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Sebastien F M Chastin - One of the best experts on this subject based on the ideXlab platform.
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impact of free living pattern of sedentary behaviour on intra day glucose regulation in type 2 diabetes
European Journal of Applied Physiology, 2020Co-Authors: Aye C Paing, Kathryn Anne Mcmillan, Alison Kirk, Andrew Collier, Allan Hewitt, Sebastien F M ChastinAbstract:To investigate how the pattern of sedentary behaviour affects intra-day glucose regulation in type 2 diabetes. This intensive longitudinal study was conducted in 37 participants with type 2 diabetes (age, 62.8 ± 10.5 years). Glucose and sedentary behaviour/physical activity were assessed with a continuous glucose monitoring (Abbott FreeStyle Libre) and an activity monitor (activPAL3) for 14 days. Multiple regression models with generalised estimating equations (GEEs) approach were used to assess the associations of sedentary time and breaks in sedentary time with pre-breakfast glucose, pre-lunch glucose, pre-dinner glucose, post-breakfast glucose, post-lunch glucose, post-dinner glucose, bedtime glucose, the Dawn Phenomenon, time in target glucose range (TIR, glucose 3.9–10 mmol/L) and time above target glucose range (TAR, glucose > 10 mmol/L). Sedentary time was associated with higher pre-breakfast glucose (p = 0.001), pre-dinner glucose (p < 0.001), post-lunch glucose (p = 0.005), post-dinner glucose (p = 0.013) and the Dawn Phenomenon (p < 0.001). Breaks in sedentary time were associated with lower pre-breakfast glucose (p = 0.023), pre-dinner glucose (p = 0.023), post-breakfast glucose (p < 0.001) and the Dawn Phenomenon (p = 0.004). The association between sedentary time and less TIR (p = 0.022) and the association between breaks in sedentary time and more TIR (p = 0.001) were also observed. Reducing sedentary time and promoting breaks in sedentary time could be clinically relevant to improve intra-day glucose regulation in type 2 diabetes.
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dose response between frequency of interruption of sedentary time and fasting glucose the Dawn Phenomenon and night time glucose in type 2 diabetes
Diabetic Medicine, 2019Co-Authors: Aye C Paing, Kathryn Anne Mcmillan, Alison Kirk, Andrew Collier, Allan Hewitt, Sebastien F M ChastinAbstract:AIM To explore the dose-response between frequency of interruption of sedentary time and basal glucose (fasting glucose, the Dawn Phenomenon and night-time glucose) in Type 2 diabetes. METHODS In a randomized three-treatment, two-period balanced incomplete block trial, 12 people with Type 2 diabetes (age, 60.0 ± 3.2 years; BMI, 30.2 ± 1.4 kg/m2 ) completed two of three conditions: sitting for 7 h interrupted every 60 min (Condition 1), 30 min (Condition 2), and 15 min (Condition 3) by 3-min light-intensity walking breaks. The activPAL3 and FreeStyle Libre were used to assess physical activity/sedentary behaviour and continuous glucose profile. Standardized meals were provided, and changes in basal glucose of the nights and early mornings before and after treatment conditions were calculated (mean ± SE). RESULTS After treatment conditions, fasting glucose and duration of the Dawn Phenomenon were lower for Condition 3 (-1.0 ± 0.2 mmol/l, P < 0.02; -3.1 ± 1.3 h, P = 0.004) compared with Condition 1 (-0.1 ± 0.2 mmol/l; 1.9 ± 1.2 h). The magnitude of the Dawn Phenomenon was reduced in Condition 3 (-0.6 ± 0.4 mmol/l, P = 0.041) compared with Condition 2 (0.6 ± 0.3 mmol/l). Night-time glycaemic variability (coefficient of variation) was reduced in Condition 3 (-9.7 ± 3.9%) relative to Condition 2 (6.1 ± 4.8%, P < 0.03) and Condition 1 (2.5 ± 1.8%, P = 0.02). There was no change in night-time mean glucose. CONCLUSIONS Frequent interruptions of prolonged sitting with 3 min of light-intensity walking breaks every 15 min improves fasting glucose, the Dawn Phenomenon and night-time glycaemic variability, and this might be a simple therapeutic intervention to improve glucose control. Clinicaltrials.gov Identifier: NCT02738996.
David R Owens - One of the best experts on this subject based on the ideXlab platform.
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the Dawn Phenomenon in type 2 diabetes how to assess it in clinical practice
Diabetes & Metabolism, 2015Co-Authors: L Monnier, C Colette, Sylvie Dejager, David R OwensAbstract:Abstract Aim The 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. Methods A 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. Results All pre-meal glucose levels and differences from pre-breakfast values (Δpre-meal) significantly correlated ( P 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. Conclusion The 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.
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response to comment on monnier et al magnitude of the Dawn Phenomenon and its impact on the overall glucose exposure in type 2 diabetes is this of concern diabetes care 2013 36 4057 4062
Diabetes Care, 2014Co-Authors: L Monnier, C Colette, S Dejager, David R OwensAbstract:Carr and Alexander (1) raise the question as to why we have classified dipeptidyl peptidase-4 (DPP-4) inhibitors as insulin secretagogues and not taken into account the features that differentiate DPP-4 inhibitors from older insulin secretagogues. First, there is cogent evidence that the actions of DPP-4 inhibitors are not solely restricted to a stimulatory effect on the insulin release by β-cells and that these agents also act through several additional effects, such as their inhibitory action on glucagon release (2). As a consequence, these drugs represent a new class of antidiabetes agents; for that reason, we …
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magnitude of the Dawn Phenomenon and its impact on the overall glucose exposure in type 2 diabetes is this of concern
Diabetes Care, 2013Co-Authors: L Monnier, C Colette, Sylvie Dejager, David R OwensAbstract:OBJECTIVE To assess the magnitude of the Dawn Phenomenon and its impact on the total glucose exposure in type 2 diabetes. RESEARCH DESIGN AND METHODS A total of 248 noninsulin-treated persons with type 2 diabetes who underwent continuous glucose monitoring were divided into three groups selected by treatments: diet alone ( n = 53); insulin sensitizers alone ( n = 82); and insulin secretagogues alone or in combination with insulin sensitizers ( n = 113). The Dawn Phenomenon (∂ glucose, mg/dL) was quantified by its absolute increment from nocturnal nadir to prebreakfast value. The participants were secondarily divided into two paired subsets after they had been separated by the presence/absence of a Dawn Phenomenon based on a threshold of 20 mg/dL and matched for glucose nadir. The impact of the Dawn Phenomenon was assessed on HbA 1c and 24-h mean glucose. RESULTS The median of ∂ glucose (interquartile range) was 16.0 (0–31.5 mg/dL) in the 248 subjects, and no differences were observed across groups selected by HbA 1c or treatments. In the overall population, the mean impacts on HbA 1c and 24-h mean glucose were 4.3 ± 1.3 mmol/mol (0.39 ± 0.12%) and 12.4 ± 2.4 mg/dL, respectively. The mean impact on 24-h mean glucose was not statistically different between those on diet alone (16.7 ± 5.9 mg/dL) compared with the two subsets treated with oral hypoglycemic agents (11.2 ± 5.3 and 8.5 ± 7.5 mg/dL). CONCLUSIONS The impact of the Dawn Phenomenon on overall glycemic control in type 2 diabetes, as depicted by the HbA 1c level, was ∼0.4% and not eliminated by any of the currently available armamentarium of oral antidiabetes agents.
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frequency and severity of the Dawn Phenomenon in type 2 diabetes relationship to age
Diabetes Care, 2012Co-Authors: L Monnier, C Colette, Mathieu Sardinoux, Gregory Baptista, Alyne Regnierzerbib, David R OwensAbstract:OBJECTIVE To know whether age has an independent effect on the Dawn Phenomenon in noninsulin-using type 2 diabetes. RESEARCH DESIGN AND METHODS Eighty-one individuals with type 2 diabetes were matched for HbA 1c and divided by age into three subgroups of 27 individuals (1: ≥70 years; 2: 60–69 years; and 3: ≤59 years). All underwent ambulatory continuous glucose monitoring for quantifying the Dawn Phenomenon (i.e., the absolute [∂G, mg/dL] or relative [∂G%] increments from nocturnal nadirs to prebreakfast time points). RESULTS HbA 1c levels and 24-h glycemic profiles were similar across the three groups. Glucose increments (mean ± SEM) were identical in the three groups: ∂G (mg/dL), 22.0 ± 4.7 (1), 21.3 ± 3.6 (2), and 18.0 ± 3.6 (3) and δG (%), 19.9 ± 4.9 (1), 21.6 ± 4.4 (2), and 17.6 ± 4.2 (3). Using the most common definition (∂G >10 mg/dL), the prevalence of the Dawn Phenomenon was 52, 70, and 59% in groups 1, 2, and 3, respectively. CONCLUSIONS The Dawn Phenomenon is present in the elderly.
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the loss of postprandial glycemic control precedes stepwise deterioration of fasting with worsening diabetes
Diabetes Care, 2007Co-Authors: L Monnier, C Colette, Gareth Dunseath, David R OwensAbstract:OBJECTIVE — The aim of the study was to determine whether the loss of fasting and postprandial glycemic control occurs in parallel or sequentially in the evolution of type 2 diabetes. RESEARCH DESIGN AND METHODS — In 130 type 2 diabetic patients, 24-h glucose profiles were obtained using a continuous glucose monitoring system. The individuals with type 2 diabetes were divided into five groups according to A1C levels: 1 ( n = 30), 2 (6.5–6.9%, n = 17), 3 (7–7.9%, n = 32), 4 (8–8.9%, n = 25), and 5 (≥9%, n = 26). The glucose profiles between the groups were compared. The overall glucose concentrations for the diurnal, nocturnal, and morning periods, which represent the postprandial, fasting, and the Dawn Phenomenon states, respectively, were also compared. RESULTS — Glucose concentrations increased steadily from group 1 to 5 in a stepwise manner. The initial differences in mean glucose concentrations reaching statistical significance occurred 1 ) between groups 1 and 2 (6.4 vs. 7.7 mmol/l, P = 0.0004) for daytime postprandial periods, followed by differences; 2 ) between groups 2 and 3 (7.5 vs. 9.3 mmol/l, P = 0.0003) for the morning periods (Dawn Phenomenon); and finally 3 ) between groups 3 and 4 (6.3 vs. 8.4 mmol/l, P CONCLUSIONS — The deterioration of glucose homeostasis in individuals with type 2 diabetes progressed from postprandial to fasting hyperglycemia following a three-step process. The first step related to the three diurnal postmeal periods considered as a whole, the second step occurred during the morning period, and the third and final step corresponded to sustained hyperglycemia over the nocturnal fasting periods. Such a description of the key stages in the evolution of type 2 diabetes may be of interest for implementing antidiabetes treatment.
Geremia B Bolli - One of the best experts on this subject based on the ideXlab platform.
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thirty years of research on the Dawn Phenomenon lessons to optimize blood glucose control in diabetes
Diabetes Care, 2013Co-Authors: Francesca Porcellati, Paola Lucidi, Geremia B Bolli, Carmine G FanelliAbstract:More than 30 years ago in Diabetes Care , Schmidt et al. (1) defined “Dawn Phenomenon,” the night-to-morning elevation of blood glucose (BG) before and, to a larger extent, after breakfast in subjects with type 1 diabetes (T1D). Shortly after, a similar observation was made in type 2 diabetes (T2D) (2), and the physiology of glucose homeostasis at night was studied in normal, nondiabetic subjects (3–5). Ever since the first description, the Dawn Phenomenon has been studied extensively with at least 187 articles published as of today (6). In this issue, Monnier et al. (7) report an additional observation on the Dawn Phenomenon in a large group of T2D subjects and quantify its role on overall BG control. Given this information and the extensive data to date, an assessment of our knowledge in this area should be determined. Specifically, what have we learned from the last 30 years of research on the Dawn Phenomenon? What is the appropriate definition, the identified mechanism(s), the importance (if any), and the treatment of the Dawn Phenomenon in T1D and T2D? Physiology of glucose homeostasis in normal, nondiabetic subjects indicates that BG and plasma insulin concentrations remain remarkably flat and constant overnight, with a modest, transient increase in insulin secretion just before Dawn (3,4) to restrain hepatic glucose production (4) and prevent hyperglycemia. Thus, normal subjects do not exhibit the Dawn Phenomenon sensu strictiori because they secrete insulin to prevent it. In T1D, the magnitude of BG elevation at Dawn first reported was impressive and largely secondary to the decrease of plasma insulin concentration overnight (1), commonly observed with evening administration of NPH or lente insulins (8) (Fig. 1). Even in early studies with intravenous insulin by the “artificial pancreas” (Biostator) (2), plasma insulin decreased overnight because of progressive inactivation …
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the Dawn Phenomenon in type 1 insulin dependent diabetes mellitus magnitude frequency variability and dependency on glucose counterregulation and insulin sensitivity
Diabetologia, 1991Co-Authors: G Perriello, Carmine G Fanelli, P De Feo, E Torlone, F Santeusanio, P Brunetti, Geremia B BolliAbstract:In 114 subjects with Type 1 (insulin-dependent) diabetes mellitus the nocturnal insulin requirements to maintain euglycaemia were assessed by means of i.v. insulin infusion by a Harvard pump. The insulin requirements decreased after midnight to a nadir of 0.102 +/- 0.03 mU.kg-1.min-1 at 02.40 hours. Thereafter, the insulin requirements increased to a peak of 0.135 +/- 0.06 mU.kg-1.min-1 at 06.40 hours (p less than 0.05). The Dawn Phenomenon (increase in insulin requirements by more than 20% after 02.40 hours lasting for at least 90 min) was present in 101 out of the 114 diabetic subjects, and its magnitude (% increase in insulin requirements between 05.00-07.00 hours vs that between 01.00-03.00 hours) was 19.4 +/- 0.54% and correlated inversely with the duration of diabetes (r = -0.72, p less than 0.001), but not with age. The nocturnal insulin requirements and the Dawn Phenomenon were highly reproducible on three separate nights. In addition, glycaemic control, state of counterregulation to hypoglycaemia and insulin sensitivity all influenced the magnitude of the Dawn Phenomenon as follows. In a subgroup of 84 subjects with Type 1 diabetes, the multiple correlation analysis showed that not only duration of diabetes (t = -9.76, p less than 0.0001), but also % HbA1 significantly influenced the magnitude of the Dawn Phenomenon (t = 2.03, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Julio V Santiago - One of the best experts on this subject based on the ideXlab platform.
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absence of the Dawn Phenomenon and abnormal lipolysis in type 1 insulin dependent diabetic patients with chronic growth hormone deficiency
Diabetologia, 1992Co-Authors: Patrick J Boyle, Philip E. Cryer, Angelo Avogaro, Lori Smith, Suresh D Shah, Julio V SantiagoAbstract:To determine the role of growth hormone in overnight insulin requirements and lipolysis, five patients with chronic growth hormone deficiency and Type 1 (insulin-dependent) diabetes mellitus and six control patients with diabetes were each studied on two separate nights. Insulin was infused at a variable rate throughout one night to maintain euglycaemia and fixed at 04.00 hours on another. During the variable infusion, euglycaemia was maintained in control patients by a 36% increase in insulin infusion rate between 03.00 and 08.00 hours while a 46% decrease in the rate was required in growth hormone deficient patients (p less than 0.02). Despite this difference, mean free insulin values were equivalent. This finding is suggestive of increased insulin clearance in growth hormone sufficient patients. Glucose levels rose in control and fell in growth hormone deficient patients when insulin infusion rates were fixed at 04.00 hours. Glycerol production and non-esterified fatty acid concentrations were significantly lower in the growth hormone deficient diabetic patients, p less than 0.001, and when normalized with a heparin infusion, had no effect on insulin requirements. We conclude that: (1) growth hormone contributes to the development of the "Dawn Phenomenon," possibly by increasing insulin clearance (2) growth hormone helps sustain nocturnal lipolysis in Type 1 diabetes and (3) non-esterified fatty acids are not involved in the Dawn Phenomenon.
M O Savage - One of the best experts on this subject based on the ideXlab platform.
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the Dawn Phenomenon in adolescents with insulin dependent diabetes mellitus possible contribution of insulin like growth factor binding protein 1
Clinical Endocrinology, 1995Co-Authors: A M Cotterill, Fiona Daly, Jeffrey M P Holly, Slan Cwyfan Hughes, Cecilia Camachohubner, Farhana A Abdulla, Edwin A M Gale, M O SavageAbstract:Summary OBJECTIVE Insulin resistance increases during adolescence, and is exaggerated in patients with insulin dependent diabetes mellitus (IDDM). A relative deficiency of insulin-like growth factor-I (IGF-I) may contribute to this increased insulin requirement. Two mechanisms have been proposed: (a) increased GH secretion, caused by failure of IGF feedback control, leading to increased insulin resistance and (b) lack of Insulin-like action of the IGFs which is reinforced by high plasma levels of IGFBP-1, an inhibitor of IGF action. The contribution of these two mechanisms to the ‘Dawn Phenomenon’ is assessed. DESIGN The two possible mechanisms were studied during the Dawn rise of glucose in pubertal adolescent patients with IDDM. Two overnight studies were performed in each subject. Patients remained on the same insulin regimen throughout. SUBJECTS Twenty-two diabetic adolescent subjects, aged (mean ± SEM) 14.0 ± 0.4 years, duration of IDDM 7.9 ± 0.8 years, were recruited. Pubertal status was: group 1 (breast stage 1–2; testicular volume < 4–8ml) 3 male and 4 female, group 2 (breast stage 3; testicular volume 10–12 ml) 0 male 4 female, group 3 (breast stage 4–5; testicular volume 15–25 ml) 4 male and 7 female. Height standard deviation score (mean ± SD) (-0.02 ± 099) and dally insulin dose (50.4 ± 3.1 U/day) did not change between studies. There were no differences in HbA1 (study A 11.26 ± 0.45%, study B 11.09 ± 0.42%). METHODS The subjects were admitted for the two studies 0.3 ± 0.03 years apart. Blood samples were taken via an indwelling cannula every 20 minutes between 1900 and 0700 h. MEASUREMENTS GH was assayed every 20 minutes, IGFBP-1, glucose and free Insulin every hour and lGF-I at 0700h. GH, IGFBP-1, IGF-I and free insulin were measured by radioimmunoassay. IGFBPs were also analysed by Western ligand blotting techniques. GH profiles were analysed by Pulsar and results compared by paired Student's t-test. The relations between the Dawn rise In glucose and the changes in IGFBP-1, GH and free insulin were examined by multiple linear regression analysis. RESULTS Serum IGFBP-1 levels rose overnight In the two studies (study A, from 9·1 at 2200 to 59 ± 9μg/l at 0700 h; study B, from 10±1 at 2100 to 64 ± 14μg/l at 0700h) whilst insulin levels fell from 47 ± 5 at 2200 to 16 ± 2mU/l at 0700 h (study A) and from 45·5 at 2000 to 14 ± 2mU/l at 0700 h (study B). Glucose levels fell from 16.0 ± 1.0 to 9.3 ± 0.9 mmol/l at 0400h, and then rose to 11.9 ± 1.1 mmol/l at 0700 h during study A, and from 13.4 ± 1.3 to 10.1 ± 1.1 mmol/l at 0400 h and then rose to 13.5 ± 1.0 mmol/l at 0700 h during study B. There were no differences in GH secretion between studies (mean GH levels (mean ± SD) (study A, 15.7 ± 6.6 mU/I; study B, 16.2 ± 7.1 mU/l; correlation within subjects between studies r= 0.77, P < 0.001), sum of GH peaks (study A, 189.9 ± 903 mU/l; study B, 185.8 ±100.2 mU/l; r= 0.57, P= 0.006)). Mean GH levels varied with pubertal stage (group 1,12.1 ± 1.5 mU/l; group 2, 23.3 ± 2.1 mU/I; group 3, 15.3 ± 1.2mU/I). Serum IGF-l levels were not different (study A, 203 ± 12 μg/l; study B, 218 ± 13 μg/l). REGRESSION ANALYSIS The change In plasma glucose between 0200 and 0700 h In both studies related to free insulin, IGFBP-1 and the sum of the GH levels over the preceding hour (log glucose =7.87 + 5.32 log IGFBP-1 (P= 0.0001) −5.05 log free insulin (P= 0.0001)-1.44 log GH (P= 0.004); R2= 72%). Mean overnight GH levels did not predict the morning rise In plasma glucose. CONCLUSION The morning rise of IGFBP-1 and plasma glucose appear to be related in this group of subjects with IDDM and this was a consistent finding In the two studies. This relation was additive to the effect of Insulin deficiency. No positive relation was noted between GH secretion and glucose levels. These findings support the hypothesis that the increased GH secretion In IDDM Is a marker of IGF-I deficiency rather than a direct causal factor in the increase In insulin resistance. The IGFs may therefore have a direct role In glucose homeostasis via the ‘free’ fraction of circulating IGFs, the availability of which may be modulated by changes in IGFBP-1 levels.
