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Nutrients Feb 2022As years progress, we are found more often in a postprandial than a postabsorptive state. Chrononutrition is an integral part of metabolism, pancreatic function, and... (Review)
Review
As years progress, we are found more often in a postprandial than a postabsorptive state. Chrononutrition is an integral part of metabolism, pancreatic function, and hormone secretion. Eating most calories and carbohydrates at lunch time and early afternoon, avoiding late evening dinner, and keeping consistent number of daily meals and relative times of eating occasions seem to play a pivotal role for postprandial glycemia and insulin sensitivity. Sequence of meals and nutrients also play a significant role, as foods of low density such as vegetables, salads, or soups consumed first, followed by protein and then by starchy foods lead to ameliorated glycemic and insulin responses. There are several dietary schemes available, such as intermittent fasting regimes, which may improve glycemic and insulin responses. Weight loss is important for the treatment of insulin resistance, and it can be achieved by many approaches, such as low-fat, low-carbohydrate, Mediterranean-style diets, etc. Lifestyle interventions with small weight loss (7-10%), 150 min of weekly moderate intensity exercise and behavioral therapy approach can be highly effective in preventing and treating type 2 diabetes. Similarly, decreasing carbohydrates in meals also improves significantly glycemic and insulin responses, but the extent of this reduction should be individualized, patient-centered, and monitored. Alternative foods or ingredients, such as vinegar, yogurt, whey protein, peanuts and tree nuts should also be considered in ameliorating postprandial hyperglycemia and insulin resistance. This review aims to describe the available evidence about the effects of diet, chrononutrition, alternative dietary interventions and exercise on postprandial glycemia and insulin resistance.
Topics: Blood Glucose; Cross-Over Studies; Diabetes Mellitus, Type 2; Diet, Fat-Restricted; Dietary Carbohydrates; Glycemic Index; Humans; Insulin; Insulin Resistance; Life Style; Meals; Postprandial Period
PubMed: 35215472
DOI: 10.3390/nu14040823 -
Nutrients Apr 2020Food ingestion induces a metered response of the digestive system. Initially, the upper digestive system reacts to process and extract meal substrates. Later, meal... (Review)
Review
Food ingestion induces a metered response of the digestive system. Initially, the upper digestive system reacts to process and extract meal substrates. Later, meal residues not absorbed in the small bowel, pass into the colon and activate the metabolism of resident microbiota. Food consumption also induces sensations that arise before ingestion (e.g., anticipatory reward), during ingestion (e.g., gustation), and most importantly, after the meal (i.e., the postprandial experience). The postprandial experience involves homeostatic sensations (satiety, fullness) with a hedonic dimension (digestive well-being, mood). The factors that determine the postprandial experience are poorly understood, despite their potential role in personalized diets and healthy eating habits. Current data suggest that the characteristics of the meal (amount, palatability, composition), the activity of the digestive system (suited processing), and the receptivity of the eater (influenced by multiple conditioning factors) may be important in this context.
Topics: Affect; Digestion; Eating; Feeding Behavior; Gastrointestinal Microbiome; Humans; Postprandial Period; Satiation; Satiety Response
PubMed: 32252402
DOI: 10.3390/nu12040986 -
International Journal of Molecular... Sep 2023Postprandial hyperlipidemia showing postprandial increases in serum triglyceride (TG) is associated with the development of atherosclerotic cardiovascular disease... (Review)
Review
Postprandial hyperlipidemia showing postprandial increases in serum triglyceride (TG) is associated with the development of atherosclerotic cardiovascular disease (ASCVD). To diagnose postprandial hyperlipidemia, the oral fat loading test (OFLT) should be performed; however, this test is very time-consuming and is difficult to perform. Elevated serum TG levels reflect an increase in TG-rich lipoproteins (TRLs), such as chylomicrons (CM), very low-density lipoproteins (VLDL), and their remnants (CM remnants [CMRs] and VLDL remnants [VLDLRs]). Understanding of elevation in CMR and/or VLDLR can lead us to understand the existence of postprandial hyperlipidemia. The measurement of apo B48, which is a constituent of CM and CMR; non-fasting TG, which includes TG content in all lipoproteins including CM and CMR; non-high-density lipoprotein cholesterol (non-HDL-C), which includes TRLs and low-density lipoprotein; and remnant cholesterol are useful to reveal the existence of postprandial hyperlipidemia. Postprandial hyperlipidemia is observed in patients with familial type III hyperlipoproteinemia, familial combined hyperlipidemia, chronic kidney disease, metabolic syndrome and type 2 diabetes. Postprandial hyperlipidemia is closely related to postprandial hyperglycemia, and insulin resistance may be an inducing and enhancing factor for both postprandial hyperlipidemia and postprandial hyperglycemia. Remnant lipoproteins and metabolic disorders associated with postprandial hyperlipidemia have various atherogenic properties such as induction of inflammation and endothelial dysfunction. A healthy diet, calorie restriction, weight loss, and exercise positively impact postprandial hyperlipidemia. Anti-hyperlipidemic drugs such pemafibrate, fenofibrate, bezafibrate, ezetimibe, and eicosapentaenoic acid have been shown to improve postprandial hyperlipidemia. Anti-diabetic drugs including metformin, alpha-glucosidase inhibitors, pioglitazone, dipeptidyl-peptidase-4 inhibitors and glucagon-like peptide 1 analogues have been shown to ameliorate postprandial hyperlipidemia. Although sodium glucose cotransporter-2 inhibitors have not been proven to reduce postprandial hyperlipidemia, they reduced fasting apo B48 and remnant lipoprotein cholesterol. In conclusion, it is important to appropriately understand the existence of postprandial hyperlipidemia and to connect it to optimal treatments. However, there are some problems with the diagnosis for postprandial hyperlipidemia. Postprandial hyperlipidemia cannot be specifically defined by measures such as TG levels 2 h after a meal. To study interventions for postprandial hyperlipidemia with the outcome of preventing the onset of ASCVD, it is necessary to define postprandial hyperlipidemia using reference values such as IGT.
Topics: Humans; Hyperlipidemias; Diabetes Mellitus, Type 2; Lipoproteins; Triglycerides; Lipoproteins, VLDL; Atherosclerosis; Postprandial Period
PubMed: 37762244
DOI: 10.3390/ijms241813942 -
Nutrients Feb 2020There is no question that elevated postprandial glycemia is a significant driver of common chronic diseases globally [...].
There is no question that elevated postprandial glycemia is a significant driver of common chronic diseases globally [...].
Topics: Diet, Healthy; Dietary Carbohydrates; Glycemic Index; Humans; Postprandial Period
PubMed: 32093020
DOI: 10.3390/nu12020536 -
Nutrients Jan 2021Glucose levels in blood must be constantly maintained within a tight physiological range to sustain anabolism. Insulin regulates glucose homeostasis via its effects on... (Review)
Review
Glucose levels in blood must be constantly maintained within a tight physiological range to sustain anabolism. Insulin regulates glucose homeostasis via its effects on glucose production from the liver and kidneys and glucose disposal in peripheral tissues (mainly skeletal muscle). Blood levels of glucose are regulated simultaneously by insulin-mediated rates of glucose production from the liver (and kidneys) and removal from muscle; adipose tissue is a key partner in this scenario, providing nonesterified fatty acids (NEFA) as an alternative fuel for skeletal muscle and liver when blood glucose levels are depleted. During sleep at night, the gradual development of insulin resistance, due to growth hormone and cortisol surges, ensures that blood glucose levels will be maintained within normal levels by: (a) switching from glucose to NEFA oxidation in muscle; (b) modulating glucose production from the liver/kidneys. After meals, several mechanisms (sequence/composition of meals, gastric emptying/intestinal glucose absorption, gastrointestinal hormones, hyperglycemia mass action effects, insulin/glucagon secretion/action, de novo lipogenesis and glucose disposal) operate in concert for optimal regulation of postprandial glucose fluctuations. The contribution of the liver in postprandial glucose homeostasis is critical. The liver is preferentially used to dispose over 50% of the ingested glucose and restrict the acute increases of glucose and insulin in the bloodstream after meals, thus protecting the circulation and tissues from the adverse effects of marked hyperglycemia and hyperinsulinemia.
Topics: Adipose Tissue; Blood Glucose; Fasting; Fatty Acids, Nonesterified; Gastric Emptying; Glucose; Homeostasis; Humans; Hyperglycemia; Hyperinsulinism; Hypoglycemia; Incretins; Insulin; Insulin Resistance; Kidney; Liver; Meals; Muscle, Skeletal; Postprandial Period
PubMed: 33419065
DOI: 10.3390/nu13010159 -
Nature Metabolism Apr 2021Understanding how to modulate appetite in humans is key to developing successful weight loss interventions. Here, we showed that postprandial glucose dips 2-3 h after...
Understanding how to modulate appetite in humans is key to developing successful weight loss interventions. Here, we showed that postprandial glucose dips 2-3 h after a meal are a better predictor of postprandial self-reported hunger and subsequent energy intake than peak glucose at 0-2 h and glucose incremental area under the blood glucose curve at 0-2 h. We explore the links among postprandial glucose, appetite and subsequent energy intake in 1,070 participants from a UK exploratory and US validation cohort, who consumed 8,624 standardized meals followed by 71,715 ad libitum meals, using continuous glucose monitors to record postprandial glycaemia. For participants eating each of the standardized meals, the average postprandial glucose dip at 2-3 h relative to baseline level predicted an increase in hunger at 2-3 h (r = 0.16, P < 0.001), shorter time until next meal (r = -0.14, P < 0.001), greater energy intake at 3-4 h (r = 0.19, P < 0.001) and greater energy intake at 24 h (r = 0.27, P < 0.001). Results were directionally consistent in the US validation cohort. These data provide a quantitative assessment of the relevance of postprandial glycaemia in appetite and energy intake modulation.
Topics: Adult; Appetite; Blood Glucose; Cohort Studies; Diet; Energy Intake; Female; Humans; Hunger; Male; Postprandial Period; Predictive Value of Tests; Satiation; Young Adult
PubMed: 33846643
DOI: 10.1038/s42255-021-00383-x -
Diabetes, Obesity & Metabolism Jul 2021To assess the effects of oral semaglutide on postprandial glucose and lipid metabolism, and gastric emptying, in subjects with type 2 diabetes (T2D). (Randomized Controlled Trial)
Randomized Controlled Trial
AIM
To assess the effects of oral semaglutide on postprandial glucose and lipid metabolism, and gastric emptying, in subjects with type 2 diabetes (T2D).
MATERIALS AND METHODS
In this randomized, double-blind, single-centre, crossover trial, subjects with T2D received once-daily oral semaglutide (escalated to 14 mg) followed by placebo, or vice versa, over two consecutive 12-week periods. Glucose and lipid metabolism, and gastric emptying (paracetamol absorption) were assessed before and after two types of standardized meals (standard and/or fat-rich) at the end of each treatment period. The primary endpoint was area under the glucose 0-5-h curve (AUC ) after the standard breakfast.
RESULTS
Fifteen subjects were enrolled (mean age 58.2 years, HbA1c 6.9%, body weight 93.9 kg, diabetes duration 3.1 years; 13 [86.7%] males). Fasting concentrations of glucose were significantly lower, and C-peptide significantly greater, with oral semaglutide versus placebo. Postprandial glucose (AUC ) was significantly lower with oral semaglutide versus placebo (estimated treatment ratio, 0.71; 95% CI, 0.63, 0.81; p < .0001); glucose incremental AUC (iAUC ) and glucagon AUC were also significantly reduced, with similar results after the fat-rich breakfast. Fasting concentrations of triglycerides, very low-density lipoprotein (VLDL) and apolipoprotein B48 (ApoB48) were significantly lower with oral semaglutide versus placebo. AUC for triglycerides, VLDL and ApoB48, and triglycerides iAUC , were significantly reduced after oral semaglutide versus placebo. During the first postprandial hour, gastric emptying was delayed (a 31% decrease in paracetamol AUC ) with oral semaglutide versus placebo. One serious adverse event (acute myocardial infarction) occurred during oral semaglutide treatment.
CONCLUSION
Oral semaglutide significantly improved fasting and postprandial glucose and lipid metabolism, and delayed gastric emptying.
Topics: Blood Glucose; Diabetes Mellitus, Type 2; Double-Blind Method; Gastric Emptying; Glucagon-Like Peptides; Glucose; Humans; Hypoglycemic Agents; Lipid Metabolism; Male; Middle Aged; Postprandial Period
PubMed: 33710717
DOI: 10.1111/dom.14373 -
Diabetologia Feb 2022Sleep, diet and exercise are fundamental to metabolic homeostasis. In this secondary analysis of a repeated measures, nutritional intervention study, we tested whether...
AIMS/HYPOTHESIS
Sleep, diet and exercise are fundamental to metabolic homeostasis. In this secondary analysis of a repeated measures, nutritional intervention study, we tested whether an individual's sleep quality, duration and timing impact glycaemic response to a breakfast meal the following morning.
METHODS
Healthy adults' data (N = 953 [41% twins]) were analysed from the PREDICT dietary intervention trial. Participants consumed isoenergetic standardised meals over 2 weeks in the clinic and at home. Actigraphy was used to assess sleep variables (duration, efficiency, timing) and continuous glucose monitors were used to measure glycaemic variation (>8000 meals).
RESULTS
Sleep variables were significantly associated with postprandial glycaemic control (2 h incremental AUC), at both between- and within-person levels. Sleep period time interacted with meal type, with a smaller effect of poor sleep on postprandial blood glucose levels when high-carbohydrate (low fat/protein) (p = 0.02) and high-fat (p = 0.03) breakfasts were consumed compared with a reference 75 g OGTT. Within-person sleep period time had a similar interaction (high carbohydrate: p = 0.001, high fat: p = 0.02). Within- and between-person sleep efficiency were significantly associated with lower postprandial blood glucose levels irrespective of meal type (both p < 0.03). Later sleep midpoint (time deviation from midnight) was found to be significantly associated with higher postprandial glucose, in both between-person and within-person comparisons (p = 0.035 and p = 0.051, respectively).
CONCLUSIONS/INTERPRETATION
Poor sleep efficiency and later bedtime routines are associated with more pronounced postprandial glycaemic responses to breakfast the following morning. A person's deviation from their usual sleep pattern was also associated with poorer postprandial glycaemic control. These findings underscore sleep as a modifiable, non-pharmacological therapeutic target for the optimal regulation of human metabolic health. Trial registration ClinicalTrials.gov NCT03479866.
Topics: Adolescent; Adult; Aged; Blood Glucose; Breakfast; Diet; Female; Glycemic Control; Glycemic Index; Humans; Male; Middle Aged; Postprandial Period; Sleep Deprivation; Young Adult
PubMed: 34845532
DOI: 10.1007/s00125-021-05608-y -
Gut Microbes 2022Non-fasting lipidemia (nFL), mainly contributed by postprandial lipidemia (PL), has recently been recognized as an important cardiovascular disease (CVD) risk as fasting... (Randomized Controlled Trial)
Randomized Controlled Trial
Combined berberine and probiotic treatment as an effective regimen for improving postprandial hyperlipidemia in type 2 diabetes patients: a double blinded placebo controlled randomized study.
Non-fasting lipidemia (nFL), mainly contributed by postprandial lipidemia (PL), has recently been recognized as an important cardiovascular disease (CVD) risk as fasting lipidemia (FL). PL serves as a common feature of dyslipidemia in Type 2 Diabetes (T2D), albeit effective therapies targeting on PL were limited. In this study, we aimed to evaluate whether the therapy combining probiotics (Prob) and berberine (BBR), a proven antidiabetic and hypolipidemic regimen via altering gut microbiome, could effectively reduce PL in T2D and to explore the underlying mechanism. Blood PL (120 min after taking 100 g standard carbohydrate meal) was examined in 365 participants with T2D from the Probiotics and BBR on the Efficacy and Change of Gut Microbiota in Patients with Newly Diagnosed Type 2 Diabetes (PREMOTE study), a random, placebo-controlled, and multicenter clinical trial. Prob+BBR was superior to BBR or Prob alone in improving postprandial total cholesterol (pTC) and low-density lipoprotein cholesterol (pLDLc) levels with decrement of multiple species of postprandial lipidomic metabolites after 3 months follow-up. This effect was linked to the changes of fecal level responding to BBR alone or Prob+BBR treatment. Four genes encoding long-chain acyl-CoA synthetase were identified in the genome of this strain, and transcriptionally activated by BBR. BBR treatment further decreased the concentration of FFA in the culture medium of compared to vehicle. Thus, the activation of by BBR could enhance FFA import and mobilization in and diliminish the intraluminal lipids for absorption to mediate the effect of Prob+BBR on PL. Our study confirmed that BBR and Prob () could exert a synergistic hypolipidemic effect on PL, acting as a gut lipid sink to achieve better lipidemia and CVD risk control in T2D.
Topics: Adult; Animals; Berberine; Cholesterol; Cholesterol, LDL; Diabetes Mellitus, Type 2; Double-Blind Method; Drug Therapy, Combination; Feces; Female; Gastrointestinal Microbiome; Humans; Hyperlipidemias; Male; Middle Aged; Postprandial Period; Probiotics
PubMed: 34923903
DOI: 10.1080/19490976.2021.2003176 -
Nutrients May 2020The increasing prevalence of type 2 diabetes (T2D) worldwide calls for effective approaches to its management. Strategies for diabetes have generally focused on... (Review)
Review
UNLABELLED
The increasing prevalence of type 2 diabetes (T2D) worldwide calls for effective approaches to its management. Strategies for diabetes have generally focused on optimizing overall glycemic control as assessed by glycated hemoglobin (HbA1c) and fasting plasma glucose (FPG) values. However, since 2001, the American Diabetes Association has established postprandial glucose (PPG) as an independent contributor to both HbA1c and diabetes complications, and increasing evidence suggests that all three glycemic parameters of HbA1c, FPG, and postprandial glucose (PPG) are independently important.
OBJECTIVES
The objective of this review was to comprehensively summarize the literature on the effects of nutritional strategies incorporating glycemic index (GI)/glycemic load (GL) on the postprandial hyperglycemia in people with T2D, as well as to provide recommendations for effective dietary strategies addressing both the dietary glycemic index and load in clinical practice.
DESIGN
An advanced Pubmed search was conducted. A total of 10 randomized controlled studies met the inclusion criteria. Six studies compared low-GI with higher GI meals, three included studies that compared reduced carbohydrate content with higher carbohydrate content, and one study compared meals of low-GI (with high or low fiber) with meals of higher GI (with high or low fiber).
RESULTS
Most of the clinical trials resulted in significant improvement ( < 0.05) of postprandial hyperglycemia. Conclusions Either reducing the amount of carbohydrate in a meal or increasing consumption of soluble fiber has a favorable effect on postprandial glucose excursions.
Topics: Blood Glucose; Diabetes Mellitus, Type 2; Diet; Dietary Fiber; Glycated Hemoglobin; Glycemic Index; Glycemic Load; Humans; Hyperglycemia; Postprandial Period
PubMed: 32471238
DOI: 10.3390/nu12061561