-
Diabetes & Metabolism Sep 2006Several experimental data suggest that single sugar intake may induce heart rate acceleration and blood pressure elevation as a result of sympathetic activation... (Review)
Review
Several experimental data suggest that single sugar intake may induce heart rate acceleration and blood pressure elevation as a result of sympathetic activation secondary to insulin response and from alterations in endothelial function due to activation of oxidative stress. These hemodynamic effects might be more marked in patients with arterial hypertension or metabolic disorders, in particular in hypertensive patients with diabetes. A high-fat load may also induce activation of oxidative stress and endothelial dysfunction. However, the long-term effect of repeated intake of single sugar and fat on blood pressure, oxidative stress, and endothelial function should be tested in controlled trials. On the contrary, a balanced mixed meal (50% carbohydrates) does not induce any significant blood pressure changes. Nevertheless, acarbose treatment is able to reduce hypertension incidence in patients with impaired glucose tolerance and to improve endothelial function. In elderly subjects, in particular with type 2 diabetes or with severe dysautonomia, sigle sugar intake may account for nonhypoglycemic postprandial dizziness.
Topics: Animals; Blood Pressure; Dietary Carbohydrates; Dietary Fats; Glucose; Models, Biological; Postprandial Period; Rats
PubMed: 17375406
DOI: 10.1016/s1262-3636(06)70484-0 -
Diabetes Care Aug 2010
Topics: Blood Glucose; Diabetes Mellitus, Type 2; Humans; Postprandial Period
PubMed: 20668158
DOI: 10.2337/dc10-0634 -
Terapevticheskii Arkhiv 1998
Comparative Study
Topics: Adult; Duodenal Ulcer; Hemodynamics; Humans; Middle Aged; Postprandial Period; Reference Values; Time Factors
PubMed: 9551560
DOI: No ID Found -
The European Journal of Neuroscience Sep 2014Elimination of granule cells (GCs) in the olfactory bulb (OB) is not a continual event but is promoted during a short time window in the postprandial period, typically...
Elimination of granule cells (GCs) in the olfactory bulb (OB) is not a continual event but is promoted during a short time window in the postprandial period, typically with postprandial sleep. However, the neuronal mechanisms for the enhanced GC elimination during the postprandial period are not understood. Here, we addressed the question of whether top-down inputs of centrifugal axons from the olfactory cortex (OC) during the postprandial period are involved in the enhanced GC elimination in the OB. Electrical stimulation of centrifugal axons from the OC of anesthetized mice increased GC apoptosis. Furthermore, pharmacological suppression of top-down inputs from the OC to the OB during the postprandial period of freely behaving mice by γ-aminobutyric acid (GABA)A receptor agonist injection in the OC significantly decreased GC apoptosis. Remarkable apoptotic GC elimination in the sensory-deprived OB was also suppressed by pharmacological blockade of top-down inputs. These results indicate that top-down inputs from the OC to the OB during the postprandial period are the crucial signal promoting GC elimination, and suggest that the life and death decision of GCs in the OB is determined by the interplay between bottom-up sensory inputs from the external world and top-down inputs from the OC.
Topics: Animals; Apoptosis; Axons; Catheters, Indwelling; Cell Count; Electric Stimulation; Electrodes, Implanted; Electroencephalography; GABA-A Receptor Agonists; Immunohistochemistry; Male; Mice, Inbred C57BL; Muscimol; Neurons; Olfactory Bulb; Olfactory Cortex; Olfactory Pathways; Postprandial Period; Receptors, GABA-A; Sensory Deprivation
PubMed: 25041475
DOI: 10.1111/ejn.12679 -
The American Journal of Clinical... Nov 2007
Topics: Animals; Cytokines; Dietary Fats; Humans; Inflammation; Leukocytes; Postprandial Period; Toll-Like Receptor 4
PubMed: 17991632
DOI: 10.1093/ajcn/86.5.1257 -
Molecular Pharmaceutics May 2013Food effects on drug release and absorption from solid oral dosage forms are a common biopharmaceutical problem. The fed state is characterized by different motility and... (Review)
Review
Food effects on drug release and absorption from solid oral dosage forms are a common biopharmaceutical problem. The fed state is characterized by different motility and secretory activity of the complete gastrointestinal (GI) tract compared to fasting conditions. Due to long gastric transit times, the postprandial stomach plays an essential role for drug release and the appearance of food effects. Therefore, a concise comprehension of the relationship between food intake and its effect on drug release from solid oral dosage forms is essential to understand their dissolution behavior under fed conditions. This review describes important aspects of stomach physiology occurring after meal ingestion with particular reference to the FDA standard breakfast. A brief overview of oral and gastric food processing and their potential influence on drug release is given. The key factors affecting the intragastric dissolution of solid oral dosage forms and their regional distribution in the stomach are discussed. Additionally, the effects of food properties on gastric emptying kinetics are presented. Mechanical aspects such as intragastric pressures and hydrodynamics caused by gastric peristalsis are defined. The initial state and the dynamic changes of the gastric content during digestion are characterized since the different physicochemical aspects such as pH value, buffer capacity, rheological properties or surface tension may be essential for the in vivo dissolution profiles of oral dosage forms. Possible effects of the discrete interplay of the physiological factors on the in vivo drug delivery behavior of solid oral dosage forms are discussed.
Topics: Administration, Oral; Biological Availability; Drug Delivery Systems; Gastric Emptying; Gastrointestinal Transit; Humans; Intestinal Absorption; Mastication; Models, Biological; Pharmaceutical Preparations; Postprandial Period; Salivation; Stomach
PubMed: 23506381
DOI: 10.1021/mp300604u -
International Journal of Clinical... Feb 2010Postprandial lipaemia-induced endothelial dysfunction is felt to be mediated by increases in oxidative stress. In this review, we have examined the cross-sectional... (Review)
Review
AIMS
Postprandial lipaemia-induced endothelial dysfunction is felt to be mediated by increases in oxidative stress. In this review, we have examined the cross-sectional relationships found among these three variables.
METHODS
We found 20 studies conducted by 16 independent investigative teams through a Medline search from 1980 to 2008; studies were required to report correlations between at least two of the three variables of interest in studies of humans. This review is divided into (i) discussions on the biomarkers and other measures of postprandial lipaemia, oxidative stress and endothelial function; (ii) associations reported among the three variables; and (iii) other considerations including alternative intervention studies.
RESULTS
Triglycerides and free fatty acids are robust and well-standardised biomarkers of lipaemia. Measures of oxidative stress ranged from electron spin techniques to measures of lipid peroxidation and are limited by lack of standardisation. Brachial artery flow-mediated dilatation is the most commonly used measure of endothelial function. The associations between postprandial lipaemia and oxidative stress and between postprandial lipaemia and endothelial function are strong and consistent. However, the association between postprandial oxidative stress and endothelial function appears weak, at least using current approaches to measurement of oxidative stress.
DISCUSSION AND CONCLUSIONS
These observations are consistent with the proposed concept that oxidative stress mediates the adverse effects of postprandial lipaemia on endothelial function; they are limited by the difficulties in measuring oxidative stress. Efforts directed at optimising and standardising the measurement of oxidative stress will be of value in future works in this area.
Topics: Cardiovascular Diseases; Endothelium, Vascular; Humans; Hyperlipidemias; Oxidative Stress; Postprandial Period
PubMed: 20456177
DOI: 10.1111/j.1742-1241.2009.02146.x -
Nutrients Oct 2022Postprandial insulinaemia, triglyceridaemia and measures of inflammation are thought to be more closely associated with cardiovascular risk than fasting measures.... (Clinical Trial)
Clinical Trial
Postprandial insulinaemia, triglyceridaemia and measures of inflammation are thought to be more closely associated with cardiovascular risk than fasting measures. Although hypertension is associated with altered fasting metabolism, it is unknown as to what extent postprandial lipaemic and inflammatory metabolic responses differ between hypertensive and normotensive individuals. Linear models adjusting for age, sex, body mass index (BMI), visceral fat mass (VFM) and multiple testing (false discovery rate), were used to investigate whether hypertensive cases and normotensive controls had different fasting and postprandial (in response to two standardised test meal challenges) lipaemic, glycaemic, insulinaemic, and inflammatory (glycoprotein acetylation (GlycA)) responses in 989 participants from the ZOE PREDICT-1 nutritional intervention study. Compared to normotensive controls, hypertensive individuals had significantly higher fasting and postprandial insulin, triglycerides, and markers of inflammation after adjusting for age, sex, and BMI (effect size: Beta (Standard Error) ranging from 0.17 (0.08), = 0.04 for peak insulin to 0.29 (0.08), = 4.4 × 10 for peak GlycA). No difference was seen for postprandial glucose. When further adjusting for VFM effects were attenuated. Causal mediation analysis suggests that 36% of the variance in postprandial insulin response and 33.8% of variance in postprandial triglyceride response were mediated by VFM. Hypertensive individuals have different postprandial insulinaemic and lipaemic responses compared to normotensive controls and this is partially mediated by visceral fat mass. Consequently, reducing VFM should be a key focus of health interventions in hypertension. The ClinicalTrials.gov registration identifier is NCT03479866.
Topics: Humans; Blood Glucose; Hypertension; Inflammation; Insulin; Intra-Abdominal Fat; Postprandial Period; Triglycerides
PubMed: 36364763
DOI: 10.3390/nu14214499 -
Diabetes Care May 2013
Review
Topics: Blood Glucose; Gastric Emptying; Humans; Incretins; Models, Biological; Postprandial Period
PubMed: 23613599
DOI: 10.2337/dc12-1609 -
Diabetologia Dec 2001That cardiovascular disease occurs more frequently in patients with Type II (non-insulin-dependent) diabetes mellitus has been recognized for a long time. However, the... (Review)
Review
That cardiovascular disease occurs more frequently in patients with Type II (non-insulin-dependent) diabetes mellitus has been recognized for a long time. However, the extent to which hyperglycaemia contributes to atherosclerosis and cardiovascular disease is still not clear. Epidemiological studies published in recent years suggest that postprandial blood glucose might be an independent risk factor of cardiovascular disease. The main results of these studies, which are reviewed in this article, are that subjects from the general population with mild to moderate hyperglycaemia, following oral glucose load, but not in the fasting state, showed an increased cardiovascular risk. Furthermore, the post-challenge as well as postprandial glucose concentrations of subjects with Type II diabetes were found to be directly associated to incident cardiovascular disease independently of fasting glucose. Also, the correction of fasting hyperglycaemia or HbA1 c or both, disregarding the specific correction of postprandial hyperglycaemia was not found to significantly reduce the incidence of cardiovascular disease in patients with Type II diabetes. Finally, the strict control of both preprandial and postprandial hyperglycaemia yielded a substantial reduction of cardiovascular disease in Type II diabetes. Trials specifically designed to address this issue are needed to determine whether postprandial hyperglycaemia plays an independent and causative role in cardiovascular disease in patients with Type II diabetes.
Topics: Blood Glucose; Diabetes Mellitus, Type 2; Diabetic Angiopathies; Epidemiologic Methods; Humans; Postprandial Period; Risk Factors
PubMed: 11793012
DOI: 10.1007/s001250100020