OBJECTIVE: To evaluate the relationship between fasting plasma glucose (FPG) and 2-hour postload plasma glucose (2hPG) measured during an oral glucose tolerance test, and the risk of developing diabetes in Chinese adults.
METHODS: We followed 3,094 participants without diabetes, categorizing them based on their oral glucose tolerance test (OGTT) results into low post load (2hPG ≤ FPG) and high post load (2hPG > FPG) at baseline. We monitored the incidence of diabetes, incidence of prediabetes, disease progression from prediabetes to diabetes and disease reversal from prediabetes to normal glucose tolerance (NGT) over an average of 3.2 years of follow-up. After the Schoenfeld residual test, Cox\'s time-varying covariate (Cox-TVC) models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CI) to compare the different clinical events between low and high post load groups.
RESULTS: In the cohort study, of the 3,094 participants, 702 (22.7 %) had low post load (2hPG ≤ FPG, mean postload-fasting gap: -0.8 ± 0.7 mmol/L) and 2,392 (77.3 %) had high post load (2hPG > FPG, mean postload-fasting gap: 1.8 ± 1.2 mmol/L). Over 3.2 ± 0.2 years of follow-up, 282 (9.1 %) developed diabetes. In the low post load group, the incidence rates per 1,000 person-years were: diabetes was 7.9, prediabetes was 70.0, disease progression from prediabetes to diabetes was 23.4 and disease reversal to NGT was 327.2. For the high post load group, incidence rates for diabetes was 13.9, prediabetes was 124.3, disease progression was 59.5 and disease reversal was 238.6 per 1,000 person-years. Participants with high post load showed higher incidence rates of diabetes, prediabetes, and progression from prediabetes to diabetes compared to those with low post load. HRs were significantly higher for incident diabetes and prediabetes, and disease progression from prediabetes to diabetes, whereas disease reversal was lower.
CONCLUSIONS: The risk of developing prediabetes/diabetes after 3.2 years of follow-up was higher in the participants with high post load. It suggested that postload-fasting gap may be a simple tool to predict the risk of developing prediabetes, diabetes or reversal to NGT.

This observational pilot study examined the association between diet, meal pattern and glucose over a 2-week period under free-living conditions in 26 adults with dysglycemia (D-GLYC) and 14 with normoglycemia (N-GLYC). We hypothesized that a prolonged eating window and late eating occasions (EOs), along with a higher dietary carbohydrate intake, would result in higher glucose levels and glucose variability (GV). General linear models were run with meal timing with time-stamped photographs in real time, and diet composition by dietary recalls, and their variability (SD), as predictors and glucose variables (mean glucose, mean amplitude of glucose excursions [MAGE], largest amplitude of glucose excursions [LAGE] and GV) as dependent variables. After adjusting for calories and nutrients, a later eating midpoint predicted a lower GV (β = -2.3, SE = 1.0, p = 0.03) in D-GLYC, while a later last EO predicted a higher GV (β = 1.5, SE = 0.6, p = 0.04) in N-GLYC. A higher carbohydrate intake predicted a higher MAGE (β = 0.9, SE = 0.4, p = 0.02) and GV (β = 0.4, SE = 0.2, p = 0.04) in N-GLYC, but not D-GLYC. In summary, our data suggest that meal patterns interact with dietary composition and should be evaluated as potential modifiable determinants of glucose in adults with and without dysglycemia. Future research should evaluate causality with controlled diets.

OBJECTIVE: To determine the relationship between point-of-care β-hydroxybutyrate (BHB) concentration and outcomes in adult patients without diabetes admitted through ED.
METHODS: This was a prospective study from 10 March to 2 July 2021. Admitted patients without diabetes had capillary BHB sampled in ED. Outcomes of length-of-stay (LOS), composite mortality/ICU admission rates and clinical severity scores (Quick Sepsis Organ Failure Assessment score/National Early Warning Score [qSOFA/NEWS]) were measured. BHB was assessed as a continuous variable and between those with BHB above and equal to 1.0 mmol/L and those below 1.0 mmol/L.
RESULTS: A total of 311 patients were included from 2377 admissions. Median length-of-stay was 4.1 days (IQR 2.1-9.8), 18 (5.8%) died and 37 (11.8%) were admitted to ICU. Median BHB was 0.2 mmol/L (IQR 0.1-0.4). Twenty-five patients had BHB ≥1.0 mmol/L and five were >3.0 mmol/L. There was no significant difference in median LOS for patients with BHB ≥1.0 mmol/L compared to non-ketotic patients, 5.3 days (IQR 2.2-7.5) versus 4.1 days, respectively (IQR 2.0-9.8) (P = 0.69). BHB did not correlate with LOS (Spearman ρ = 0.116, 95% confidence interval: 0.006-0.223). qSOFA and NEWS also did not differ between these cohorts. For those 25 patients with BHB ≥1.0 mmol/L, an infective/inflammatory diagnosis was present in 11 (44%), at least 2 days of fasting in 10 (40%) and ethanol intake >40 g within 48 h in 4 (16%).
CONCLUSIONS: Routine BHB measurement in patients without diabetes does not add to clinical bedside assessment and use should be limited to when required to confirm a clinical impression.

OBJECTIVE: To evaluate whether the extent of return to fasting state 2-hours after a glucose challenge among normoglycemic individuals is associated with lower risk of incident prediabetes/ type 2 diabetes in the Coronary Artery Risk Development in Young Adults (CARDIA) cohort study.
METHODS: We evaluated this association among 1879 normoglycemic adults who were categorized into three groups: \'Low post load\' (2hPG < FPG); \'Medium post load\' (2hPG ≥ FPG and < 75th percentile of the difference); and \'High post load\' (2hPG > FPG and ≥ 75th percentile of the difference). We used Cox proportional hazards regression to evaluate the association of the difference in 2hPG and FPG with incident diabetes/prediabetes after adjustment for demographic and clinical covariates.
RESULTS: During 20 years of follow-up, 8% developed type 2 diabetes and 35% developed prediabetes. Compared to those with \'Low post load\', the risk of type 2 diabetes was higher for participants with \'High post load\' [HR: 1.56, 95% CI (1.03, 2.37)] and similar for participants with \'Medium post load\' [HR: 0.99, 95% CI (0.64, 1.52)]. However, HRs for incident prediabetes among participants with \'High post load\' [HR = 1.2, 95 %CI = (0.98, 1.46)] was not significantly different compared to participants with \'Low post load\'.
CONCLUSIONS: Among normoglycemic individuals, a difference between 2hPG and FPG concentration > 0.9 mmol/L can be used to stratify individuals at higher risk for developing type 2 diabetes.

OBJECTIVE: To evaluate pancreatic β-cell function (βf) in patients with normoglycemia (NG) and normal glucose tolerance (NGT) and related risk factors.
METHODS: An observational and comparative study in 527 patients with NG and NGT that were divided by quartiles of βf according to the disposition index derived from OGTT. Anthropometrical, clinical, nutritional, and biochemical variables were measured and associated with βf.
RESULTS: Quartiles of βf were Q1 = DI < 1.93 n = 131, Q2 = DI 1.93-2.45 n = 134, Q3 = DI 2.46-3.1 n = 133, and Q4 = DI > 3.1 n = 129. There was a progressive reduction in pancreatic β-cell function and it is negatively correlated with age, weight, BMI, total body fat and visceral fat, waist circumference, total cholesterol, LDL, and triglycerides (p < 0.01). Glucose levels during OGTT had a negative correlation with βf; the product of fasting glucose by 1-h glucose had the best correlation with βf (r = 0.611, p < 0.001) and was the best predictor of βdf (AUC 0.816, CI 95% 0.774-0.857), even better than 1-h glucose (r = 0.581, p < 0.001). Energy, fat, and carbohydrate intake were negatively correlated with βf (p < 0.05). Glucose levels at 1-h OGTT > 110 mg/dl were positively associated with pancreatic βdf (OR 6.85, CI 95% 3.86-12.4). In the multivariate analysis, glucose levels during OGTT, fasting insulin, and BMI were the main factors associated with βf.
CONCLUSIONS: A subgroup of patients with NG and NGT may have a loss of 40% of their βf. Factors related to this βdf were age, adiposity, glucose during OGTT, and the product of fasting and 1-h glucose, as well as food intake.

Diabetic ketoacidosis is defined as hyperglycemia >250 mg/dL with metabolic acidosis of arterial pH <7.3, serum bicarbonate <18 mEq/L with positive urine and serum ketones and an anion gap >10. Euglycemic ketoacidosis has been reported in patients with type 2 diabetes and in patients with type 1 diabetes. However, as a surgical complication, euglycemic ketoacidosis has not been reported. We report 2 cases from 2 teaching tertiary care centers of patients with type 2 diabetes who developed high-gap ketoacidosis in an intensive care unit while recovering from emergent abdominal surgery. Both patients developed altered mental status, metabolic acidosis with a bicarbonate level as low as 14 mEq/L, and an anion gap > 18, without hyperglycemia. Both patients had β-hydroxybutyrate levels > 5 mmol/L.

We investigated the effect of a canola oil-supplemented diet on the metabolic state and diabetic renal function of a type I diabetes experimental model. Male Sprague-Dawley rats were randomly divided into four groups: (1) normoglycemic+chow diet, (2) normoglycemic+a canola oil-supplemented chow diet, (3) diabetic+chow diet, and (4) diabetic+a canola oil-supplemented chow diet. For 15 weeks, animals were fed a diet of Purina rat chow alone or supplemented with 30% canola oil. Energetic intake, water intake, body weight, and adipose tissue fat pad were measured; renal function, electrolyte balance, glomerular filtration rate, and the plasmatic concentration of free fatty acids, cholesterol, triglycerides, and glucose were evaluated. The mesenteric, retroperitoneal, and epididymal fat pads were dissected and weighed. The kidneys were used for lipid peroxidation (LP) and reactive oxygen species (ROS) quantifications. Diabetic rats fed with a canola oil-supplemented diet had higher body weights, were less hyperphagic, and their mesenteric, retroperitoneal, and epididymal fat pads weighed more than diabetic rats on an unsupplemented diet. The canola oil-supplemented diet decreased plasmatic concentrations of free fatty acids, triglycerides, and cholesterol; showed improved osmolarity, water clearances, and creatinine depuration; and had decreased LP and ROS. A canola oil-supplemented diet decreases hyperphagia and prevents lipotoxicity and renal dysfunction in a type I diabetes mellitus model.

OBJECTIVE: The aim was to study the effect of family history of type 2 diabetes mellitus (T2DM) on insulin sensitivity and β-cell function in normoglycemic offspring.
METHODS: Offspring of T2DM patients (cases) and individuals without family history of T2DM (controls) were the subjects for this cross-sectional study. All participants underwent 75 g OGTT and samples were collected for plasma insulin, C-peptide, and proinsulin at 0, 30, 60, and 120 minutes.
RESULTS: A total of 271 cases (age 22 ± 10 years; 53% males) and 259 controls (28 ± 10 years, 66% males) were enrolled for the study. BMI, plasma insulin, C-peptide, proinsulin, HOMA-IR, and insulinogenic index (0-120) were significantly higher and whole-body insulin sensitivity (WBISI) and disposition index (0-120) [DI 120] were lower in cases compared to controls. After adjusting for BMI, proinsulin at 120 minutes, area under the curve (AUC) of proinsulin (during OGTT) and AUC proinsulin/AUC C-peptide were significantly higher in cases. Cases were subdivided into four groups according to inheritance pattern; paternal DM (PDM), maternal DM (MDM), grandparental DM (GPDM), and both parents DM (BPDM). The magnitude of differences varied with relationship (greater when both parents and grandparents were affected). Mean HOMA-IR was higher by 127% and 50% and DI 120 was lower by 33% and 18% (adjusted for age and gender) in the BPDM and GPDM groups respectively compared to controls.
CONCLUSIONS: We observed higher BMI, plasma insulin, C-peptide, and proinsulin and lower insulin sensitivity and β-cell compensation in normoglycemic offspring of T2DM subjects compared to controls. Differences were greater when both parents and grandparents had T2DM.