were conducted on days 1-4 and days 15-18, involving weighed food diaries, physical activity measurements (ActiHeart™), and visual analogue scales of appetite across the day. After study completion, participants were asked whether they believed they had a sweet tooth or not; n = 27 responded and were included in these analyses. Analyses were exploratory with no significance testing or a priori hypothesis. Results: 16 participants reported not having a sweet tooth. Average body mass index was higher in those without a sweet tooth (25.9 ± 6.0 kg/m2 versus 24.4 ± 4.3 kg/m2 for those with a sweet tooth), but waist-to-hip ratio was lower. Having a sweet tooth was associated with a higher desire for sweet across the day during both interventions compared to those without a sweet tooth, but also lower sugar intake. Sweet sensory-specific satiety was achieved in both groups post-breakfast during SWEET, whilst savoury sensory-specific satiety was achieved post-breakfast after both PLAIN and SWEET. Fasting plasma fibroblast growth factor 21 was higher in those with a sweet tooth, whilst fasting glucagon-like peptide-1 increased pre- to post-PLAIN (Δ 6.2, 95 % CI 1.1, 11.4 pmol∙L-1), but was otherwise similar across interventions and between groups. Those without a sweet tooth reduced their energy intake from week 1 to week 3 of PLAIN (Δ -152, 95 % CI -349, 45 kcal/d), whereas those with a sweet tooth (less reliably) increased their energy intake (Δ 131, 95 % CI -131, 395 kcal/d). No changes in energy intake were noted during SWEET. Physical activity energy expenditure largely remained consistent between groups and across interventions, though those without a sweet tooth increased their physical activity energy expenditure from week 1 to week 3 of SWEET (Δ 166, 95 % CI -8, 241 kcal/d).Conclusion: Having a sweet tooth was associated with distinct characteristics, such as lower body mass index and higher fasted plasma fibroblast growth factor 21 concentrations. Sweet preference may moderate biopsychological metabolic and appetitive responses to savoury or sweet primes. Due to the small sample size and other methodological features of these analyses, future work should establish the causality of these findings, and may need to consider sweet preference a priori when designing health and appetite research relating to sweetness.

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“…As direct effects of GLP-1 on peripheral insulin sensitivity are unclear, the mechanism(s) by which GLP-1 may contribute to metabolic control are thought to also include microvascular recruitment and glucose-stimulated insulin secretion (Drucker 2018 ). Whilst enteral feeding pattern does not modulate the decline in peripheral insulin sensitivity during bed rest (Dirks et al 2019a ), other strategies that increase endogenous GLP-1 concentrations, such as enteral delivery mode (Luttikhold et al 2016 ) and/or nutrient composition (Gonzalez et al 2015 ; Gonzalez and Stevenson 2014b ; Chen et al 2019 ), warrant exploring as potential approaches to preserve GLP1 concentrations during bed rest.…”

Section: Discussionmentioning

confidence: 99%

Intermittent versus continuous enteral nutrition attenuates increases in insulin and leptin during short-term bed rest

et al. 2020

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Purpose To compare endocrine responses to intermittent vs continuous enteral nutrition provision during short-term bed rest. Methods Twenty healthy men underwent 7 days of bed rest, during which they were randomized to receive enteral nutrition (47%E as carbohydrate, 34%E as fat, 16%E as protein and 3%E as fibre) in a continuous (CONTINUOUS; n = 10; 24 h day −1 at a constant rate) or intermittent (INTERMITTENT; n = 10; as 4 meals per day separated by 5 h) pattern. Daily plasma samples were taken every morning to assess metabolite/hormone concentrations. Results During bed rest, plasma leptin concentrations were elevated to a lesser extent with INTERMITTENT vs CONTINUOUS (iAUC: 0.42 ± 0.38 vs 0.95 ± 0.48 nmol L −1 , respectively; P = 0.014) as were insulin concentrations (interaction effect, P < 0.001) which reached a peak of 369 ± 225 pmol L −1 in CONTINUOUS, compared to 94 ± 38 pmol L −1 in INTERMITTENT ( P = 0.001). Changes in glucose infusion rate were positively correlated with changes in fasting plasma GLP-1 concentrations ( r = 0.44, P = 0.049). Conclusion Intermittent enteral nutrition attenuates the progressive rise in plasma leptin and insulinemia seen with continuous feeding during bed rest, suggesting that continuous feeding increases insulin requirements to maintain euglycemia. This raises the possibility that hepatic insulin sensitivity is impaired to a greater extent with continuous versus intermittent feeding during bed rest. To attenuate endocrine and metabolic changes with enteral feeding, an intermittent feeding strategy may, therefore, be preferable to continuous provision of nutrition. This trial was registered on clinicaltrials.gov as NCT02521025.

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Co-ingestion of whey protein hydrolysate with milk minerals rich in calcium potently stimulates glucagon-like peptide-1 secretion: an RCT in healthy adults

Cited by 18 publications

References 40 publications

Protein- and Calcium-Mediated GLP-1 Secretion: A Narrative Review

Protein- and Calcium-Mediated GLP-1 Secretion: A Narrative Review

Effect of plain versus sugar‐sweetened breakfast on energy balance and metabolic health: A secondary data analysis stratified by participant-defined sweet preference

Intermittent versus continuous enteral nutrition attenuates increases in insulin and leptin during short-term bed rest

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