Preprandial Values Research Articles

Assessment of Liver Perfusion by IntraVoxel Incoherent Motion (IVIM) Magnetic Resonance-Diffusion-Weighted Imaging: Correlation With Phase-Contrast Portal Venous Flow Measurements.

To prospectively verify, in vivo, Le Bihan's model of signal decay in magnetic resonance/diffusion-weighted imaging (intravoxel incoherent motion) in healthy liver parenchyma. Informed consent and institutional board approval were obtained. To measure both underfasting and postprandial conditions, apparent, slow, and fast diffusion (D*) coefficients and perfusion fraction of liver parenchyma, 40 healthy volunteers (19 women and 21 men) underwent a 3.0-T magnetic resonance imaging examination, including portal venous flow measurements by a 2-dimensional phase-contrast sequence, and multi-b diffusion-weighted imaging acquired before and 30 minutes after a 600-Kcal meal. Parameters were measured by fitting procedure with regions of interest drawn on the right liver lobe. Paired-sample t test was performed to search for any statistically significant difference between preprandial and postprandial values of each parameter and of portal flow. Pearson correlation coefficients were calculated to evaluate the relationship between portal flow increase and diffusion-weighted imaging parameter changes in postprandial conditions. Interobserver agreement for measurement of the intravoxel incoherent motion parameters was determined, both for preprandial and postprandial values. Mean increase in postprandial portal flow was 98% (P < 0.0009). The t test did not show any statistically significant difference between the preprandial and postprandial values for apparent, slow diffusion coefficients and perfusion fraction (P ≥ 0.05), whereas a statistically significant postprandial increase (P < 0.01) of D* was detected. Correlation with portal venous flow increase at Pearson test was statistically significant for D* (P = 0.04) and nonsignificant for the other parameters. All the parameters showed wide variability, with a higher percent coefficient of variation for D*. Interobserver agreement was always greater than 0.70. This study verifies Le Bihan's theory, confirming that in the liver, D* is influenced by perfusional changes related to portal venous flow.

The dawn phenomenon in type 2 diabetes: How to assess it in clinical practice?

AimThe study was aimed at determining whether the dawn phenomenon in type 2 diabetes (T2D) can be predicted and quantified using simple and easily accessible glucose determinations. MethodsA total of 210 non-insulin-treated persons with T2D underwent continuous glucose monitoring (CGM). The dawn phenomenon was quantified as the absolute increment from the nocturnal glucose nadir to the pre-breakfast value (Δdawn, mg/dL). Pre-lunch (preL) and pre-dinner (preD) glucose, and their averaged values (preLD), were compared with the nocturnal nadir. These pre-meal values were subtracted from the pre-breakfast values. The differences obtained (Δpre-mealL, Δpre-meal D and Δpre-meal LD) were correlated with Δdawn values. The receiver operating characteristic (ROC) curve was used to select the optimal Δpre-meal value that best predicted a dawn phenomenon, set at a threshold of 20mg/dL. ResultsAll pre-meal glucose levels and differences from pre-breakfast values (Δpre-meal) significantly correlated (P<0.0001) with the nocturnal nadir and Δdawn values, respectively. The strongest correlations were observed for the parameters averaged at preL and preD time points: r=0.83 for preLD and r=0.58 for Δpre-meal LD. ROC curve analysis indicated that the dawn phenomenon at a threshold of 20mg/dL can be significantly predicted by a Δpre-meal LD cut off value of 10mg/dL. The relationship between Δdawn (Y, mg/dL) and Δpre-meal LD (X, mg/dL) was Y=0.49 X+15. ConclusionThe self-monitoring of preprandial glucose values at the three main mealtimes can predict the presence/absence of the dawn phenomenon, and permits reliable assessment of its magnitude without requiring continuous overnight glucose monitoring.

PS-190 The Effect Of Enteral Feeding On Regional Intestinal Oxygen Saturation In Preterm Born Infants

<h3>Background</h3> Term born infants demonstrate an increase in intestinal perfusion after receiving enteral feeding (postprandial intestinal hyperemia). It remains unclear whether enteral feeding influences intestinal perfusion in preterm infants. <h3>Aim</h3> To assess the effect of enteral feeding on intestinal perfusion in preterm infants. <h3>Methods</h3> This study was part of a larger prospective cohort study. We used near-infrared spectroscopy to measure regional intestinal oxygen saturation (r_intSO₂), which is indicative for intestinal perfusion. We measured during two hours on postnatal days 2–5, 8, 15, 22, 29, and 36. Feeding times were manually recorded. We used Multi-level analyses to compare preprandial (baseline) r_intSO₂ values to postprandial r_intSO₂values, both 10–30 min and 30–60 min after feeding. <h3>Results</h3> We included 29 preterm infants with a median GA of 28+1/7 (range 25+1/7–30+4/7) weeks, and a median birth weight of 1025 (range 580–1495) grams. Compared to preprandial values, we only found decreased postprandial r_intSO₂values 30–60 min after feeding (mean[SD]: from 47%[22] to 41%[19], p = 0.007) on day 5. We observed increased r_intSO₂ values 10–30 min after feeding compared to preprandial values on day 29 (mean[SD]: from 51%[14] to 42%[14], p = 0.005). <h3>Conclusion</h3> Our results suggest that in preterm infants during their first three weeks of life, intestinal oxygen saturation does not increase, and sometimes even decreases, the first hour after feeding. One might speculate that preterm infants are not yet able to increase intestinal perfusion rates after feeding, an increase which might be necessary to meet metabolic demands.

Reversal time of postprandial changes of the thickness of abdominal muscles employing ultrasound measurements

ObjectivesLow thickness of Transversus Abdominis, Internal Oblique and External Oblique muscles may play a role in development of low back pain. Ultrasonography is increasingly utilized to measure the thickness of these muscles. Prandial state has recently been proposed as a confounding factor in such measurements. We aimed to compare the reversal time of the postprandial thickness of these muscles with preprandial values. The measurement errors of ultrasonographic values were also assessed in both immediate preprandial and postprandial states. DesignInterventional cross-sectional study. MethodsThe ultrasonographic thickness of lateral abdominal muscles was measured at rest and during abdominal drawing-in maneuver in 20 healthy participants before and after consumption of a specific meal. Postprandial ultrasound measurements continued every 15 min until their thickness reached 95% of their preprandial values. ResultsThere was a statistically significant reduction in postprandial thickness of these muscles (all p-values <0.001 on both sides). The reversal times were 1.5, 1.3 and 1.2 h for Transversus Abdominis, Internal Oblique, and External Oblique muscles, respectively. Standard Error of Measurement and Smallest Detectable Change were in the range of 0.007–0.013 mm and 0.020–0.035 mm, respectively. ConclusionsTo limit the effects of prandial state on the sonographic thickness of lateral abdominal muscles, we recommend measuring these values at least 1.5–2 h after food consumption. For the future studies, controlling the participants according to their prandial state is recommended.

Sonographic evaluation of gallbladder motility in children with chronic functional constipation.

Background/AimsStudies in adults suggest that constipation may not be a purely colonic pathology and may be a component of a generalized gastrointestinal (GI) motor disorder in which proximal GI motility can be impaired. Pediatric data are scarce, and the natural history of the disorder remains undefined. We aimed to evaluate gallbladder motility in a subset of Asian children with chronic functional constipation.MethodsAbdominal ultrasound was performed on 105 children, including 55 patients (aged 3 to 13 years) with chronic functional constipation who met the inclusion criteria and 50 age- and gender-matched controls. The gallbladder contractility index was calculated based on the preprandial and postprandial gallbladder areas. Preprandial and postprandial values for gallbladder volume and wall thickness were evaluated.ResultsThe mean value of the contractility index for the patients (15.77±24.68) was significantly lower than the mean value for the controls (43.66±11.58) (p=0.001). The mean postprandial gallbladder volumes and areas were larger in children with gallbladder hypomotility (p<0.05). The mean duration of constipation (4.8 months) was significantly higher (p=0.004) in the children with gall-bladder hypomotility.ConclusionsGallbladder motility is significantly impaired in children with chronic functional constipation. This study contributes to the understanding of the underlying pathophysiology, which will enable advancement in and improved management of children with chronic constipation and associated gallbladder hypomotility.

Effect of orally administered electrolyte solution formulation on abomasal luminal pH and emptying rate in dairy calves

To determine the effects of 3 commercially available, orally administered electrolyte solutions (OAEs) on abomasal luminal pH and emptying rate in dairy calves, compared with the effect of orally administered milk replacer. Randomized crossover study. 6 male dairy calves (age, 12 to 31 days). Calves were surgically instrumented with an abomasal cannula and were administered 4 treatments in randomized order: all-milk protein milk replacer, high-glucose high-bicarbonate OAE, high-glucose high-bicarbonate OAE containing glycine, and low-glucose OAE containing acetate and propionate. Abomasal luminal pH was measured with a miniature glass pH electrode prior to treatment administration and every second afterward for 24 hours. Feeding of orally administered milk replacer resulted in a rapid increase in mean abomasal luminal pH from 1.3 to 5.8, followed by a gradual decrease to preprandial values by 8 hours afterward (mean 24-hour pH, 3.2). High-glucose high-bicarbonate OAEs caused a large and sustained increase from 1.3 to 7.5 (mean 24-hour pH, 4.1 for the solution without glycine and 3.5 for the solution with glycine). In contrast, feeding of the acetate-containing OAE was followed by only a mild and transient increase (mean 24-hour pH, 2.1); luminal pH returned to preprandial values by 3 hours after ingestion. Ingestion of a bicarbonate-containing OAE resulted in sustained abomasal alkalinization in dairy calves. Because persistently high abomasal luminal pH may facilitate growth of enteropathogenic bacteria, administration of OAEs containing a high bicarbonate concentration (> 70mM) is not recommended for calves with diarrhea.

Tooth and Periodontal Clinical Attachment Loss Are Associated With Hyperglycemia in Patients With Diabetes

Periodontal disease has been associated with diabetes, but there is still controversy on the relationship between periodontal clinical parameters and glycemic control. The purpose of this study is to assess the relationship between blood glucose levels and clinical parameters of periodontal disease in individuals with diabetes. A total of 65 individuals with diabetes and 81 individuals without diabetes were included in the study. A full-mouth periodontal examination and preprandial fasting glycemia values were recorded for each individual. Glycosylated hemoglobin was only measured in patients with diabetes. A comparative analysis between groups (Mann-Whitney U test) and a correlation analysis between glycemia and periodontal parameters were performed (Spearman test). Patients without diabetes presented more teeth than individuals with diabetes (P <0.05). Patients with diabetes with periodontitis displayed loss of periodontal clinical attachment compared to patients without diabetes, but the highest value was observed in patients with periodontitis that reported a smoking habit. Furthermore, patients with diabetes with periodontitis presented higher glycemia and glycated hemoglobin values in contrast to patients with gingivitis. Patients with diabetes with hyperglycemia had a higher risk to develop periodontitis (odds ratio = 2.24; 95% confidence interval = 1.02 to 4.93). A positive correlation was observed between glycemia and clinical attachment loss (AL), whereas a negative correlation between glycemia and the number of teeth present was found (P <0.05). Tooth and periodontal AL were increased by hyperglycemia in individuals with diabetes. This study contributes additional evidence that diabetes could aggravate periodontal disease and affect the systemic health of individuals.

Effect of Glucose Control on Delayed Gastric Emptying in Diabetic Patients: Author's Reply

TO THE EDITOR: We thank Dr. Kim for her interest in our paper.1 We agree regarding the issues raised in the correspondence to the editor. The study under discussion was a retrospective analysis of an available serum hemoglobin A1C (HbA1C) level near the performance of a gastric emptying scan. As a result of this limitation, assessment of preprandial or postprandial glucose values as well as duration of diabetes and presence of diabetic complications could not be performed.2-5

Insulin dosage optimization based on prediction of postprandial glucose excursions under uncertain parameters and food intake

Considering the difficulty in selecting correct insulin doses and the problem of hyper- and hypoglycemia episodes in type 1 diabetes, dosage-aid systems are very useful for these patients. A model-based approach to this problem must unavoidably consider uncertainty sources such as large intra-patient variability and food intake. In the present study, postprandial glucose is predicted considering this uncertain information using modal interval analysis. This approach calculates a safer prediction of possible hyper- and hypoglycemia episodes induced by insulin therapy for an individual patient's parameters and integrates this information into a dosage-aid system. Predictions of a patient's postprandial glucose at 5-h intervals are used to predict the risk for a given therapy. Then the insulin dose and injection-to-meal time with the lowest risk are calculated. The method has been validated for three different scenarios corresponding to preprandial glucose values of 100, 180 and 250 mg/dl.

Changes in blood pancreatic polypeptide and ghrelin concentrations in response to feeding in sheep1

The roles of pancreatic polypeptide (PP) have not been determined in ruminant animals. The aim of the present study was to examine the role of PP in the regulation of ghrelin secretion in sheep. Two experiments were conducted using four 2-yr-old Suffolk wethers fed a maintenance diet of alfalfa hay cubes. In Exp. 1, the effects of feeding on blood ghrelin and PP concentrations were examined in scheduled-fed sheep. Blood samples were collected every 10 min from 30 min before to 360 min after feeding. Plasma PP concentrations were transiently increased from the preprandial average value to the values from 30 to 60 min after feeding and gradually decreased (P < 0.05) to stable values from 150 to 180 min. The values from 30 to 60 min were greater (P < 0.05) than those from 150 to 360 min. In contrast, plasma ghrelin concentrations were gradually decreased (P < 0.01) by feeding. The values from 60 to 360 min were less (P < 0.01) than the preprandial average value. In Exp. 2, the effects of continuous PP infusion on ghrelin secretion were examined in feed-deprived sheep. The animals were deprived of feed for 48 h before PP infusion. The PP-treated group intravenously received synthetic bovine PP at a rate of 10 pmol.kg(-1 )of BW.min(-1) for 180 min. Blood samples were collected every 10 min from 30 min before to 180 min after the commencement of PP infusion. Plasma PP concentrations reached a plateau within 30 min after the commencement of PP infusion. Plasma ghrelin concentrations were decreased (P = 0.002, 0.016, 0.007) by PP infusion at 160, 170, and 180 min, respectively. In conclusion, plasma ghrelin and PP concentrations were decreased and increased, respectively, in response to feeding in ruminant animals. Furthermore, PP could depress ghrelin secretion.

Associations Between Features of Glucose Exposure and A1C

OBJECTIVEVarious methods are used to quantify postprandial glycemia or glucose variability, but few have been compared and none are standardized. Our objective was to examine the relationship among common indexes of postprandial glycemia, overall hyperglycemia, glucose variability, and A1C using detailed glucose measures obtained during everyday life and to study which blood glucose values of the day provide the strongest prediction of A1C.RESEARCH DESIGN AND METHODSIn the A1C-Derived Average Glucose (ADAG) study, glucose levels were monitored in 507 participants (268 type 1 diabetic, 159 type 2 diabetic, and 80 nondiabetic subjects) with continuous glucose monitoring (CGM) and frequent self-monitoring of blood glucose (SMBG) during 16 weeks. We calculated several indexes of glycemia and analyzed their intercorrelations. The association between glucose measurements at different times of the day (pre- and postprandial) and A1C was examined using multiple linear regression.RESULTSIndexes of glucose variability showed strong intercorrelation. Among postprandial indexes, the area under the glucose curve calculated from CGM 2 h after a meal correlated well with the 90-min SMBG postprandial measurements. Fasting blood glucose (FBG) levels were only moderately correlated with indexes of hyperglycemia and average or postprandial glucose levels. Indexes derived with SMBG strongly correlated with those from CGM. Some SMBG time points had a stronger association with A1C than others. Overall, preprandial glucose values had a stronger association with A1C than postprandial values for both diabetes types, particularly for type 2 diabetes.CONCLUSIONSIndexes of glucose variability and average and postprandial glycemia intercorrelate strongly within each category. Variability indexes are weakly correlated with the other categories, indicating that these measures convey different information. FBG is not a clear indicator of general glycemia. Preprandial glucose values have a larger impact on A1C levels than postprandial values.

Computing the Risk of Postprandial Hypo- and Hyperglycemia in Type 1 Diabetes Mellitus considering Intrapatient Variability and other Sources of Uncertainty

The objective of this article was to develop a methodology to quantify the risk of suffering different grades of hypo- and hyperglycemia episodes in the postprandial state. Interval predictions of patient postprandial glucose were performed during a 5-hour period after a meal for a set of 3315 scenarios. Uncertainty in the patient's insulin sensitivities and carbohydrate (CHO) contents of the planned meal was considered. A normalized area under the curve of the worst-case predicted glucose excursion for severe and mild hypo- and hyperglycemia glucose ranges was obtained and weighted accordingly to their importance. As a result, a comprehensive risk measure was obtained. A reference model of preprandial glucose values representing the behavior in different ranges was chosen by a xi(2) test. The relationship between the computed risk index and the probability of occurrence of events was analyzed for these reference models through 19,500 Monte Carlo simulations. The obtained reference models for each preprandial glucose range were 100, 160, and 220 mg/dl. A relationship between the risk index ranges <10, 10-60, 60-120, and >120 and the probability of occurrence of mild and severe postprandial hyper- and hypoglycemia can be derived. When intrapatient variability and uncertainty in the CHO content of the meal are considered, a safer prediction of possible hyper- and hypoglycemia episodes induced by the tested insulin therapy can be calculated.

Large-for-gestational-age infants of type 1 diabetic mothers: An effect of preprandial hyperglycemia?

Objective. To determine how the frequency, timing and magnitude of hyperglycemia are associated with large-for-gestational-age (LGA) infants in pregnancies complicated by type 1 diabetes.Methods. Charts from pregnant women with type 1 diabetes (n = 70) were reviewed. Indices of maternal glycemic control were determined for seven gestational periods (weeks 7–10, 11–15, 16–19, 20–24, 25–28, 29–32 and 33–38) and compared between women who delivered LGA infants and appropriate-for-gestational-age (AGA) infants.Results. Of the 70 pregnancies, 57% of the infants were LGA (4.3 ± 0.4 kg) and 43% were AGA (3.2 ± 0.4 kg). Total maternal weight gain and rate of weight gain were significantly higher in mothers with LGA infants. The glycemic variables associated with an LGA infant were percentage of preprandial values above target for weeks 11–15, 25–28 and 29–32, and percentage of all values above target for weeks 33–38. For the entire pregnancy, the strongest predictors of an LGA infant were percentage of preprandial blood glucose values above target during weeks 29–32 and maternal weight gain.Conclusions. In pregnant women with type 1 diabetes, frequent episodes of preprandial hyperglycemia in the third trimester significantly impact the development of LGA infants.

Effects of a patent ductus arteriosus on postprandial mesenteric perfusion in premature baboons.

Superior mesenteric artery flow increases after a feeding to meet the intestines' increased metabolic demands. Although a patent ductus arteriosus can affect superior mesenteric artery perfusion in nonfeeding infants, there is no information about its effects on the hyperemic response that follows a feeding. Our goal was to study the effects of a patent ductus arteriosus on superior mesenteric artery perfusion in preterm baboons. Preterm baboons were delivered at 67% gestation and ventilated for 14 days. Enteral feedings were begun and advanced per protocol. Feeding studies were performed between days 10 and 14. Thirty-one studies were performed in animals with a closed ductus; 21 studies in those with a moderate patent ductus arteriosus shunt (pulmonary-to-systemic blood flow ratio>or=2:1). Two-dimensional echocardiographic and Doppler examinations were performed before and 10 and 30 minutes after a feeding. The groups were similar in birth weights, feeding volumes, and age at time of study. During the preprandial period, baboons with a moderate patent ductus arteriosus had significantly lower blood pressures and systemic blood flows than animals with a closed ductus. Preprandial superior mesenteric artery-blood flow velocities did not differ between the open and closed ductus groups. Animals with a closed ductus increased their superior mesenteric artery-velocities (diastolic and mean) and decreased their superior mesenteric artery relative-vascular-resistance (mean blood pressure/mean superior mesenteric artery-velocity) by 10 minutes after the feeding. By 30 minutes after the feeding, the values were returning to their preprandial values. In contrast, in baboons in the patent ductus arteriosus group, there were no significant changes in superior mesenteric artery-velocity or resistance after the feeding, and superior mesenteric artery-velocities were significantly lower than those in the closed ductus group. A moderate patent ductus arteriosus shunt limits the ability of the preterm newborn baboon to increase its postprandial mesenteric blood flow velocity. We speculate that this may interfere with its ability to meet increased intestinal metabolic demands and may contribute to feeding difficulties.

Respuesta secretora de PYY1-36 y PYY3-36 en sujetos normales tras la ingesta de una comida mixta

Peptide YY (PYY) is a 36 amino acid peptide synthesized mostly by intestinal L cells. This peptide reaches its nadir during fasting and increases immediately after meals. After food intake, two molecular forms are released, PYY(1-36) and PYY(3-36). PYY(3-36) reduces food intake in both humans and rodents. There is scarce information about plasmatic concentrations of PYY, especially of PYY(3-36), after food ingestion, and their relationship to ghrelin. To study PYY(1-36) and PYY(3-36) secretory response after a mixed meal, and its relationship to total and acylated ghrelin secretion in healthy subjects. We studied eight healthy subjects, 4 women and 4 men, with a median age of 53 (range, 36-59) years. After an overnight fast, the subjects received either a mixed standard meal (400ml Isosource Energy® [159kcal/100ml]) or placebo (400ml of water) orally in random order on two different days. Blood samples were obtained at 0, 30, 45, 60 and 120 min for measurement of PYY(1-36), PYY(3-36), total ghrelin and acylated ghrelin. Comparisons were made by Wilcoxon's test. Numerical correlations were performed using Spearman's test. P-values ≤ 0.05 were considered significant. After a mixed meal, PYY(1-36) reached a peak of (median [range]) 141.5 (81-198) pg/ml. There was no response to placebo, with a peak of 92.5 (46-219) pg/ml (p=0.04). The area under the curve (AUC) of PYY(1-36) levels after a mixed meal were 14,865 (8,032-19,822) pg/ml/min and after placebo were 8,992 (4,455-21,382) pg/ml/min (p=0.06). After ingestion of a mixed meal, PYY(3-36) reached a peak of 92.5 (59-135) pg/ml, with no response to placebo (46.5 [30-66] pg/ml) (p = 0.02). The AUC of PYY(3-36) levels after a mixed meal were 9,086 (6,412-14,970) pg/ml/min, and after placebo were 4,984 (3,142-6,772) pg/ml/min (p=0.012). The quotient between nadir total ghrelin/peak PYY(1-36) was markedly diminished after food ingestion, with preprandial values of 7.44 (3.64-14.56) and postprandial values of 3.55 (1.64-7.16) (p=0.03). The former quotient was unmodified by placebo. The quotient between nadir acylated ghrelin/peak PYY(3-36) was markedly diminished after ingestion of a mixed meal, with preprandial values of 2.03 (0.92-3) and postprandial values of 0.73 (0.26-1.27) (p=0.02). This quotient was unmodified by placebo. In healthy subjects, blood levels of both PYY(1-36) and PYY(3-36) increase after ingestion of a mixed meal. Simultaneously, total and acylated ghrelin levels diminish. The quotient between nadir acylated ghrelin/peak PYY(3-36) diminishes after a mixed meal. All these data suggest the possible contribution of these peptides to appetite regulation after ingestion.

Self-Monitoring of Blood Glucose—Epidemiological and Practical Aspects

Self-monitoring of blood glucose (SMBG) is a cornerstone in glucose management. This paper is an oversight article and describes epidemiological and practical aspects of SMBG. It looks into the worldwide frequency of diabetes, the correlation of blood glucose and glycosylated hemoglobin (HbA1c), the effect of SMBG itself upon HbA1c, and confounders and sources of error of SMBG. Then it goes into recommendations for the use of SMBG in diabetes. Issues regarding the frequency of SMBG as well as goals are described. It also examines to what extent postprandial monitoring should be balanced with fasting and preprandial values.

Acyl and Total Ghrelin Are Suppressed Strongly by Ingested Proteins, Weakly by Lipids, and Biphasically by Carbohydrates

Ghrelin is an orexigenic hormone that can increase body weight. Its circulating levels increase before meals and are suppressed after food ingestion. Understanding the effects of specific types of ingested macronutrients on ghrelin regulation could facilitate the design of weight-reducing diets. We sought to understand how ingestion of carbohydrates, proteins, or lipids affect acyl (bioactive) and total ghrelin levels among human subjects, hypothesizing that lipids might suppress ghrelin levels less effectively than do either carbohydrates or proteins. This was a randomized, within-subjects cross-over study. The study was conducted at a University Clinical Research Center. There were 16 healthy human subjects included in the study. Isocaloric, isovolemic beverages composed primarily of carbohydrates, proteins, or lipids were provided. The magnitude of postprandial suppression of total and acyl ghrelin levels (measured with a novel acyl-selective, two-site ELISA) was determined. All beverages suppressed plasma acyl and total ghrelin levels. A significant effect of macronutrient class on decremental area under the curve for both acyl and total ghrelin was observed; the rank order for magnitude of suppression was protein more than carbohydrate more than lipid. Total ghrelin nadir levels were significantly lower after both carbohydrate and protein, compared with lipid beverages. In the first 3 postprandial hours, the rank order for acyl and total ghrelin suppression was carbohydrate more than protein more than lipid. In the subsequent 3 h, there was a marked rebound above preprandial values of acyl and total ghrelin after carbohydrate ingestion alone. These findings suggest possible mechanisms contributing to the effects of high-protein/low-carbohydrate diets to promote weight loss, and high-fat diets to promote weight gain.

Parameters Affecting Postprandial Blood Glucose: Effects of Blood Glucose Measurement Errors

The Diabetes Error Test Model (DETM) has been developed to characterize the clinical relevance of the large and varying margins of error of parameters affecting postprandial blood glucose (BG) levels, which increase the risk for hypo- or hyperglycemia. The DETM is based on a treatment concept aimed at normoglycemia after meals. The model includes as parameters (a) preprandial BG measurement by patient self-monitoring (SMBG), (b) patient estimate of carbohydrate amounts (CARB-P) in food, (c) effect of CARB-P on maximum BG increase, (d) effect of insulin on maximum BG decrease, and (e) insulin dosage. Covering the relevant range of preprandial BG (30-330 mg/dl), the DETM simulates the maximum effect of these parameters and their margins of error on postprandial BG values. According to the DETM, a SMBG error of +20% results in normoglycemia (BG range: 60-160 mg/dl) as the postprandial outcome if preprandial BG values are in the range of 30-130 or 260-330 mg/dl, but can unexpectedly result in hypoglycemia if preprandial BG values are between 131 and 259 mg/dl. If the SMBG error of +20% is combined, e.g., with an error of CARB-P estimate in the food of +20%, hypoglycemia as the postprandial outcome is worsened. If one combines the effects of errors of more than two parameters, even with errors that are so small that they have no clinically relevant dysglycemic effect on postprandial BG per se (e.g., +/-6%), this can result in postprandial hypo- or hyperglycemic values. The DETM simulates the effects of errors of parameters affecting postprandial BG within the clinically relevant BG range. The DETM offers the opportunity to evaluate the clinical relevance of these errors and their contribution to the increased risk of meal-related excessive glucose excursions during intensified insulin therapy.

Protein metabolism in adult patients with phenylketonuria

Objective Protein intake recommendations in phenylketonuria (PKU) are frequently the subject of discussion. For healthy adults, the recommended daily allowance (RDA) is 0.8 g · kg −1 · d −1, which is generally lower than that observed in the general Western population. We investigated whether whole-body protein metabolism in patients with PKU is comparable to that of healthy controls at a RDA rate of protein intake. Methods Six adult patients with well-controlled PKU and six healthy subjects of comparable age, height, and weight were studied using a primed continuous infusion of [1- 13C]-valine for 8 h after an overnight fast before and during frequent meals. Normal protein was given to controls, whereas patients with PKU received a combination of an amino acid mixture and natural protein. Results No significant differences were observed between patients with PKU and controls in preprandial and prandial rates of valine appearance and oxidation and protein breakdown, protein synthesis, and net protein balance. Feeding resulted in a significant ( P < 0.01) decrease in protein breakdown (PKU: 94 ± 15 μmol · kg −1 · h −1 preprandial to 49 ± 10 μmol · kg −1 · h −1 prandial; controls: 97 ± 10 μmol · kg −1 · h −1 preprandial to 55 ± 10 μmol · kg −1 · h −1 prandial), whereas no effects were observed in protein synthesis (PKU: 77 ± 10 μmol · kg −1 · h −1 preprandial to 73 ± 7 μmol · kg −1 · h −1 prandial; controls: 76 ± 8 μmol · kg −1 · h −1 preprandial to 71 ± 5 μmol · kg −1 · h −1 prandial). Net protein balance increased from negative prandial to positive preprandial values (PKU: −17 ± 6 μmol · kg −1 · h −1 preprandial to +23 ± 8 μmol · kg −1 · h −1 prandial; controls: −21 ± 4 μmol · kg −1 · h −1 preprandial to +16 ± 9 μmol · kg −1 · h −1 prandial). Conclusion Whole-body protein metabolism in adult patients with PKU is fully comparable to that in healthy controls at the RDA level of protein intake.

The effect of acute exercise on endothelial function following a high-fat meal

The transient impairment of endothelial function following a high-fat meal is well established. Brachial artery flow-mediated dilation (FMD) decreases between 2 and 6 h post ingestion. Whether this impairment can be reduced with acute aerobic exercise has not been investigated. The purpose of this study was to investigate if a single sustained aerobic exercise session can counteract the postprandial attenuation in brachial artery FMD associated with the ingestion of a high-fat meal. Eight apparently healthy adults (five men, three women), age 25.5 +/- 0.8 years, performed three treatment conditions in a counter-balanced design: (1) low-fat meal alone (LFM), (2) high-fat meal alone (HFM), and (3) one session of aerobic exercise presented 2 h after ingesting a high-fat meal (HFM-EX). The examination of brachial artery FMD was performed at baseline and 4 h following the ingestion of the meal for each treatment condition. A 3 x 2 (treatment x time) repeated measures ANOVA exhibited a significant interaction (P = 0.019). Preprandial FMDs were similar (P = 0.863) among all three treatment conditions. The FMDs following the LFM (7.18 +/- 1.31%) and HFM-EX (8.72 +/- 0.94%) were significantly higher (P = 0.001) than the FMD following the HFM (4.29 +/- 1.64%). FMD was significantly elevated above preprandial values following the HFM-EX (5.61 +/- 1.54 to 8.72 +/- 0.94%, P = 0.005) but was unchanged following the LFM (6.17 +/- 0.94 to 7.18 +/- 1.31%, P = 0.317) and the HFM (5.73 +/- 1.23 to 4.29 +/- 1.64%, P = 0.160). These findings suggest that a single aerobic exercise session cannot only counteract the postprandial endothelial dysfunction induced by the ingestion of a high-fat meal, but also increase brachial artery FMD in apparently healthy adults.