Faculty Bibliography

BACKGROUND:Dietary self-monitoring is central to effective personalized nutrition, providing critical data to inform tailored feedback and support behavior change. OBJECTIVE:To examine the impact of dietary self-monitoring adherence and the indirect effect of personalized scores to predict postprandial glycemic response (PPGR) on weight loss. METHODS:Post-hoc analysis of the Personal Diet Study that investigated the impact of a machine algorithm-based diet that integrates clinical and microbiome features (Personalized) compared to a standard, low-fat diet (Standardized) on weight loss. All participants received behavioral counseling and were encouraged to self-monitor dietary intake via a smartphone app. Personalized received algorithm-based scores (1 to 5) on predicted PPGR to foods logged (PPGR score; 1-2 indicating optimal; 3-5 suboptimal). Dietary self-monitoring adherence was the percentage of days logging ≥50% of target calories, classified as high or low. PPGR score quality was calculated by the proportion of optimal predicted PPGR scores per day; defined as "high-PPGR quality" days when this exceeded the group average. Mediation analysis assessed whether PPGR quality mediated the relationship between dietary self-monitoring adherence and weight loss. RESULTS:Participants with high self-monitoring adherence lost an average of 4.2% of their baseline weight, compared to 1.9% among those with low adherence (p=0.016). High self-monitoring adherence was associated with a greater likelihood of achieving ≥5% weight loss (aOR=3.67, 95% CI: 1.63-8.50). Within Personalized, high PPGR quality mediated 53.4% of the total effect of self-monitoring adherence on weight loss (p<0.001). CONCLUSION/CONCLUSIONS:Consistent self-monitoring coupled with personalized feedback may significantly enhance weight loss in a precision nutrition approach. CLINICAL TRIAL REGISTRATION/BACKGROUND:NCT03336411.

AIMS/HYPOTHESIS/OBJECTIVE:plus FPG. METHODS:, individually and in combination, for diagnosing diabetes. Random-effects meta-analyses were applied to pooled data to summarise the overall diagnostic accuracy across studies. RESULTS:, with pooled AUCs (95% CI) of 0.97 (0.96, 0.98) vs 0.85 (0.82, 0.88). CONCLUSIONS/INTERPRETATION/CONCLUSIONS:for diagnosing type 2 diabetes.

BACKGROUND:High 1-h-post-load plasma glucose (1 h-PG) is an early diabetes risk marker. We hypothesized that isolated high 1 h-PG represents an intermediate state between normal glucose regulation (NGR) and impaired glucose regulation (IGR) and is amendable to greater lifestyle intervention (LI) benefit. METHODS:In the Tübingen Lifestyle Intervention Program, 317 people with either NGR, IGR or isolated high 1 h-PG without IGR underwent LI for 9 months to achieve ≥5 % weight loss. RESULTS:Before LI initiation, insulin sensitivity and β-cell function declined progressively from NGR (n = 106) to high 1 h-PG (n = 96) and to IGR (n = 115). Visceral adipose tissue (VAT) volume and liver fat content increased from NGT to high 1 h-PG and to IGR. LI improved insulin sensitivity and ß-cell function in the high 1 h-PG group to levels observed in NGR together with a marked reduction in hepatic fat content. Compared to the IGR group, T2D risk was reduced by 80 % (37-96 %, p = 0.005) in the high 1 h-PG group during a 12-year follow-up period. The odds of remission to complete normoglycemia were doubled in the high 1 h-PG group compared to the IGR group (2.18 [1.13-4.28], p = 0.021). CONCLUSION/CONCLUSIONS:High 1 h-PG indicates an intermediate metabolic state with pathophysiological changes more severe than in NGR but milder than in IGR. In people with high 1 h-PG, LI significantly improved insulin sensitivity and β-cell function and reduced ectopic lipid deposition and the risk of developing T2D compared to IGR. These findings highlight the value of 1 h-PG as a clinically useful biomarker, providing a critical window for early intervention to reverse core metabolic defects driving prediabetes and T2D.

AIMS/OBJECTIVE:To evaluate a previously proposed type 2 diabetes staging schema by examining the decline in oral beta-cell compensation and the increase in diabetes risk. METHODS:We analyzed 1,235 participants (43-85 years) from one ELSA-Brasil center. We defined stages as previously proposed: stage 1, isolated 1-h PG ≥155 mg/dL; stage 2, also having prediabetes/intermediate hyperglycemia (preDM/IH) defined by the American Diabetes Association (ADA); and stage 3, diabetes. We made additional evaluations defining IH based on the World Health Organization (WHO)/International Expert Committee (IEC) criteria. We estimated beta-cell compensation with the insulin secretion-sensitivity index-2 (ISSI-2). RESULTS:ISSI-2 declined (p < 0.001) across stages. After 5.29 (0.44) years (n = 850), the adjusted diabetes incidence increased from stage 0 (normoglycemia) to stage 1 (RR = 2.64;1.12,6.22) and stage 2 (RR = 5.94;2.83,12.44), considering WHO/IEC criteria. With the ADA criteria, RRs were larger but not progressive. Adding 1-h PG testing doubled the detection of unknown diabetes. A strategy combining FPG with 1-h PG performed just as well as using all four tests. CONCLUSIONS:Staging captured progressive deterioration to type 2 diabetes. Adding 1-h PG improved current and future case detection, which represents a major advance in diabetes prevention. However, refinements in staging will require further evaluation of tests and their thresholds.

AIMS/OBJECTIVE:To characterize changes in continuous glucose monitoring (CGM)-derived time in tight range (TIR) measures in individuals with prediabetes or non-insulin-treated type 2 diabetes undergoing dietary weight loss intervention and to quantify the association between weight loss and TIR improvement. METHODS:) were analysed. The association between weight change and TIR change adjusted for demographic and clinical covariates was computed using linear regression. RESULTS:. There were no associations between weight loss and change in any overnight TIR measure. CONCLUSION/CONCLUSIONS:in individuals with prediabetes and non-insulin-treated type 2 diabetes undergoing dietary intervention. The daytime time in tight range measures can complement traditional markers like HbA1c, offering a more comprehensive view of glycaemic variations during dietary weight loss programmes for individuals with prediabetes and type 2 diabetes not on insulin.

Sodium-glucose cotransporter-2 inhibitors (SGLT2i) and glucagon-Like peptide-1 receptor agonists (GLP-1 RA) are recommended in people with type 2 diabetes (T2D) for glycaemic control and for people with high cardiovascular risk. However, current guidelines do not specifically address the role of initial early combination therapy with SGLT2i and GLP-1 RA or dual gastric inhibitory polypeptide (GIP)/GLP-1 RA, but rather sequential initiation with either in T2D. This review synthesizes the available evidence on the use of SGLT2i and GLP-1-based therapies for T2D and provides a rationale for their combination. The combination of SGLT2i with GLP-1-based therapies addresses complementary pathophysiological mechanisms and enhances efficacy in achieving target haemoglobin A1C (HbA1c) levels. SGLT2i and GLP-1 RA also have been shown to prevent complications of T2D. While both classes reduce adverse cardiorenal events, SGLT2i has a predominant effect on prevention of kidney dysfunction and heart failure, whereas GLP-1 RA has a more marked effect on the risk of atherosclerotic cardiovascular disease. Both drug classes have favourable safety profiles. Finally, weight loss with combination therapy may have disease-modifying effects that may reverse T2D progression. We propose that the combination of SGLT2i with GLP-1 RA or dual GIP/GLP-1 RA should be considered for most patients with T2D who do not have contraindications.

AIMS/OBJECTIVE:Because one-hour post-load plasma glucose (1h-PG) ≥ 155 mg/dL (8.6 mmol/L) has been proposed as an early marker for future diabetes but lacks sufficient longitudinal confirmation of its risk, we aimed to evaluate the risk of T2D based on 1h-PG and track changes of insulin sensitivity and β-cell function over time by 1h-PG in a longitudinal cohort. METHODS:OGTTs were conducted every 2 years in the 10-year longitudinal Korean Genome Epidemiology study (n = 6144) with three groups characterized at baseline: Low 1h-PG (< 155 mg/dL) with Normal Glucose Tolerance (NGT), High 1h-PG (≥155 mg/dL) with NGT, and prediabetes (PreDM). RESULTS:T2D risk was higher in people with High 1h-PG with NGT and PreDM than those with Low 1h-PG with NGT. Baseline insulin sensitivity in Low 1h-PG as measured by the insulin sensitivity and secretion (ISS) model and Matsuda insulin sensitivity index (ISI) was higher than in High 1h-PG, which was comparable to PreDM. β-cell function as assessed by ISS and the insulinogenic index decreased from Low 1h-PG to High 1h-PG to PreDM. Over time, insulin sensitivity decreased in the three groups. Time from High 1h-PG to T2D was 0.9 years shorter than from Low 1h-PG. All participants passed the 1h-PG threshold for T2D (209 mg/dL, 11.6 mmol/L) first, and 74 % passed the 1h-PG threshold for impaired glucose tolerance (IGT; 155 mg/dL) first. CONCLUSIONS:High 1h-PG NGT is an intermediate risk category between Low 1h-PG NGT and PreDM and may provide an opportunity for early intervention to prese rve ß-cell function.