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PubMed2026

Early Cardiomyopathy in Prediabetic NDPK-B-Deficient Mice Is Associated with Remodeling of the Mitochondrial O-GlcNAc Proteome.

Diabetic cardiomyopathy (DCM) is characterized by myocardial remodeling that may already be evident during prediabetes, yet the molecular alterations accompanying these early changes remain poorly understood. The present study examined mouse models of Nucleoside diphosphate kinase B (NDPK-B)-deficient prediabetes and streptozotocin-induced diabetes using O-GlcNAc-associated proteomic profiling to define stage-specific molecular alterations during the progression from prediabetic to diabetic cardiomyopathy. Both models exhibited increased left ventricular extracellular matrix deposition and impaired diastolic function, together with activation of the hexosamine biosynthesis pathway. Profiling of O-GlcNAc-associated proteins uncovered extensive remodeling of the mitochondrial proteome already at the prediabetic stage, with respiratory complex I among the most prominently altered targets, alongside changes in substrate metabolism and inflammatory signaling. In overt DCM, the putative O-GlcNAc proteomic profile was associated with a shift toward wider lipid-dependent metabolic reprogramming and remodeling of mitochondrial proteins. These findings identify early remodeling of the mitochondrial O-GlcNAc-associated proteome as a molecular signature of prediabetic cardiomyopathy and highlight respiratory complex I proteins as candidate targets for future mechanistic investigations.

Animals↗

PubMed2026

Effects of time-restricted eating on markers of glucose metabolism and regulation in individuals with prediabetes or type 2 diabetes: a systematic review and meta-analysis of randomised controlled trials.

AIMS/HYPOTHESIS: This systematic review and meta-analysis aimed to investigate the effects of time-restricted eating (TRE) on glucose metabolism and regulation in individuals with prediabetes (fasting blood glucose of 5.6-6.9 mmol/l or HbA1c of 39-47 mmol/mol [5.7-6.4%]) or type 2 diabetes (fasting blood glucose ≥7 mmol/l or HbA1c ≥48 mmol/mol [6.5%]). METHODS: A literature search was performed in MEDLINE, Embase and CENTRAL from inception to 5 August 2025. Moreover, forward and backward citation searches were performed. Eligible studies were RCTs in adults with prediabetes or type 2 diabetes, lasting ≥2 weeks, reporting markers of glucose metabolism and regulation, comparing TRE (≤12 h eating window) with a non-time-restricted control diet. Studies involving pregnancy, other fasting regimens, or non-peer-reviewed publications were excluded. Data were pooled as weighted mean differences with 95% CIs using random-effects generic inverse variance models in Cochrane Review Manager Web, and results are presented as forest plots. The certainty of evidence was defined using Grading of Recommendations, Assessment, Development and Evaluations methodology, and risk of bias was estimated by using the Revised Cochrane risk-of-bias tool for randomised trials (RoB 2). RESULTS: Out of 2043 records identified through the database search, as well as 1249 from forward and backward citation searches, ten RCTs including 599 participants were included. The mean length of the studies was 4 months, and the eating windows ranged from 4 to 10 h per day. The pooled meta-analysis showed no overall effect of TRE on HbA1c (-3.33 mmol/mol; 95% CI -6.87, 0.20 (-0.30% points; -0.63, 0.02); p=0.06, moderate certainty). Nevertheless, following stratification by subgroups, TRE resulted in a reduction in HbA1c of 0.93 mmol/mol (-1.70, -0.17 [-0.09% points; -0.16, -0.02]; p=0.02) in individuals with prediabetes but not in individuals with type 2 diabetes (-4.68 mmol/mol; -10.08, 0.72 (-0.43% points; -0.92, 0.07); p=0.09). TRE reduced fasting blood glucose in the pooled analysis (-0.30 mmol/l; -0.53, -0.07; p<0.01, moderate certainty) as well as in the subgroup analyses in individuals with prediabetes (-0.14 mmol/l; -0.27, -0.01; p=0.03) and with type 2 diabetes (-0.48 mmol/l; -0.78, -0.17; p<0.01). Moreover, TRE lowered body weight by 1.6 kg (-2.2, -1.0; p<0.001) in the pooled analysis. The evidence was limited by imprecision arising from wide confidence intervals in some of the included studies, which may be due to small sample sizes. Lastly, the effects of TRE on markers of insulin sensitivity, beta cell function and continuous glucose monitoring measurements were inconclusive. CONCLUSIONS/INTERPRETATION: Moderate-certainty evidence indicates that TRE reduces fasting blood glucose but not HbA1c. The subgroup analyses revealed that TRE improved HbA1c and fasting glucose in individuals with prediabetes and improved fasting glucose in individuals with type 2 diabetes. Future large-scale studies should investigate long-term effects of TRE in prevention and treatment of type 2 diabetes. TRIAL REGISTRATION: PROSPERO CRD42024523591 FUNDING: This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors. Three authors (JS, A-DT, THA) are employed at Steno Diabetes Center Copenhagen, a public hospital and research institution under the Capital Region of Denmark, partly funded by a grant from the Novo Nordisk Foundation.

Humans↗

PubMed1978

[Pathogenesis of diabetes in adulthood. I. Insulin secretion at different evolutionary phases of diabetes].

Intravenous loading with glucose and glucose+tolbutamid was conduced in five groups of subjects, selected in a way that the intensity of insulin secretion gradually decreases from one group to the other (control group, relatives of patients with diabetes, diabetics sensitive to SUP and diabetics resistant to SUP). With insulin deficiency (in the last three groups) the early insulin secretion (absence of summit in IRI curve at the tenth minute), was established to grow weak, whereas in latent diabetes and in SUP sensitive diabetics it was preserved and insulinemia was protracted during the second half of the test. Early insulin secretion, in the control group and in the relatives of the diabetics, with loading with glucose-tolbutamid was twice as high as compared with that, obtained with loading solely with glucose. Diabetes at a mature age is concluded to be with a changed sensitivity of B-cells, at the beginning, versus glucose as a stimulator with signaling character, but the ability for synthesis and secretion of insulin, in general, is preserved. With the evolution of diabetes defect, the falling-off of insulin-synthesis ability is included in the pathogenetic mechanisms. A state of complete insulin deficiency develops--hence non-sensitivity to SUP.

Adult↗

PubMed2026

Molecular Signature of Prediabetes With High-Risk of Diabetes Revealed by Deep Plasma Proteome.

AIMS: Prediabetes is biologically heterogeneous, but molecular subtypes linked to diabetes progression remain poorly defined. We aimed to identify plasma proteome-based subtypes of impaired fasting glucose (IFG), characterise their molecular features and assess their association with future diabetes risk. MATERIALS AND METHODS: We quantified 2584 plasma proteins using liquid chromatography-mass spectrometry in 538 IFG participants from a prospective discovery cohort (Nutrition and Health of Aging Population in China, NHAPC). Proteomic subtypes were defined by consensus clustering, linked to longitudinal changes in insulin sensitivity and incident type 2 diabetes mellitus (T2DM), which were further validated in an independent Shanghai Brain Aging Study (SBAS) cohort. RESULTS: Two reproducible IFG molecular subtypes based on plasma proteomics were identified. The high-risk subtype showed higher incident diabetes and a greater 6-year decline in insulin sensitivity and was characterised by enrichment of glycolysis/gluconeogenesis, insulin signalling and neutrophil degranulation, together with a dyslipidemic lipidomic profile indicating co-dysregulation of glucose and lipid homeostasis. The low-risk subtype demonstrated a higher complement cascade and high-density lipoprotein particle remodelling signature. In the high-risk subtype, key proteins and lipids showed stronger associations with longitudinal declines in insulin sensitivity, including PPBP, PGK1 and ALDOA, as well as PE-P 18:0/20:3 and PE-P 18:1/20:3. CONCLUSIONS: Proteome-based molecular subtyping stratifies IFG individuals with similar fasting glucose levels but distinct biology and future diabetes risk, supporting earlier and more targeted prevention.

Humans↗

PubMed2026

Acute mild cold exposure with shivering reduces 24 h glucose levels in individuals with type 2 diabetes but not prediabetes.

AIMS/HYPOTHESIS: Repeated cold exposure with shivering has been proposed as a potential strategy to enhance glucose metabolism by increasing energy expenditure and substrate utilisation. However, acute effects/benefits of cold-induced shivering on glucose homeostasis in metabolically compromised individuals are unknown. Here, we aimed to determine whether cold exposure at two different intensities improves 24 h glucose homeostasis in individuals with prediabetes and type 2 diabetes. METHODS: In a randomised crossover trial conducted in the South Limburg/Maastricht region of the Netherlands, men and postmenopausal women with prediabetes (n=12) and stable type 2 diabetes (n=12), aged 40-75 years, body mass index ≥27 and ≤35 kg/m2, non-smoking and sedentary, underwent two whole-body cold exposure sessions using a water-perfused suit. Session order was randomised using an online randomisation tool (randomizer.org); participants were masked to the cold exposure intensity received, but investigators were not. Sessions were designed to elicit ~1.5-fold (mild, 15°C) and ~2.5-fold (moderate, 4°C) increases in resting metabolic rate (RMR). Continuous glucose monitoring assessed interstitial glucose concentrations over 24 h periods before and after each intervention, with controlled diet and activity. Shivering was confirmed via indirect calorimetry and electromyography. RESULTS: In both study groups and periods, RMR increased significantly vs baseline (p<0.001 for all). In prediabetes, the increase in the final 1 h of cold was 1.53 × RMR in mild and 1.94 × RMR in moderate cold. In type 2 diabetes, the increase was 1.57 × RMR and 2.09 × RMR in the final 1 h of mild and moderate cold, respectively. In prediabetes, neither mild nor moderate cold exposure altered mean 24 h glucose levels. In contrast, after mild cold exposure the type 2 diabetes group exhibited a significant reduction in mean 24 h glucose levels (-0.6 ± 0.5 mmol/l, p=0.003) and fasting glucose (-0.6 ± 0.8 mmol/l, p=0.019), as well as an increase in time in normal range (+8.8 ± 10.3%, p=0.013) and reduced time in hyperglycaemia (-10.9 ± 12.9%, p=0.014). Moderate cold did not significantly affect any of the glucose outcomes in type 2 diabetes. Baseline fasting glucose, age and ALT levels were predictors of the glucose-lowering response, suggesting greater benefits in individuals who have higher baseline glucose levels, are younger and/or have more optimal liver health, i.e. lower ALT. CONCLUSIONS/INTERPRETATION: Acute mild cold exposure with shivering reduced 24 h glucose levels in individuals with type 2 diabetes. No changes were observed in prediabetes. The observed effects appear to depend on baseline metabolic status rather than acute substrate utilisation during cold exposure. These findings support the potential of cold exposure as an adjunct non-pharmacological therapy for type 2 diabetes, although further mechanistic studies and validation in larger cohorts are warranted. TRIAL REGISTRATION: ClinicalTrials.gov NCT05576025 FUNDING: Dutch Organisation for Knowledge and Innovation in Health, Healthcare and Well-being (ZonMw): 09120012010062.

Humans↗

PubMedDate not supplied

[State of the microcirculation in the relatives of diabetes mellitus patients].

The biomicroscopic study of the conjunctival vessels demonstrated microcirculation disturbances in 43.8% of 105 relatives of diabetic patients, and in 8.5% changes of the optic fundus vessels, irrespective of the glucose tolerance test results. There was a statistically significant difference between the total conjunctival index and its partial values in the relatives of diabetic patients in comparison with the control (healthy) group, and in patients with newly diagnosed diabetes mellitus as compared with the control group and with the group of relatives with a normal glucose tolerance test.

Adolescent↗

PubMed1977

[Pregnancy and diabetes].

There is a mutual effect between gravidity and diabetes. Diabetes can have disadvantageous effect over gravidity, but the state of gravidity can contribute to the earlier diagnosis of diabetes. The author had 4850 cases of gravidity of 1686 women, indiscriminately, suffering from diabetes observed and on the basis of his observation he found that the manifestations of diabetes in the state of gravidity are respectively infrequent nowadays but the number of manifestation increases parallel with the fatness of women. The transitional diabetogen effect, the pathologic gravidities and the huge-embryos are, however, able to indicate the early stage of diabetes, that other methods or medical examinations could not still indicate. The birth of huge-embryos is the earliest and most characteristic praediabetic sign and it can appear 30 to 50 years before the development of diabetic trouble of metabolism. The number of pathological gravidities increases parallel with the advance of diabetic manifestation. The author emphasises on basis of his observations the importance of obstetrical and pregnancy-anamnesis in the prevention of diabetic manifestation and in the reduction of foetal losses.

Adult↗

PubMed1976

Locating the site(s) of insulin resistance in patients with nonketotic diabetes mellitus.

Insulin resistance and the ability of insulin to inhibit hepatic glucose production and to increas efficiency of glucose uptake were determined in 24 nonobese individuals: eight subjects with normal oral glucose tolerance, eight patients with chemical diabetes, and eight nonketotic patients with fasting hyperglycemia (greater than 150 mg. per cent). Insulin resistance was estimated by measuring the steady-state plasma glucose response to a continuous infusion of insulin, glucose, epinephrine, and propranolol. This approach permits us to inhibit levels of exogenous insulin, and use the height of the steady-state plasma glucose response as a direct estimate of insulin resistance. The ability of insulin to inhibit hepatic glucose production and to increase efficiency of glucose uptake was calculated from the results of two studies in which a continuous infusion of 3H-2-glucose was used to measure glucose turnover rate. The first study was performed after an overnight fast, under conditions of basal insulin levels, while the second was conducted during the infusion of insulin, glucose, epinephrine, and propranolol. Hepatic glucose production is equal to glucose turnover rate during the basal study and is equal to glucose turnover rate minus the infusion rate of cold glucose during the second study. Glucose uptake in both studies is equal to glucose turnover rate minus urinary glucose loss, and the efficiency of glucose uptake is calculated by dividing glucose uptake by the plasma glucose pool size. The mean (+/- S.E.) steady-state plasma glucose response was 113 +/- 9 mg. per cent in normal subjects, 205 +/- 14 mg. per cent in chemical diabetics, and 346 +/- 30 mg. per cent in patients with fasting hyperglycemia. Thus, insulin resistance exists in monoketotic diabetes, and the greater the degree of glucose intolerance, the greater the insulin resistance. The resistance to the insulin infusion in patients with chemical diabetes seemed to be mainly a function of the inability of insulin to increase efficiency of glucose uptake, since insulin did retain its ability to inhibit glucose production (although not to normal levels). In contrast, the infusion of insulin neither inhibited hepatic glucose production nor increased efficienty of glucose uptake in patients with fasting hyperglycemia. Thus, the insulin resistance that exists in patients with nonketotic diabetes cannot be considered to be a global phenomenon. Significant differences exist in the responsiveness of various tissues to the two general aspects of insulin's action on glucose homeostasis, and these differences provide a physiologic basis for the variations in degree of over-all insulin resistance that are present in the three groups of subjects.

Adult↗

PubMedDate not supplied

Congenital anomalies and the diabetic and prediabetic pregnancy.

Congenital anomalies are two to four times more frequent in the offspring of diabetic mothers than in those of non-diabetic mothers, and represent an increasingly important cause of perinatal mortality. These anomalies involve multiple organ systems more often than those found in the children of non-diabetic mothers. The excess of anomalies associated with maternal diabetes occurs in many organ systems. Anomalies are no more frequent in the offspring of diabetic fathers and pre-diabetic mothers than among those of non-diabetics, suggesting that non-genetic factors are the important determinants. Anomalies are most frequent in the offspring of mothers who have developed diabetes at an early age, many of whom have diabetes of long duration, are insulin-treated, and may have vascular complications. The relative importance of each of these factors in the pathogenesis of anomalies is unknown, but present evidence is consistent with a hypothesis that anomalies are the result of metabolic disturbances in the intrauterine environment during the first trimester of pregnancy. Whether or not their incidence can be reduced by optimum metabolic control of maternal diabetes during this period is unknown.

Congenital Abnormalities↗

PubMed1979