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Mean ( SEM) postprandial concentrations of C-peptide in serum, of insulin in serum, and of oligosaccharides and arginine in plasma in 24 normolipidemic subjects after 4 different meals in each case: 1) 1 g fat/kg body wt (continuous line), 2) fat combined with 75 g oligosaccharides (broken line), 3) fat combined with 50 g sodium caseinate (dotted line), and 4) fat combined with oligosaccharides and caseinate (dot-dash line). For all panels, there were significant effects of time (P 0.001) and meal (P 0.001) and a significant meal time interaction (P 0.001), ANOVA for repeated measures.
Source publication
Postprandial lipemia is markedly modulated when carbohydrates are added to a fatty meal. The effect of added protein is less known, however, and the data are controversial.
We investigated the effects of casein added to various fat-rich meals in the absence and presence of oligosaccharides.
Four different test meals were given to 24 healthy volunte...
Contexts in source publication
Context 1
... was to be expected, fat alone did not significantly alter concentrations of C-peptide, insulin, or glucose (Figure 3). When oligosaccharides and oligosaccharides plus casein were added, however, these variables were affected in 2 phases: in an early phase up to 3 h, which was dominated by glucose regula- tion, and in a second phase, between 4 and 8 h, when the specific effect of casein was observed. ...
Context 2
... reason for these late elevations is probably again the release of insulinotropic amino acids from casein. The kinetics of arginine as a representative amino acid are shown in Figure 3. Interestingly enough, the variable reacting most sensi- tively to this late and continuous insulin elevation was not glu- cose but FFAs. ...
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Citations
... This finding could be explained by the fact that almond crackers have a higher energy density than cashew nut, white kidney bean, and wheat crackers. In a prior study, there was a positive correlation between increased energy and gastricemptying time after consumption of a meal containing different energy and macronutrients (Westphal et al., 2004). Food products with a higher energy density and fat content would slow down the rate of gastric emptying, consequently reducing postprandial glycaemic response and increasing satiety (Tan, Dhillon & Mattes, 2014). ...
Introduction: Crackers, one of the most consumed baked products, primarily contain refined wheat flour and have a moderate glycaemic index (GI). Nut and legume powders are used in baked goods to help regulate postprandial glycaemia; however, their glycaemic responses remain controversial. Our study aimed to compare the postprandial glycaemic responses between crackers with 30% wheat flour substitution by white kidney beans, cashew nuts, and almonds versus standard wheat crackers. Methods: Twelve adults were recruited for a five-session randomised controlled crossover study. In each session, they were randomly assigned to receive 50g carbohydrates from either a glucose solution or one of the four crackers. Plasma glucose levels were measured at baseline and 15, 30, 45, 60, 90, and 120 minutes after consumption. Satiety and hunger were evaluated using 100mm visual analogue scales at baseline and every 30 minutes until 120 minutes. Results: Mean incremental area under the curve (IAUC) for plasma glucose did not differ between the alternatives and wheat crackers, but was lowest for almond crackers. Compared with GI value of glucose solution, that of wheat, cashew nut, white kidney bean, and almond crackers were 39.97±23.13, 37.66±24.66, 35.85±10.86, and 28.09±17.92, respectively. Almond cracker consumption resulted in the highest mean IAUC for satiety and lowest for hunger, though non-significant. Conclusion: Crackers with 30% wheat flour substitution by nut and legume powders tended to improve postprandial glycaemia more than the standard crackers; however, acute responses on insulin and glucagon-like peptide-1 require further examination.
... In addition to the "calcium theory," it has been claimed that the magnesium content of milk and lactose or caseins could alter lipid and fat metabolism through insulin. [113] Moreover, help to enhance insulin sensitivity, which could have health implications. Furthermore, it has recently been proposed that milk contains bioactive molecules (rare in other dairy meals) that may function independently of calcium in regulating body fat storage. ...
Over the past four decades, overweight, obesity, and related metabolic disorders have reached epidemic proportions. According to a report from the World Health Organization (WHO), over 1.9 billion (accounting for 39%) adults were overweight, and 650 million of these were obese in 2016 [1]. Obesity is a leading contributor to numerous diseases, such as diabetes mellitus, cardiovascular diseases, and cancers. Therefore, seeking effective and safe approaches to control obesity is essential. Gut microbiota has been demonstrated to play a critical role in the occurrence of obesity via the regulation of energy metabolism. The diet can alter the composition and abundance of gut microbiota. This chapter reviews the gut environment and normal colonic microbiota, the mechanism Linking the microbiota to obesity, the gut microbiota in obese patients, and the effects of bioactive compounds in the modulation of gut microbiota.
... Other markers of lipid metabolism including HDL cholesterol, total cholesterol and β-hydroxybutyrate were not altered after adaptation to the different diets. These results agree with observations that high dietary protein acutely affects lipid metabolism, with lowering effects on cholesterol synthesis and lipogenic enzymes [10,29] and a potential reduction of lipidemia [30][31][32]. High protein diets can stimulate postprandial gluconeogenesis in the liver, with a reduced inhibition of glucose production by the meal [33,34]. They also have the potential to acutely stimulate postprandial insulin secretion [35]. ...
The western dietary pattern is known for its frequent meals rich in saturated fat and protein, resulting in a postprandial state for a large part of the day. Therefore, our aim was to investigate the postprandial glucose and lipid metabolism in response to high (HP) or normal (NP) protein, high-fat hypercaloric diet and to identify early biomarkers of protein intake and hepatic lipid accumulation. In a crossover design, 17 healthy subjects were randomly assigned to consume a HP or NP hypercaloric diet for two weeks. In parallel, a control group (CD; n = 10) consumed a weight-maintaining control diet. Biomarkers of postprandial lipid and glucose metabolism were measured in 24 h urine and in plasma before and following a meal challenge. The metabolic profile of urine but not plasma, showed increased excretion of 13C, carnitine and short chain acyl-carnitines after adaptation to the HP diet. Urinary excretion of decatrienoylcarnitine and octenoylcarnitine increased after adaptation to the NP diet. Our results suggest that the higher excretion of short-chain urinary acyl-carnitines could facilitate the elimination of excess fat of the HP diet and thereby reduce hepatic fat accumulation previously reported, whereas the higher excretion medium-chains acyl-carnitine could be early biomarkers of hepatic lipid accumulation.
... Prolonging exposure of saturated fats within the circulation through reduced insulin sensitivity aggravates the renin angiotensin response through oxidative mechanisms, especially among overweight and obese individuals [138]. Dietary proteins have been demonstrated to offset the oxidative effects and exert vascular protective effects [156,157]. However, no study has yet demonstrated the degree to which dairy proteins offset the hypertensive effects contributable to saturated fats found in dairy. ...
... Previous investigations have noted acute postprandial effects of saturated fats to increase RAS, proinflammatory markers, and oxidative species to promote endothelial dysfunction [138,152,154]. When protein is added to a meal rich in saturated fat, the effects of endothelial dysfunction from elevated saturated fat intake are ameliorated [156,157]. Therefore, a lack of hypotensive effects may be attributed to a counterbalancing of healthy vascular effects from dairy proteins and negative consequences to the saturated fat (Fig. 1) [198]. In this context, a modified higher-fat DASH diet, incorporating full-fat dairy products in place of non-and low-fat dairy products from the original DASH diet [17], reduced BP to a similar degree as the original DASH diet. ...
Lifestyle modifications in the form of diet and exercise are generally a first-line approach to reduce hypertensive risk and overall cardiovascular disease (CVD) risk. Accumulating research evidence has revealed that consumption of non- and low-fat dairy products incorporated into the routine diet is an effective means to reduce elevated blood pressure and improve vascular functions. However, the idea of incorporating whole-fat or full-fat dairy products in the normal routine diet as a strategy to reduce CVD risk has been met with controversy. The aim of this review is to review both sides of the argument surrounding saturated fat intake and CVD risk from the standpoint of dairy intake. Throughout the review, we examined observational studies on relationships between CVD risk and dairy consumption, dietary intervention studies using non-fat and whole-fat dairy, and mechanistic studies investigating physiological mechanisms of saturated fat intake that may help to explain increases in cardiovascular disease risk. Currently available data have demonstrated that whole-fat dairy is unlikely to augment hypertensive risk when added to the normal routine diet but may negatively impact CVD risk. In conclusion, whole-fat dairy may not be a recommended alternative to non- or low-fat dairy products as a means to reduce hypertensive or overall CVD risk.
... The addition of glucose or digestible oligosaccharides to a fatty meal results in a delay in gastric emptying [91,92]. More importantly, regarding lipid digestion, high levels of digestible carbohydrates in the diet attenuate the lipase secretion by the gastric mucosa or the pancreas into the small intestine [93,94], while indigestible carbohydrates, i.e., dietary fibers, can lower the extent of lipolysis either through the reduction of lipid emulsification or through forming aggregates with lipid globules [95,96]. ...
Many recent studies have acknowledged postprandial hypetriglyceridemia as a distinct risk factor for cardiovascular disease. This dysmetabolic state is the result of the hepatic overproduction of very low-density lipoproteins (VLDLs) and intestinal secretion of chylomicrons (CMs), which leads to highly atherogenic particles and endothelial inflammation. Postprandial lipid metabolism does not only depend on consumed fat but also on the other classes of nutrients that a meal contains. Various mechanisms through which carbohydrates exacerbate lipidemia have been identified, especially for fructose, which stimulates de novo lipogenesis. Glycemic index and glycemic load, despite their intrinsic limitations, have been used as markers of the postprandial glucose and insulin response, and their association with metabolic health and cardiovascular events has been extensively studied with contradictory results. This review aims to discuss the importance and pathogenesis of postprandial hypertriglyceridemia and its association with cardiovascular disease. Then, we describe the mechanisms through which carbohydrates influence lipidemia and, through a brief presentation of the available clinical studies on glycemic index/glycemic load, we discuss the association of these indices with atherogenic dyslipidemia and address possible concerns and implications for everyday practice.
... However, more studies are needed to conclude that fructose or sucrose has more adverse effects than glucose. Conversely, carbohydrates from starchy food did not influence PPL in healthy people (41). In addition, postprandial TAG increased linearly with the glycemic index of different foods containing the same amount of carbohydrates in individuals with insulin resistance (42). ...
... Overall, no significant differences in fasting TAG were detected in all studies investigating protein quality or quantity, suggesting that the possible effect is related to the postprandial period. As for PPL, the addition of casein (45-50 g) during an 8-h high fat meal challenge (80 g of fat) significantly reduced the TAG response (evaluated as 8 h-iAUC) in healthy volunteers and in individuals with type 2 diabetes (41,64). However, no difference was detected for TAG in the VLDL-fraction or whole plasma (41,64). ...
... As for PPL, the addition of casein (45-50 g) during an 8-h high fat meal challenge (80 g of fat) significantly reduced the TAG response (evaluated as 8 h-iAUC) in healthy volunteers and in individuals with type 2 diabetes (41,64). However, no difference was detected for TAG in the VLDL-fraction or whole plasma (41,64). These results have been confirmed in the medium-term, although only one study is available to date ( Table 5). ...
Abnormalities in postprandial lipemia (PPL), particularly those related to triglyceride-rich lipoproteins, are considered an independent cardiovascular risk factor. As diet is known to be one of the main modulators of PPL, the aim of this review was to summarize and discuss current knowledge on the impact of diet and its components on PPL in humans; specifically, the impact of weight loss, different nutrients (quantity and quality of dietary fats, carbohydrates, and proteins), alcohol and other bioactive dietary components (i.e., polyphenols), as well as the effect of different dietary patterns. The possible mechanisms behind the metabolic effects of each dietary component were also discussed.
... Only 1 trial (2 comparisons) was included for this analysis (42), with the overall pooled Hedges' g value being −0.16 (95% CI: −0.52, 0.20) with I 2 = 0.0% for iAUC (Supplemental Figure 4). ...
... Six trials (15 comparisons) were considered for this analysis to give an overall pooled Hedges' g value of 0.30 (95% CI: −0.12, 0.73) with I 2 = 57.9% for iAUC (15 comparisons) (Supplemental Figure 12) (17,42,(76)(77)(78)(79). Sensitivity testing attributed the high heterogeneity to the findings of Pal et al. (76) due to differences in the control meal for this study (glucose) compared with the others (whey protein or isolate). ...
... max , peak concentration; iAUC, incremental area under the curve.2 Includes double counting of Westphal et al.(42).3 Includes double counting of Naissides et al.(73). ...
The use of postprandial triglyceride (ppTG) as a cardiovascular disease risk indicator has gained recent popularity. However, the influence of different foods or food ingredients on the ppTG response has not been comprehensively characterized. A systematic literature review and meta-analysis was conducted to assess the effects of foods or food ingredients on the ppTG response. PubMed, MEDLINE, Cochrane, and CINAHL databases were searched for relevant acute (<24-h) randomized controlled trials published up to September 2018. Based on our selection criteria, 179 relevant trials (366 comparisons) were identified and systematically compiled into distinct food or food ingredient categories. A ppTG-lowering effect was noted for soluble fiber (Hedges' giAUC = -0.72; 95% CI: -1.33, -0.11), sodium bicarbonate mineral water (Hedges' gAUC = -0.42; 95% CI: -0.79, -0.04), diacylglycerol oil (Hedges' giAUC = -0.38; 95% CI: -0.75, -0.00), and whey protein when it was contrasted with other proteins. The fats group showed significant but opposite effects depending on the outcome measure used (Hedges' giAUC = -0.32; 95% CI: -0.61, -0.03; and Hedges' gAUC = 0.16; 95% CI: 0.06, 0.26). Data for other important food groups (nuts, vegetables, and polyphenols) were also assessed but of limited availability. Assessing for oral fat tolerance test (OFTT) recommendation compliance, most trials were ≥4 h long but lacked a sufficiently high fat challenge. iAUC and AUC were more common measures of ppTG. Overall, our analyses indicate that the effects on ppTG by different food groups are diverse, largely influenced by the type of food or food ingredient within the same group. The type of ppTG measurement can also influence the response.
... A trend towards higher NEFA concentrations following maximal eating in the present study may indicate spillover of dietary fatty acids into the circulating NEFA pool (23) . When fat is ingested alone, postprandial TAG responses across a 4 h period increase in direct proportion to the increase in fat ingested (24) , but when carbohydrate (25,26) or protein (27) are added to oral fat ingestion, postprandial triglyceridaemia is attenuated. This potentially explains the relatively modest increase in postprandial TAG in the present study, which was ~1.5-fold, despite a 2-fold increase in fat intake. ...
This study investigated metabolic, endocrine, appetite, and mood responses to a maximal eating occasion in fourteen men (mean ±SD: age 28 ±5 y, body mass 77.2 ±6.6 kg, body mass index 24.2 ±2.2 kg·m ⁻² ) who completed two trials in a randomised crossover design. On each occasion participants ate a homogenous mixed-macronutrient meal (pizza). On one occasion, they ate until ‘comfortably full’ ( ad libitum ) and on the other until they ‘could not eat another bite’ ( maximal ). Mean [95% CI] energy intake was double in the maximal (13,024 [10964, 15084] kJ; 3113 [2620,3605] kcal) compared with the ad libitum trial (6627 [5708,7547] kJ; 1584 [1364,1804] kcal). Serum insulin iAUC increased ~1.5-fold in the maximal compared with ad libitum trial (mean [95% CI] ad libitum 51.1 [33.3,69.0] nmol·L ⁻¹ ·4 h, maximal 78.8 [55.0,102.6] nmol·L ⁻¹ ·4 h, p < 0.01), but glucose iAUC did not differ between trials ( ad libitum 94.3 [30.3,158.2] mmol·L ⁻¹ ·4 h, maximal 126.5 [76.9,176.0] mmol·L ⁻¹ ·4 h, p = 0.19). TAG iAUC was ~1.5-fold greater in the maximal versus ad libitum trial ( ad libitum 98.6 [69.9,127.2] mmol·L ⁻¹ ·4 h, maximal 146.4 [88.6,204.1] mmol·L ⁻¹ ·4 h, p < 0.01). Total GLP-1, GIP, and PYY iAUC were greater in the maximal compared with ad libitum trial ( p < 0.05). Total ghrelin concentrations decreased to a similar extent, but AUC was slightly lower in the maximal versus ad libitum trial ( p = 0.02). There were marked differences on appetite and mood between trials, most notably maximal eating caused a prolonged increase in lethargy. Healthy men have capacity to eat twice the calories required to achieve comfortable fullness at a single meal. Postprandial glycaemia is well-regulated following initial overeating, with elevated postprandial insulinaemia likely contributing.
... The second limitation of this study was the difference in the protein content among trials. The acute effect of the ingestion of additional protein into an HF meal may reduce the postprandial TG concentration [21,22]. However, no study has investigated the long-term effect of protein ingestion or the effect of protein on the day before the HF meal test. ...
Background:
This study investigated the effects of ingesting meals with the same calorie intake but distinct nutritional contents after exercise on postprandial lipemia the next day.
Methods:
Eight healthy male participants completed two 2-day trials in a random order. On day 1, the participants underwent five 12 min bouts of cycling exercise with a bout of higher intensity exercise (4 min) after each and then a bout of lower intensity cycling (2 min). The total exercise time was 90 min. After the exercise, the participants ingested three high-fat or low-fat meals. On Day 2, the participants were asked to rest in the laboratory and ingest a high-fat meal. Their postprandial reaction after a high-fat meal was observed.
Results:
Postprandial triglyceride concentrations in the high-fat diet trial and low-fat diet trial exhibited nonsignificant differences. Total TG AUC were no significantly different on HF trial and LF trial (HF: 6.63 ± 3.2; LF: 7.20 ± 3.4 mmol/L*4 h. p = 0.586). However, the postprandial fat oxidation rate total AUC (HF: 0.58 ± 0.1; LF: 0.39 ± 0.2 g/min*4 h. p = 0.045), plasma glucose, and insulin concentration of the high-fat trial were significantly higher than those of the low-fat trial.
Conclusions:
This study revealed that meals with distinct nutritional contents after a 90-min exercise increased the postprandial fat oxidation rate but did not influence the postprandial lipemia after a high-fat meal the next day.
... In a pioneering work, Westphal and colleagues showed that adding dietary protein (milk or soy protein) to a high-fat meal prevented postprandial endothelial dysfunction [112]. This effect could, however, be explained by a quantitative effect of protein, because a high intake of protein (as compared to fat), (i) slowed down gastric emptying and decreased postprandial exposure to fatty acids in the meal [113], and (ii), raised postprandial insulin, which in this context could have anti-inflammatory and anti-atherogenic properties [114]. However, specific effects of protein quality or specific amino acids have also been documented [115]. ...
The purpose of this review is to provide an overview of diets, food, and food components that affect postprandial inflammation, endothelial function, and oxidative stress, which are related to cardiometabolic risk. A high-energy meal, rich in saturated fat and sugars, induces the transient appearance of a series of metabolic, signaling and physiological dysregulations or dysfunctions, including oxidative stress, low-grade inflammation, and endothelial dysfunction, which are directly related to the amplitude of postprandial plasma triglycerides and glucose. Low-grade inflammation and endothelial dysfunction are also known to cluster together with insulin resistance, a third risk factor for cardiovascular diseases (CVD) and type-II diabetes, thus making a considerable contribution to cardiometabolic risk. Because of the marked relevance of the postprandial model to nutritional pathophysiology, many studies have investigated whether adding various nutrients and other substances to such a challenge meal might mitigate the onset of these adverse effects. Some foods (e.g., nuts, berries, and citrus), nutrients (e.g., l-arginine), and other substances (various polyphenols) have been widely studied. Reports of favorable effects in the postprandial state have concerned plasma markers for systemic or vascular pro-inflammatory conditions, the activation of inflammatory pathways in plasma monocytes, vascular endothelial function (mostly assessed using physiological criteria), and postprandial oxidative stress. Although the literature is fragmented, this topic warrants further study using multiple endpoints and markers to investigate whether the interesting candidates identified might prevent or limit the postprandial appearance of critical features of cardiometabolic risk.
