Obese post-menopausal women with diabetes had a higher FNBMD (8.8%, p = 0.008) and LSBMD (12.2%, p < 0.001), but those with IFG were not different from the normoglycaemia group.
A higher number of ideal CVH components was associated with a dose-dependent lower risk of diabetes for participants with normal fasting glucose but not IFG.
The prevalence in gestational diabetes of these autoimmune markers of type 1 diabetes (T1D) has been assessed in many studies, together with the risk of progression of AABs-positive GDM towards impaired glucose regulation (IFG or IGT) and overt diabetes after pregancy.
Using a CD4<sup>+</sup> T cell-mediated adoptive transfer model of autoimmune diabetes we observed that even though diabetes does not develop in recipient mice lacking IFNγ receptors, mice with MHC class II-deficient IEC were not protected from disease.
Questions remain about whether dietary cholesterol has adverse cardiovascular effects among individuals with impaired fasting glucose or diabetes (IFG/T2DM).
FBS, serving as the criterion to assess the progression of diabetes, was classified into four states including (a) normal (FBS<100mg/dl), (b) impaired fasting glucose I (IFG I) (100mg/dl<FBS<110mg/dl), (c) impaired fasting glucose II (IFG II) (110mg/dl<FBS<126mg/dl), and (d) diabetes status (FBS>126mg/dl).
The HRQOL-15D scores of 172 people with pre-diabetes (108 with Impaired Fasting Glucose [IFG], 64 with Impaired Glucose Tolerance [IGT], aged 58.3 ± 10.3 years) and 198 with NGT (aged 54.4 ± 10.1 years) from the Greek part of the DEPLAN study (Diabetes in Europe - Prevention using Lifestyle, Physical Activity and Nutritional Intervention), were compared to 100 diabetes patients' scores (aged 60.9 ± 12.5 years, diabetes duration 17.0 ± 10.0 years, HbA1c 7.2 ± 1.2%), derived from the outpatient Diabetes Clinic of a University Hospital.
Diabetes increased malondialdehyde (MDA) concentration by 39%; elevated levels of TNF-α (44%) and IFN-γ (20%); and reduced the antioxidant status in the kidney in comparison to normal control rats.
We included observational studies that applied either the tuberculin skin test or the interferon gamma release assay for diagnosis of LTBI and that provided adjusted effect estimate for the association between diabetes and LTBI.
After adjusting for age, body mass index, systolic blood pressure, triacylglycerol, high-density lipoprotein cholesterol, uric acid, creatinine, family history of diabetes, alcohol consumption, and current smoking, a positive association was found between fatty liver and the onset of IFG in both sexes with the highest quartile of FPG levels [men: adjusted hazard ratio (aHR) 1.823, 95 % confidence interval (CI) 1.316-2.534, p < 0.001; women: aHR 2.016, 95 % CI 1.117-3.6, p = 0.02].
After adjusting for confounders, the association of sarcopenia with severe fibrosis was maintained (OR 2.36, CI 1.16-4.77, P = 0.01), together with age > 50 (OR 6.53, CI 2.95-14.4, P < 0.001), IFG/Diabetes (OR 2.14, CI 1.05-4.35, P = 0.03) and NASH (OR 13.3, CI 1.64-108.1, P = 0.01).
Those with an elevated fasting plasma glucose [impaired fasting glucose or IFG] with or without an elevated HbA1c [non -diabetic hyperglycaemia; NDH] are randomised into three treatment arms: a control arm receiving no trial intervention, an arm receiving an intensive bespoke group-based diet and physical activity intervention, and an arm receiving the same intervention with enhanced support from people with T2DM trained as diabetes prevention mentors [DPM].
Rats were studied 30 days after the STZ treatment, and the diabetes untreated model group presented significantly higher kidney index, blood glucose, triglyceride (TG), total cholesterol (TC), malondialdehyde (MDA), interferon-γ (IFN-γ), and IFN-γ/IL-4 levels, lower body weight, fasting blood insulin (FPI), IL-4, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and nitric oxide (NO) levels and worse renal function (higher blood urea nitrogen (BUN), serum creatinine (SCr), urine protein (UP) levels and glomerular extracellular matrix (relative area)) compared with the normal control group (p < 0.05).
GLIS3 KD increased beta cell apoptosis basally and sensitized the cells to death induced by pro-inflammatory cytokines (interleukin 1β + interferon-γ) or palmitate, agents that may contribute to beta cell loss in respectively type 1 and 2 diabetes.
Inhibition of lysine deacetylases (KDACi) counteracts β-cell toxicity induced by the combination of IL-1 and IFNγ and reduces diabetes incidence in non-obese diabetic (NOD) mice.
IFNG-induced up-regulation of indoleamine 2,3-dioxygenase (IDO), rate-limiting enzyme of TRY-KYN pathway, decreases TRY conversion into serotonin (substrate of antidepressant effect) and increases production of KYN associated with diabetes [xanthurenic acid (XA)], anxiety (KYN), psychoses and cognitive impairment (kynurenic acid).
IFG has partly same risk factors as diabetes, and prevalence of some cardiovascular risk factors and number of risk factor in diabetes were higher than that in IFG.
Lowering the threshold to 5.6 mmol/l raised the population-attributable risk of IFG to 23% (95% CI: 20-25); its contribution to diabetes progression, however, was largely due to co-existent IGT.
IFG and IGT identified in general practice during a stepwise, high-risk screening programme for type 2 diabetes have high 1-year progression rates to diabetes.