Gastrointestinal digestion of dietary advanced glycation endproducts using an<i>in vitro</i>model of the gastrointestinal tract (TIM-1)

Lugt, Timme van der; Venema, Koen; Leeuwen, S.P.J. van; Vrolijk, Misha F.; Opperhuizen, Antoon; Bast, Aalt

doi:10.1039/d0fo00450b

Cited by 37 publications

(18 citation statements)

References 43 publications

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“…Advanced glycation end-products (AGEs) and their receptors may play important roles in the development and progression of CHD [68]. Recent biochemical [69][70][71][72] and other findings [73] are consistent with the possibility that AGEs form in the gut. Notably, n-carboxymethyl lysine (CML)-a well studied AGEformed under conditions consistent with the intestines, well within the time window of digestion, but not with glucose [69][70][71].…”

Section: Discussionmentioning

confidence: 68%

High fructose corn syrup, excess-free-fructose, and risk of coronary heart disease among African Americans– the Jackson Heart Study

2020

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Background Researchers have sought to explain the black-white coronary heart disease (CHD) mortality disparity that increased from near parity to ~ 30% between 1980 and 2010. Contributing factors include cardiovascular disease prevention and treatment disparities attributable to disparities in insurance coverage. Recent research suggests that dietary/environmental factors may be contributors to the disparity. Unabsorbed/luminal fructose alters gut bacterial load, composition and diversity. There is evidence that such microbiome disruptions promote hypertension and atherosclerosis. The heart-gut axis may, in part, explain the black-white CHD disparity, as fructose malabsorption prevalence is higher among African Americans. Between 1980 and 2010, consumption of excess-free-fructose–the fructose type that triggers malabsorption-exceeded dosages associated with fructose malabsorption (~ 5 g–10 g), as extrapolated from food availability data before subjective, retroactively-applied loss adjustments. This occurred due to an industrial preference shift from sucrose to high-fructose-corn-syrup (HFCS) that began ~ 1980. During this period, HFCS became the main sweetener in US soda. Importantly, there has been more fructose in HFCS than thought, as the fructose-to-glucose ratio in popular sodas (1.9-to-1 and 1.5-to-1) has exceeded generally-recognized-as-safe levels (1.2-to-1). Most natural foods contain a ~ 1-to-1 ratio. In one recent study, ≥5 times/wk. consumers of HFCS sweetened soda/fruit drinks/and apple juice-high excess-free-fructose beverages–were more likely to have CHD, than seldom/never consumers. Methods Jackson-Heart-Study data of African Americans was used to test the hypothesis that regular relative to low/infrequent intake of HFCS sweetened soda/fruit drinks increases CHD risk, but not orange juice-a low excess-free-fructose juice. Cox proportional hazards models were used to calculate hazard ratios using prospective data of 3407–3621 participants, aged 21–93 y (mean 55 y). Results African Americans who consumed HFCS sweetend soda 5-6x/wk. or any combination of HFCS sweetened soda and/or fruit drinks ≥3 times/day had ~ 2 (HR 2.08, 95% CI 1.03–4.20, P = 0.041) and 2.5–3 times higher CHD risk (HR 2.98, 95% CI 1.15–7.76; P = 0.025), respectively, than never/seldom consumers, independent of confounders. There were no associations with diet-soda or 100% orange-juice, which has a similar glycemic profile as HFCS sweetened soda, but contains a ~ 1:1 fructose-to-glucose ratio. Conclusion The ubiquitous presence of HFCS in the food supply may pre-dispose African Americans to increased CHD risk.

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Section: Discussionmentioning

confidence: 68%

High fructose corn syrup, excess-free-fructose, and risk of coronary heart disease among African Americans– the Jackson Heart Study

2020

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“…Additionally, an increase of almost 200% free form MG-H1 in the digests of apple juice. This formation was both dependent on the type of food products and thermal treatment, as the unheated glucose-lactose-casein meal system did not lead to any intestinal AGE formation [25]. Other studies have also shown intestinal AGE formation: Simulated digestion of ovalbumine with fructose alone produced compounds with a fluorescence spectrum that is characteristic for AGEs [48].…”

Section: Formation Of Ages In the Gi Tractmentioning

confidence: 86%

“…The data showed that new AGEs are being formed in the intestine and not necessarily released from their structures. In addition, AGEs were only formed endogenously after digestion of products that also contained AGEs, which might indicate an underlying need for the presence of dAGE precursors in food, such as glyoxal and methylglyoxal [25]. To our knowledge, no studies have focused on the role of dAGE precursors on AGE formation in the GI tract and this might be an interesting topic for future research.…”

Section: Formation Of Ages In the Gi Tractmentioning

confidence: 99%

“…Unfortunately, the static in vitro models as used by the above discussed studies do not take such physiological parameters into account. Since these studies all used static in vitro models, we conducted a recent study using a sophisticated in vitro GI model to assess the digestion of dAGEs and their protein binding [25]. The TNO gastroIntestinal Model-1 (TIM-1) is a dynamic in vitro model which mimics the upper human GI tract.…”

Section: Digestion Of Agesmentioning

confidence: 99%

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Dietary Advanced Glycation Endproducts and the Gastrointestinal Tract

et al. 2020

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The prevalence of inflammatory bowel diseases (IBD) is increasing in the world. The introduction of the Western diet has been suggested as a potential explanation of increased prevalence. The Western diet includes highly processed food products, and often include thermal treatment. During thermal treatment, the Maillard reaction can occur, leading to the formation of dietary advanced glycation endproducts (dAGEs). In this review, different biological effects of dAGEs are discussed, including their digestion, absorption, formation, and degradation in the gastrointestinal tract, with an emphasis on their pro-inflammatory effects. In addition, potential mechanisms in the inflammatory effects of dAGEs are discussed. This review also specifically elaborates on the involvement of the effects of dAGEs in IBD and focuses on evidence regarding the involvement of dAGEs in the symptoms of IBD. Finally, knowledge gaps that still need to be filled are identified.

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“…1,2 Since the protein binding appeared essential for this pro-inflammatory effect, it was investigated whether dAGEs were stable during digestion in the human intestinal tract by using the TNO GastroIntestinal Model (TIM-1). 3 The results of that study revealed an intact protein/peptide binding of the dAGEs during digestion. The question remains if these digested dAGEs can still have pro-inflammatory effects on macrophagelike cells.…”

Section: Introductionmentioning

confidence: 81%

Gastrointestinal digestion of dietary advanced glycation endproducts increases their pro-inflammatory potential

et al. 2021

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Gastrointestinal digestion of dietary advanced glycation endproducts using anin vitromodel of the gastrointestinal tract (TIM-1)

Abstract: In a sophisticated gastrointestinal model, dietary advanced glycation endproducts (dAGEs) in food products remain bound to proteins after digestion and concentrations increase.

Cited by 37 publications

References 43 publications

High fructose corn syrup, excess-free-fructose, and risk of coronary heart disease among African Americans– the Jackson Heart Study

High fructose corn syrup, excess-free-fructose, and risk of coronary heart disease among African Americans– the Jackson Heart Study

Dietary Advanced Glycation Endproducts and the Gastrointestinal Tract

Gastrointestinal digestion of dietary advanced glycation endproducts increases their pro-inflammatory potential

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