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Sökning: WFRF:(Delahanty Linda M.)

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1.
  • Bermingham, Kate M., et al. (författare)
  • Menopause is associated with postprandial metabolism, metabolic health and lifestyle : The ZOE PREDICT study
  • 2022
  • Ingår i: EBioMedicine. - : Elsevier BV. - 2352-3964. ; 85
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The menopause transition is associated with unfavourable alterations in health. However, postprandial metabolic changes and their mediating factors are poorly understood. Methods: The PREDICT 1 UK cohort (n=1002; pre- n=366, peri- n=55, and post-menopausal females n=206) assessed phenotypic characteristics, anthropometric, diet and gut microbiome data, and fasting and postprandial (0–6 h) cardiometabolic blood measurements, including continuous glucose monitoring (CGM) data. Differences between menopausal groups were assessed in the cohort and in an age-matched subgroup, adjusting for age, BMI, menopausal hormone therapy (MHT) use, and smoking status. Findings: Post-menopausal females had higher fasting blood measures (glucose, HbA1c and inflammation (GlycA), 6%, 5% and 4% respectively), sugar intakes (12%) and poorer sleep (12%) compared with pre-menopausal females (p<0.05 for all). Postprandial metabolic responses for glucose2hiauc and insulin2hiauc were higher (42% and 4% respectively) and CGM measures (glycaemic variability and time in range) were unfavourable post- versus pre-menopause (p<0.05 for all). In age-matched subgroups (n=150), postprandial glucose responses remained higher post-menopause (peak0-2h 4%). MHT was associated with favourable visceral fat, fasting (glucose and insulin) and postprandial (triglyceride6hiauc) measures. Mediation analysis showed that associations between menopause and metabolic health indicators (visceral fat, GlycA360mins and glycaemia (peak0-2h)) were in part mediated by diet and gut bacterial species. Interpretation: Findings from this large scale, in-depth nutrition metabolic study of menopause, support the importance of monitoring risk factors for type-2 diabetes and cardiovascular disease in mid-life to older women to reduce morbidity and mortality associated with oestrogen decline. Funding: Zoe Ltd.
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2.
  • Merino, Jordi, et al. (författare)
  • Validity of continuous glucose monitoring for categorizing glycemic responses to diet : Implications for use in personalized nutrition
  • 2022
  • Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165. ; 115:6, s. 1569-1576
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Continuous glucose monitor (CGM) devices enable characterization of individuals' glycemic variation. However, there are concerns about their reliability for categorizing glycemic responses to foods that would limit their potential application in personalized nutrition recommendations. Objectives: We aimed to evaluate the concordance of 2 simultaneously worn CGM devices in measuring postprandial glycemic responses. Methods: Within ZOE PREDICT (Personalised Responses to Dietary Composition Trial) 1, 394 participants wore 2 CGM devices simultaneously [n = 360 participants with 2 Abbott Freestyle Libre Pro (FSL) devices; n = 34 participants with both FSL and Dexcom G6] for ≤14 d while consuming standardized (n = 4457) and ad libitum (n = 5738) meals. We examined the CV and correlation of the incremental area under the glucose curve at 2 h (glucoseiAUC0-2 h). Within-subject meal ranking was assessed using Kendall τ rank correlation. Concordance between paired devices in time in range according to the American Diabetes Association cutoffs (TIRADA) and glucose variability (glucose CV) was also investigated. Results: The CV of glucoseiAUC0-2 h for standardized meals was 3.7% (IQR: 1.7%-7.1%) for intrabrand device and 12.5% (IQR: 5.1%-24.8%) for interbrand device comparisons. Similar estimates were observed for ad libitum meals, with intrabrand and interbrand device CVs of glucoseiAUC0-2 h of 4.1% (IQR: 1.8%-7.1%) and 16.6% (IQR: 5.5%-30.7%), respectively. Kendall τ rank correlation showed glucoseiAUC0-2h-derived meal rankings were agreeable between paired CGM devices (intrabrand: 0.9; IQR: 0.8-0.9; interbrand: 0.7; IQR: 0.5-0.8). Paired CGMs also showed strong concordance for TIRADA with a intrabrand device CV of 4.8% (IQR: 1.9%-9.8%) and an interbrand device CV of 3.2% (IQR: 1.1%-6.2%). Conclusions: Our data demonstrate strong concordance of CGM devices in monitoring glycemic responses and suggest their potential use in personalized nutrition.
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4.
  • Berry, Sarah E., et al. (författare)
  • Human postprandial responses to food and potential for precision nutrition
  • 2020
  • Ingår i: Nature Medicine. - : Springer Science and Business Media LLC. - 1078-8956 .- 1546-170X. ; 26:6, s. 964-973
  • Tidskriftsartikel (refereegranskat)abstract
    • Metabolic responses to food influence risk of cardiometabolic disease, but large-scale high-resolution studies are lacking. We recruited n = 1,002 twins and unrelated healthy adults in the United Kingdom to the PREDICT 1 study and assessed postprandial metabolic responses in a clinical setting and at home. We observed large inter-individual variability (as measured by the population coefficient of variation (s.d./mean, %)) in postprandial responses of blood triglyceride (103%), glucose (68%) and insulin (59%) following identical meals. Person-specific factors, such as gut microbiome, had a greater influence (7.1% of variance) than did meal macronutrients (3.6%) for postprandial lipemia, but not for postprandial glycemia (6.0% and 15.4%, respectively); genetic variants had a modest impact on predictions (9.5% for glucose, 0.8% for triglyceride, 0.2% for C-peptide). Findings were independently validated in a US cohort (n = 100 people). We developed a machine-learning model that predicted both triglyceride (r = 0.47) and glycemic (r = 0.77) responses to food intake. These findings may be informative for developing personalized diet strategies. The ClinicalTrials.gov registration identifier is NCT03479866.
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5.
  • Davis, Nichola J., et al. (författare)
  • Predictors of Sustained Reduction in Energy and Fat Intake in the Diabetes Prevention Program Outcomes Study Intensive Lifestyle Intervention
  • 2013
  • Ingår i: Journal of the American Dietetic Association. - : Elsevier BV. - 0002-8223. ; 113:11, s. 1455-1464
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Few lifestyle intervention studies examine long-term sustainability of dietary changes. Objective To describe sustainability of dietary changes over 9 years in the Diabetes Prevention Program and its outcomes study, the Diabetes Prevention Program Outcomes Study, among participants receiving the intensive lifestyle intervention. Design One thousand seventy-nine participants were enrolled in the intensive lifeStyle intervention arm of the Diabetes Prevention Program; 910 continued participation in the Diabetes Prevention Program Outcomes Study. Fat and energy intake derived from food frequency questionnaires at baseline and post-randomization Years 1 and 9 were examined. Parsimonious models determined whether baseline characteristics and intensive lifestyle intervention session participation predicted sustainability. Results Self-reported energy intake was reduced from a median of 1,876 kcal/day (interquartile range [IQR]=1,452 to 2,549 kcal/day) at baseline to 1,520 kcal/day (IQR=1,192 to 1,986 kcal/day) at Year 1, and 1,560 kcal/day (IQR=1,223 to 2,026 kcal/ day) at Year 9. Dietary fat was reduced from a median of 70.4 g (IQR=49.3 to 102.5 g) to 45 g (IQR=32.2 to 63.8 g) at Year 1 and increased to 61.0 g (IQR=44.6 to 82.7 g) at Year 9. Percent energy from fat was reduced from a median of 34.4% (IQR=29.6% to 38.5%) to 27.1% (IQR=23.1% to 31.5%) at Year 1 but increased to 35.3% (IQR=29.7% to 40.2%) at Year 9. Lower baseline energy intake and Year 1 dietary reduction predicted lower energy and fat gram intake at Year 9. Higher leisure physical activity predicted lower fat gram intake but not energy intake. Conclusions Intensive lifestyle intervention can result in reductions in total energy intake for up to 9 years. Initial success in achieving reductions in fat and energy intake and success in attaining activity goals appear to predict long-term success at maintaining changes.
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6.
  • Papandonatos, George D, et al. (författare)
  • Genetic Predisposition to Weight Loss and Regain With Lifestyle Intervention : Analyses From the Diabetes Prevention Program and the Look AHEAD Randomized Controlled Trials
  • 2015
  • Ingår i: Diabetes. - : American Diabetes Association. - 0012-1797 .- 1939-327X. ; 64:12, s. 4312-4321
  • Tidskriftsartikel (refereegranskat)abstract
    • Clinically relevant weight loss is achievable through lifestyle modification, but unintentional weight regain is common. We investigated whether recently discovered genetic variants affect weight loss and/or weight regain during behavioral intervention. Participants at high-risk of type 2 diabetes (Diabetes Prevention Program [DPP]; N = 917/907 intervention/comparison) or with type 2 diabetes (Look AHEAD [Action for Health in Diabetes]; N = 2,014/1,892 intervention/comparison) were from two parallel arm (lifestyle vs. comparison) randomized controlled trials. The associations of 91 established obesity-predisposing loci with weight loss across 4 years and with weight regain across years 2-4 after a minimum of 3% weight loss were tested. Each copy of the minor G allele of MTIF3 rs1885988 was consistently associated with greater weight loss following lifestyle intervention over 4 years across the DPP and Look AHEAD. No such effect was observed across comparison arms, leading to a nominally significant single nucleotide polymorphism x treatment interaction (P = 4.3 x 10-3). However, this effect was not significant at a study-wise significance level (Bonferroni threshold P < 5.8 x 10-4). Most obesity-predisposing gene variants were not associated with weight loss or regain within the DPP and Look AHEAD trials, directly or via interactions with lifestyle.
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7.
  • Rockette-Wagner, Bonny, et al. (författare)
  • The impact of lifestyle intervention on sedentary time in individuals at high risk of diabetes
  • 2015
  • Ingår i: Diabetologia. - : Springer Science and Business Media LLC. - 1432-0428 .- 0012-186X. ; 58:6, s. 1198-1202
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims/hypothesis The Diabetes Prevention Program (DPP) lifestyle intervention successfully achieved its goal of increasing leisure physical activity levels. This current study examines whether the lifestyle intervention also changed time spent being sedentary and the impact of sedentary time on diabetes development in this cohort. Methods 3,232 DPP participants provided baseline data. Sedentary behaviour was assessed via an interviewer-administered questionnaire and reported as time spent watching television specifically (or combined with sitting at work). Mean change in sedentary time was examined using repeated measures ANCOVA. The relationship between sedentary time and diabetes incidence was determined using Cox proportional hazards models. Results During the DPP follow-up (mean: 3.2 years), sedentary time declined more in the lifestyle than the metformin or placebo participants (p < 0.05). For the lifestyle group, the decrease in reported mean television watching time (22 [95% CI 26, 17] min/day) was greater than in the metformin or placebo groups (p < 0.001). Combining all participants together, there was a significantly increased risk of developing diabetes with increased television watching (3.4% per hour spent watching television), after controlling for age, sex, treatment arm and leisure physical activity (p < 0.01), which was attenuated when time-dependent weight was added to the model. Conclusions/interpretation In the DPP, the lifestyle intervention was effective at reducing sedentary time, which was not a primary goal. In addition, in all treatment arms, individuals with lower levels of sedentary time had a lower risk of developing diabetes. Future lifestyle intervention programmes should emphasise reducing television watching and other sedentary behaviours in addition to increasing physical activity.
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8.
  • Tsereteli, Neli, et al. (författare)
  • Impact of insufficient sleep on dysregulated blood glucose control under standardised meal conditions
  • 2022
  • Ingår i: Diabetologia. - : Springer Science and Business Media LLC. - 0012-186X .- 1432-0428. ; 65:2, s. 356-365
  • Tidskriftsartikel (refereegranskat)abstract
    • 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) (pinteraction = 0.02) and high-fat (pinteraction = 0.03) breakfasts were consumed compared with a reference 75 g OGTT. Within-person sleep period time had a similar interaction (high carbohydrate: pinteraction = 0.001, high fat: pinteraction = 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 registrationClinicalTrials.gov NCT03479866. Graphical abstract: [Figure not available: see fulltext.]
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9.
  • Billings, Liana K., et al. (författare)
  • The Influence of Rare Genetic Variation in SLC30A8 on Diabetes Incidence and beta-Cell Function
  • 2014
  • Ingår i: Journal of Clinical Endocrinology and Metabolism. - : The Endocrine Society. - 1945-7197 .- 0021-972X. ; 99:5, s. 926-930
  • Tidskriftsartikel (refereegranskat)abstract
    • Context/Objective: The variant rs13266634 in SLC30A8, encoding a beta-cell-specific zinc transporter, is associated with type 2 diabetes. We aimed to identify other variants in SLC30A8 that increase diabetes risk and impair beta-cell function, and test whether zinc intake modifies this risk. Design/Outcome: We sequenced exons in SLC30A8 in 380 Diabetes Prevention Program (DPP) participants and identified 44 novel variants, which were genotyped in 3445 DPP participants and tested for association with diabetes incidence and measures of insulin secretion and processing. We examined individual common variants and used gene burden tests to test 39 rare variants in aggregate. Results: We detected a near-nominal association between a rare-variant genotype risk score and diabetes risk. Five common variants were associated with the oral disposition index. Various methods aggregating rare variants demonstrated associations with changes in oral disposition index and insulinogenic index during year 1 of follow-up. We did not find a clear interaction of zinc intake with genotype on diabetes incidence. Conclusions: Individual common and an aggregate of rare genetic variation in SLC30A8 are associated with measures of beta-cell function in the DPP. Exploring rare variation may complement ongoing efforts to uncover the genetic influences that underlie complex diseases.
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10.
  • Delahanty, Linda M., et al. (författare)
  • Genetic Predictors of Weight Loss and Weight Regain After Intensive Lifestyle Modification, Metformin Treatment, or Standard Care in the Diabetes Prevention Program
  • 2012
  • Ingår i: Diabetes Care. - : American Diabetes Association. - 1935-5548 .- 0149-5992. ; 35:2, s. 363-366
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE-We tested genetic associations with weight loss and weight regain in the Diabetes Prevention Program, a randomized controlled trial of weight-loss inducing interventions (lifestyle and metformin) versus placebo. RESEARCH DESIGN AND METHODS-Sixteen obesity-predisposing single nucleotide polymorphisms (SNPs) were tested for association with short-term (baseline to 6 months) and long-term (baseline to 2 years) weight loss and weight regain (6 months to study end). RESULTS-Irrespective of treatment, the Ala12 allele at PPARG associated with short- and long-term weight loss (-0.63 and -0.93 kg/allele, P <= 0.005, respectively). Gene-treatment interactions were observed for short-term (LYPLAL1 rs2605100, P-lifestyle*SNP = 0.032; GNPDA2 rs10938397, P-lifestyle*SNP = 0.016; MTCH2 rs10838738, P-lifestyle*SNP = 0.022) and long-term (NEGR1 rs2815752, P-metformin*SNP = 0.028; FTO rs9939609, P-lifestyle*SNP = 0.044) weight loss. Three of 16 SNPs were associated with weight regain (NEGR1 rs2815752, BDNF rs6265, PPARG rs1801282), irrespective of treatment. TMEM18 rs6548238 and KTCD15 rs29941 showed treatment-specific effects (P-lifestyle*SNP < 0.05). CONCLUSIONS-Genetic information may help identify people who require additional support to maintain reduced weight after clinical intervention.
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