Добірка наукової літератури з теми "Glycemic excursions"

Studies on nutrient sequences during meals suggest that consuming carbohydrates last lowers postprandial glucose excursions more than consuming carbohydrates first. However, this phenomenon has not been studied in gestational diabetes mellitus (GDM). Ten women with GDM consumed the same caloric foods in different sequences over five successive days: (A) dish first, followed by carbohydrate and soup last; (B) carbohydrate first, followed by dish and soup last; (C) soup first, followed by dish and carbohydrate last; (D) three meals a day ad libitum; and (E) six meals a day as ad libitum. Continuous glucose monitoring (CGM) was used to assess diurnal glycemia. Decreases in mean glucose levels and the largest glucose levels in A were similar to group C. The peak glucose of breakfast and lunch in group B was more significant than in groups A and C. The B meal pattern showed more marked glycemic excursions than groups A and C. Increasing the number of meals reduced the peak glucose level and the glycemic excursions with the same total calories. Changing meal sequences or increasing the number of meals may reduce glycemic excursions in GDM. Our trial was registered retrospectively and the trial registration number is ChiCTR2200057044.

ABSTRACT Background The breakfast meal often results in the largest postprandial hyperglycemic excursion in people with type 2 diabetes. Objective Our purpose was to investigate whether restricting carbohydrates at breakfast would be a simple and feasible strategy to reduce daily exposure to postprandial hyperglycemia. Design Adults with physician-diagnosed type 2 diabetes [n = 23; mean ± SD age: 59 ± 11 y; glycated hemoglobin: 6.7% ± 0.6%; body mass index (kg/m2): 31 ± 7] completed two 24-h isocaloric intervention periods in a random order. Participants consumed one of the following breakfasts: 1) a very-low-carbohydrate high-fat breakfast (LCBF; <10% of energy from carbohydrate, 85% of energy from fat, 15% of energy from protein) or 2) a breakfast with dietary guidelines–recommended nutrient profile (GLBF; 55% of energy from carbohydrate, 30% of energy from fat, 15% of energy from protein), with the same lunch and dinner provided. Continuous glucose monitoring was used to assess postprandial glucose responses over 24 h, and visual analog scales were used to assess ratings of hunger and fullness. Results The LCBF significantly reduced postprandial hyperglycemia after breakfast (P < 0.01) and did not adversely affect glycemia after lunch or dinner. As such, overall postprandial hyperglycemia (24-h incremental area under the glucose curve) and glycemic variability (mean amplitude of glycemic excursions) were reduced with the LCBF (24-h incremental area under the glucose curve: −173 ± 361 mmol/L; P = 0.03; mean amplitude of glycemic excursions: −0.4 ± 0.8 mmol/L · 24 h; P = 0.03) compared with the GLBF. Premeal hunger was lower before dinner with the LCBF than with the GLBF (P-interaction = 0.03). Conclusions A very-low-carbohydrate high-fat breakfast lowers postbreakfast glucose excursions. The effects of this simple strategy appear to be sufficient to lower overall exposure to postprandial hyperglycemia and improve glycemic variability. Longer-term interventions are warranted. This trial was registered at clinicaltrials.gov as NCT02982330.

Background: Most standalone real-time continuous glucose monitoring (RT-CGM) systems provide predictive low and high sensor glucose (SG) threshold alerts. The durations and risk of low and high SG excursions following Guardian™ Connect CGM system predictive threshold alerts were evaluated. Methods: Continuous glucose monitoring system data uploaded between January 2, 2017 and May 22, 2018 by 3133 individuals using multiple daily injections (MDIs) or continuous subcutaneous insulin infusion (CSII) therapy were deidentified and retrospectively analyzed. Glucose excursions were defined as SG values that went beyond a preset low or high SG threshold for ≥15 minutes. For a control group, thresholds were based on the median of the low SG threshold limit (70 mg/dL) and the high SG threshold limit (210 mg/dL) preset by all system users. During periods when alerts were not enabled, timestamps were identified when a predictive alert would have been triggered. The time before low horizon was 17.5 minutes and the time before high horizon was 15 minutes, of all users who enabled alerts. Excursions occurring after a low SG or high SG predictive alert were segmented into prevented, ≤20, 20-60, and >60 minutes. Results: Excursions were prevented after 59% and 39% of low and high SG predictive alerts, respectively. The risk of a low or high excursion occurring was 1.9 ( P < 0.001, 95% CI, 1.88-1.93) and 3.3 ( P < 0.001, 95% CI, 3.20-3.30) times greater, respectively, when alerts were not enabled. Conclusions: The predictive alerts of the RT-CGM system under study can help individuals living with diabetes prevent some real-world low and high SG excursions. This can be especially important for those unable to reach or maintain glycemic control with basic RT-CGM or CSII therapy.

Purpose. Patients treated with therapeutic hypothermia (TH) and continuous insulin may be at increased risk of hyperglycemia or hypoglycemia, particularly during temperature transitions. This study aimed to evaluate frequency of glucose excursions during each phase of TH and to characterize glycemic control patterns in relation to survival.Methods. Patients admitted to a tertiary care hospital for circulatory arrest and treated with both therapeutic hypothermia and protocol-based continuous insulin between January 2010 and June 2013 were included. Glucose measures, insulin, and temperatures were collected through 24 hours after rewarming.Results. 24 of 26 patients experienced glycemic excursions. Hyperglycemic excursions were more frequent during initiation versus remaining phases (36.3%, 4.3%, 2.5%, and 4.0%,p=0.002). Hypoglycemia occurred most often during rewarming (0%, 7.7%, 23.1%, and 3.8%,p=0.02). Patients who experienced hypoglycemia had higher insulin doses prior to rewarming (16.2 versus 2.1 units/hr,p=0.03). Glucose variation was highest during hypothermia and trended higher in nonsurvivors compared to survivors (13.38 versus 9.16,p=0.09). Frequency of excursions was also higher in nonsurvivors (32.3% versus 19.8%,p=0.045).Conclusions. Glycemic excursions are common and occur more often in nonsurvivors. Excursions differ by phase but risk of hypoglycemia is increased during rewarming.

ABSTRACT Background High postprandial glucose excursions may increase risk for disease. Individuals have widely varying glucose responses to different meals, and precision nutrition approaches often seek to personalize diets to minimize postprandial glycemic responses as measured by continuous glucose monitors (CGMs). However, it is unknown whether different CGM devices result in concordant meal rankings according to postprandial glycemic excursions. Objective We explored whether meal rankings according to postprandial glycemic excursions differ between 2 simultaneously worn CGMs. Methods We collected 27,489 simultaneous measurements from Dexcom G4 Platinum and Abbott Freestyle Libre Pro CGMs during 28 inpatient days in 16 adults without diabetes. Simultaneous glucose measurements obtained for 2 h following 760 ad libitum meals were used to compare within-subject meal rankings between the CGM devices according to their incremental glucose response. Results Postprandial responses to ad libitum meals were highly variable, with the Abbott and Dexcom systems resulting in within-subject incremental mean ± SD glucose CVs of 91.7 ± 1.9% and 94.2 ± 2.7%, respectively. Within-subject meal rankings for incremental glycemic responses were relatively discordant between CGMs, with a mean Kendall rank correlation coefficient of 0.43 ± 0.05. Meals in the bottom compared with those in the top half of incremental glycemic responses ranked by Abbott resulted in 50 ± 10% (P = 0.0002) less glycemic reduction as measured by Dexcom, and vice versa. The missing glycemic reduction by eating meals ranked according to the discordant CGM was inversely correlated with each subject's Kendall rank correlation coefficient (r = −0.95; P &lt; 0.0001). Conclusions Precision nutrition approaches that use CGMs to personalize meal recommendations for minimizing glycemic excursions may be premature given the discordance of within-subject meal rankings between simultaneous CGM devices. More research is needed to clarify the source of this imprecision. This trial was registered at clinicaltrials.gov as NCT03407053.

This article reviews the role of fasting and postprandial glycemia to the overall glycemic control of patients with type 2 diabetes and glucose intolerance, as well as their causal relationship upon micro and macrovascular complications. Recent studies have suggested that a third component of the glucose triad, the postprandial glucose excursions, might have a role in the overall glycemic load and might also reflect glycemic control. Epidemiological and intervention studies are presented in the article, supporting the conclusion that postprandial hyperglycemia in impaired glucose tolerance and diabetic subjects is a more powerful marker of cardiovascular disease risk than fasting hyperglycemia, then the treatment directed at specifically lowering postprandial glucose is crucial, as underlined by the American Diabetes Association.

Type 2 diabetes (T2D) is a rapidly growing yet largely preventable chronic disease. Exaggerated increases in blood glucose concentration following meals is a primary contributor to many long-term complications of the disease that decrease quality of life and reduce lifespan. Adverse health consequences also manifest years prior to the development of T2D due to underlying insulin resistance and exaggerated postprandial concentrations of the glucose-lowering hormone insulin. Postprandial hyperglycemic and hyperinsulinemic excursions can be improved by exercise, which contributes to the well-established benefits of physical activity for the prevention and treatment of T2D. The aim of this review is to describe the postprandial dysmetabolism that occurs in individuals at risk for and with T2D, and highlight how acute and chronic exercise can lower postprandial glucose and insulin excursions. In addition to describing the effects of traditional moderate-intensity continuous exercise on glycemic control, we highlight other forms of activity including low-intensity walking, high-intensity interval exercise, and resistance training. In an effort to improve knowledge translation and implementation of exercise for maximal glycemic benefits, we also describe how timing of exercise around meals and post-exercise nutrition can modify acute and chronic effects of exercise on glycemic control and insulin sensitivity. Novelty: Exaggerated postprandial blood glucose and insulin excursions are associated with disease risk. Both a single session and repeated sessions of exercise improve postprandial glycemic control in individuals with and without T2D. The glycemic benefits of exercise can be enhanced by considering the timing and macronutrient composition of meals around exercise.

Postprandial hyperglycemia (PPHG) is strongly linked with the future development of cardiovascular complications in type 2 diabetes (T2D). Hence, reducing postprandial glycemic excursions is essential in T2D treatment to slow progressive deficiency of β-cell function and prevent cardiovascular complications. Most of the metabolic processes involved in PPHG, i.e., β-cell secretory function, GLP-1 secretion, insulin sensitivity, muscular glucose uptake, and hepatic glucose production, are controlled by the circadian clock and display daily oscillation. Consequently, postprandial glycemia displays diurnal variation with a higher glycemic response after meals with the same carbohydrate content, consumed at dusk compared to the morning. T2D and meal timing schedule not synchronized with the circadian clock (i.e., skipping breakfast) are associated with disrupted clock gene expression and is linked to PPHG. In contrast, greater intake in the morning (i.e., high energy breakfast) than in the evening has a resetting effect on clock gene oscillations and beneficial effects on weight loss, appetite, and reduction of PPHG, independently of total energy intake. Therefore, resetting clock gene expression through a diet intervention consisting of meal timing aligned to the circadian clock, i.e., shifting most calories and carbohydrates to the early hours of the day, is a promising therapeutic approach to improve PPHG in T2D. This review will focus on recent studies, showing how a high-energy breakfast diet (Bdiet) has resetting and synchronizing actions on circadian clock genes expression, improving glucose metabolism, postprandial glycemic excursions along with weight loss in T2D.

Background: Postprandial glycemic excursions are associated with impairment control of diabetes mellitus. Long-term consumption of flaxseed can lower blood glucose levels; however, its effects on the postprandial glycemic response remain unknown. Therefore, this study aimed to evaluate the acute effects of raw flaxseed consumption on the 2 h postprandial glycemic curve in men with type 2 diabetes mellitus (T2DM). Methods: This was a randomized crossover clinical trial. Nineteen men with T2DM were randomly assigned a standardized breakfast without (control) or with a previous intake of 15 g of ground raw golden flaxseed (flax). Glycemia was measured at fasting and postprandial at 15, 30, 45, 60, 90, and 120 min. Palatability markers (visual appeal, smell, and pleasantness of taste) and taste intensity (sweetness, saltiness, bitterness, sourness, and creaminess) were evaluated. Results: The peak glucose rise and the 2 h AUC glycemic response reduced in the flax group by 17% (p = 0.001) and 24% (p < 0.001), respectively. The glucose peak time, palatability, and taste parameters did not differ between the two groups. Conclusions: Ingestion of 15 g of ground raw golden flaxseed before breakfast decreases the 2 h postprandial glycemic response in men with T2DM.

1,5 AG is a six carbon chain monosaccharide and is one of the major polyols present in humans. The approximate normal levels of 1,5AG are about 20 -40 µg/mL. The main source of 1,5AG is diet containing carbohydrates, and this 1,5AG undergoes similar metabolic pathways like other saccharides and is distributed in all organs and tissues. Once DM is confirmed and treatment initiated, it is important to monitor glycemic control at regular intervals of time. While HbA1c has been used as a gold standard to monitor diabetic control during the preceding 2-3 months, GA and FA were used to monitor short time glycemic control. But none of the above three serves to monitor glycemic excursion after meals. 1,5AG has been emerging as an alternative short-term diabetic control monitoring marker to assess short term glycemic excursions. 1,5 AG has also been found to be useful to monitor CVD, CLD patients as well in the clinical usefulness of subtypes of DM. This review article gives a condensed version of research findings during the last two decades and will be very useful for future researchers to expand the clinical usefulness of 1,5AG in other areas of human health.

Le diabète de type 1 (DT1) se caractérise par la destruction auto-immune des cellules ß des îlots de Langerhans du pancréas productrices d'insuline, entraînant un état d'hyperglycémie chronique. Malgré une prise en charge très fine de la maladie, s'appuyant sur l'insulinothérapie fonctionnelle, les personnes vivant avec le DT1 sont fréquemment sujettes à des épisodes hypoglycémiques et hyperglycémiques en raison de difficultés à adapter le traitement insulinique, notamment lors de l'activité physique. L'activité physique procure de nombreux bénéfices pour la santé que l'on ait ou non un diabète. Cependant, dans le cadre du DT1, les excursions glycémiques lors de l'activité physique peuvent conduire à des barrières à l'activité physique dans cette population ou peuvent limiter les performances sportives d'athlètes vivant avec le DT1.L'objectif de cette thèse était triple : 1) S'intéresser aux barrières à l'activité physique chez les enfants et adultes vivant avec le DT1 et à leurs liens avec les excursions glycémiques réellement vécues dans la vie quotidienne et d'autant plus autour de l'activité physique, 2) Chez des enfants vivant avec le DT1, comparer deux modalités d'exercice (exercice aérobie continu vs. intermittent intense), représentatifs de leur activité physique spontanée, et explorer leurs effets sur les variations glycémiques à l'exercice et à la récupération précoce et tardive et, 3) Mesurer la glycémie en continu, à l'exercice et à la récupération, chez des sportifs en endurance qui n'ont pas de diabète, afin de comprendre les mécanismes impliqués dans la régulation de la glycémie lors d'épreuves d'ultra-endurance et de transposer ces résultats chez des sportifs vivant avec le DT1.Les résultats montrent que : 1) Chez les enfants, plus le temps passé à <54 mg/dL les nuits suivant les séances d'activités physiques augmente, plus la peur de l'hypoglycémie est importante. Chez les adultes, étonnamment, ceux qui déclarent le moins l'hypoglycémie comme une barrière à l'activité physique sont ceux qui ont le plus grand pourcentage de séances d'activités physiques entraînant une baisse de glycémie; 2) Le risque hypoglycémique n'est pas supérieur lors d'un exercice continu modéré représentatif de l'activité physique spontanée des enfants, et cet exercice semble même avoir un effet protecteur vis-à-vis de l'hyperglycémie transitoire retrouvée en récupération de l'exercice intermittent intense; 3) Un risque hyperglycémique existe lors des phases intenses de la course et pendant 48 heures de récupération lors d'un ultra-trail réalisé chez des athlètes qui n'ont pas de diabète. Ce risque hyperglycémique à la récupération pourrait être en lien avec les dommages musculaires
Type 1 diabetes (T1D) is characterized by the autoimmune destruction of the insulin-producing ß-cells of the islets of Langerhans in the pancreas, leading to a state of chronic hyperglycemia. Despite very sophisticated management of the disease, based on functional insulin therapy, people living with T1D are frequently subject to hypoglycemic and hyperglycemic episodes because of difficulties in adapting insulin treatment, particularly during physical activity. Physical activity has many health benefits, whether or not you have diabetes. However, in the context of T1D, glycemic excursions during physical activity may lead to barriers to physical activity in this population or may limit the sporting performance of athletes living with T1D.The aim of this thesis was threefold: 1) Investigate the barriers to physical activity in children and adults living with T1D and their links with the glycemic excursions actually experienced in daily life and all the more so around physical activity, 2) In children living with T1D, compare two exercise modalities (continuous aerobic exercise vs. intense intermittent), representative of their spontaneous physical activity, and explore their effects on glycemic variations during exercise and early and late recovery, and 3) Measure glycemia continuously, during exercise and recovery, in endurance athletes without diabetes in order to understand the mechanisms involved in regulating glycaemia during ultra-endurance events and transpose these results to athletes living with T1D.The results show that: 1) In children, the greater the time spent at <54 mg/dL on the nights following physical activity sessions, the greater the fear of hypoglycemia. Surprisingly, among adults, those who least reported hypoglycemia as a barrier to physical activity were those who had the highest percentage of physical activity sessions resulting in a drop in blood glucose levels; 2) The risk of hypoglycemia is no greater during moderate continuous exercise representative of the spontaneous physical activity of children, and that this exercise even seems to have a protective effect against the transient hyperglycemia found during recovery from intense intermittent exercise; 3) A hyperglycemic risk exists during the intense phases of the race and during 48 hours of recovery during an ultra-trail run carried out in athletes who do not have diabetes. This hyperglycemic risk during recovery could be related to muscle damage