Galactose Ingested with a High-Fat Beverage Increases Postprandial Lipemia Compared with Glucose but Not Fructose Ingestion in Healthy Men

Watkins, Jonathan D.; Simpson, Aaron; Betts, James A.; Thompson, Dylan; Holliday, Adrian; Deighton, Kevin; Gonzalez, Javier T.

doi:10.1093/jn/nxaa105

Cited by 10 publications

(7 citation statements)

References 28 publications

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“…However, whether the same concepts apply to other alternate metabolic substrates such as alcohol or aminoacids, or combination of them, remain largely unexplored. Interestingly, a recent report indicates that ingestion of galactose with a mixed meal causes a similar postprandial increase in blood triglyceride than fructose [71].…”

Section: Role Of Splanchnic Organs In the Metabolism Of Nonubiquitous Substratesmentioning

confidence: 99%

Metabolism of sugars: A window to the regulation of glucose and lipid homeostasis by splanchnic organs

Tappy

2021

Clinical Nutrition

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Background &aims: Dietary sugars are absorbed in the hepatic portal circulation as glucose, fructose, or galactose. The gut and liver are required to process fructose and galactose into glucose, lactate, and fatty acids. A high sugar intake may favor the development of cardio-metabolic diseases by inducing Insulin resistance and increased concentrations of triglyceride-rich lipoproteins. Methods: A narrative review of the literature regarding the metabolic effects of fructose-containing sugars.Results: Sugars' metabolic effects differ from those of starch mainly due to the fructose component of sucrose. Fructose is metabolized in a set of fructolytic cells, which comprise small bowel enterocytes, hepatocytes, and kidney proximal tubule cells. Compared to glucose, fructose is readily metabolized in an insulin-independent way, even in subjects with diabetes mellitus, and produces minor increases in glycemia. It can be efficiently used for energy production, including during exercise. Unlike commonly thought, fructose when ingested in small amounts is mainly metabolized to glucose and organic acids in the gut, and this organ may thus shield the liver from potentially deleterious effects. Conclusions: The metabolic functions of splanchnic organs must be performed with homeostatic constraints to avoid exaggerated blood glucose and lipid concentrations, and thus to prevent cellular damages leading to non-communicable diseases. Excess fructose intake can impair insulin-induced suppression of glucose production, stimulate de novo lipogenesis, and increase intrahepatic and blood triglyceride concentrations. With chronically high fructose intake, enterocyte can switch to lipid synthesis and accumulation of triglyceride, possibly causing an enterocyte dysfunction.

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Section: Role Of Splanchnic Organs In the Metabolism Of Nonubiquitous Substratesmentioning

confidence: 99%

Metabolism of sugars: A window to the regulation of glucose and lipid homeostasis by splanchnic organs

Tappy

2021

Clinical Nutrition

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“…The postprandial circulating lactate concentrations in response to a meal are the net result of changes in the uptake and release of lactate from tissues. Insulin-stimulated glycolysis can increase lactate production in splanchnic and peripheral tissues(36-38), and the inclusion of speci c monosaccharides within a meal, such as fructose and galactose, may further increase lactate concentrations due to their interconversion by the liver and splanchnic bed (30,(39)(40)(41). Accordingly, it might be expected that lactate concentrations display inter-individual variability in response to a xed size meal due to differences in insulin-stimulated peripheral glycolysis and relative availability of lactate precursors.…”

Section: Discussionmentioning

confidence: 99%

Are there interindividual differences in the reactive hypoglycaemia response to breakfast? A replicate crossover trial

Gonzalez,

Lolli,

Veasey

et al. 2024

Preprint

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Background Following consumption of a meal, circulating glucose concentrations can rise and then fall briefly below the basal/fasting concentrations. This phenomenon is known as reactive hypoglycaemia but to date no study explored potential inter-individual differences in response to meal consumption. Objective We conducted a secondary analysis of existing data to examine inter-individual variability of reactive hypoglycaemia in response to breakfast consumption. Methods Using a replicate crossover design, 12 healthy men completed two identical control (continued overnight fasting) and two breakfast (444 kcal) conditions in randomised sequences. Blood glucose and lactate concentrations, serum insulin and non-esterified fatty acid concentrations, whole-body energy expenditure, carbohydrate and fat oxidation rates, and appetite ratings were determined before and 2 hours after the interventions. Inter-individual differences were explored using Pearson’s product-moment correlations between the first and second replicates of the control-adjusted breakfast response. Within-participant covariate-adjusted linear mixed models and a random-effects meta-analytical approach were used to quantify participant-by-condition interactions. Results Breakfast consumption lowered 2-h blood glucose 0.44 mmol/L (95%CI: 0.76 to 0.12 mmol/L) and serum NEFA concentrations, whilst increasing blood lactate and serum insulin concentrations (all p < 0.01). Large, positive correlations were observed between the first and second replicates of the control-adjusted insulin, lactate, hunger, and satisfaction responses to breakfast consumption (all r > 0.5, 90%CI ranged from 0.03 to 0.91). The participant-by-condition interaction response variability (SD) for serum insulin concentration was 11 pmol/L (95%CI: 5 to 16 pmol/L), which was consistent with the τ-statistic from the random-effects meta-analysis (11.7 pmol/L, 95%CI 7.0 to 22.2 pmol/L) whereas effects were unclear for other outcome variables (e.g., τ-statistic value for glucose: 0 mmol/L, 95%CI 0.0 to 0.5 mmol/L). Conclusions Despite observing reactive hypoglycaemia at the group level, we were unable to detect any meaningful inter-individual variability of the reactive hypoglycaemia response to breakfast. There was, however, evidence that 2-h insulin responses to breakfast display meaningful inter-individual variability, which may be explained by relative carbohydrate dose ingested and variation in insulin sensitivity of participants.

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“…The modern diet consists of three to five feeding times a day, and individuals spend a significant amount of time in a non-fasting and postprandial state, meaning the levels of CM, VLDL, and other TRLs and their remnants are enhanced, which leads a continually fluctuating level of blood lipid ( 15 ). The postprandial metabolic status can be better reflected by postprandial TG concentration, and with the combination of fasting TG concentration, the degree of exposure of total TG in the arterial wall within 24 h can be described more comprehensively and accurately ( 16 ).…”

Section: Postprandial Lipemia and Postprandial Hyperlipidemiamentioning

confidence: 99%

Mechanisms of Atherosclerosis Induced by Postprandial Lipemia

Zhao

Liu

Yang

et al. 2021

Front. Cardiovasc. Med.

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Postprandial lipemia plays an important role in the formation, occurrence, and development of atherosclerosis, and it is closely related to coronary heart disease and other diseases involving endothelial dysfunction, oxidative stress, inflammation, and other mechanisms. Therefore, it has become a focus area for further research. The studies on postprandial lipemia mainly include TG, TRL, VLDL, CM, and remnant cholesterol. Diurnal triglyceride patterns and postprandial hyperlipidemia are very relevant and are now insufficiently covered. The possible mechanisms between postprandial lipemia and cardiovascular disease have been reviewed in this article by referring to relevant literature in recent years. The research progress on the effects of postprandial lipemia on endothelial function, oxidative stress, and inflammation is highlighted. The intervention of postprandial lipemia is discussed. Non-medicinal intervention such as diet and exercise improves postprandial lipemia. As medicinal intervention, statin, fibrate, ezetimibe, omega-3 fatty acids, and niacin have been found to improve postprandial lipid levels. Novel medications such as pemafibrate, PCSK9, and apoCIII inhibitors have been the focus of research in recent years. Gut microbiota is closely related to lipid metabolism, and some studies have indicated that intestinal microorganisms may affect lipid metabolism as environmental factors. Whether intervention of gut microbiota can reduce postprandial lipemia, and therefore against AS, may be worthy of further study.

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Galactose Ingested with a High-Fat Beverage Increases Postprandial Lipemia Compared with Glucose but Not Fructose Ingestion in Healthy Men

Abstract: ABSTRACT Background Fructose ingestion with a high-fat beverage increases postprandial lipemia when compared with glucose. It is unknown whether other sugars, such as galactose, also increase postprandial lipemia. Objectives The objective was to assess whether gal… Show more

Cited by 10 publications

References 28 publications

Metabolism of sugars: A window to the regulation of glucose and lipid homeostasis by splanchnic organs

Metabolism of sugars: A window to the regulation of glucose and lipid homeostasis by splanchnic organs

Are there interindividual differences in the reactive hypoglycaemia response to breakfast? A replicate crossover trial

Mechanisms of Atherosclerosis Induced by Postprandial Lipemia

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