Acta Diabetologica

Inequalities in diabetes prevalence among immigrants from Andean countries remain unknown. Andean populations are one of the largest groups of immigrants in Madrid city. We examined the association between country of birth and type 2 diabetes mellitus (T2DM) prevalence in Andean immigrant population relative to Spanish-natives; and whether this association varied by age, sex and length of residence. We analyzed 1,258,931 electronic medical records from Spanish native and Andean immigrant adults aged 40–75 years of Madrid city. We used logistic regression and test interaction terms to address our aims. Andean immigrants showed 1.13 (95% CI 1.10–1.17) greater adjusted odds for T2DM than Spanish natives. This association was positive in Ecuadorians and Bolivians but protective in Peruvians and Colombians. There was heterogeneity of this association according to age and sex. Relative to Spanish natives, odds of T2DM in Andeans of all ages and women were higher but lower in men. Andean adults showed greater odds of T2DM compared with Spanish native adults in Madrid, with variation observed by age and sex. These findings emphasize the need for studying immigrant populations in a disaggregated manner to implement specific clinical and preventive approaches.

There are several pieces of evidence indicating that Mycobacterium avium subspecies paratuberculosis (MAP) infection is linked to type 1 diabetes (T1D) in Sardinian patients. An association between MAP and T1D was recently observed in an Italian cohort of pediatric T1D individuals, characterized by a different genetic background. It is interesting to confirm the prevalence of anti-MAP antibodies (Abs) in another pediatric population from continental Italy, looking at several markers of MAP presence. New-onset T1D children, compared to age-matched healthy controls (HCs), were tested by indirect enzyme-linked immunosorbent assay for the presence of Abs toward the immunodominant MAP3865c/ZnT8 homologues epitopes, the recently identified C-terminal MAP3865c281–287 epitope and MAP-specific protein MptD. Abs against MAP and ZnT8 epitopes were more prevalent in the sera of new-onset T1D children compared to HCs. These findings support the view that MAP3865c/ZnT8 cross-reactivity is involved in the pathogenesis of T1D, and addition of Abs against these peptides to the panel of existing T1D biomarkers should be considered. It is important now to investigate the timing of MAP infection during prospective follow-up in at-risk children to elucidate whether Ab-titers against these MAP/ZnT8 epitopes are present before T1D onset and if so if they wane after diagnosis.

Bovine insulin was glycated by in vitro incubation with 20–220 mM d-glucose for 1–48 h. The percentage of glycation was dependent on time, glucose concentration, temperature and pH, attaining values up to 28%. Glucose-lowering activities of glycated and control (non-glycated) insulin preparations were assessed in mice by intraperitoneal injection in a 39% (w/v) glucose solution (2 g/kg body weight) at doses of 0.05 and 0.25 units/kg body weight. Injection of glucose alone significantly (P<0.001) increased plasma glucose concentrations at 30 min. Simultaneous administration of non-glycated insulin with glucose significantly decreased the 30-min glycaemic excursion (P<0.001) in a dose-dependent manner. Glycated insulin exhibited a significant reduction (P<0.001) in glucose-lowering activity under these conditions. The relationship between the extent of insulin glycation and glucose-lowering activity at 0.25 units/kg was assessed using five different insulin preparations glycated between 6%–28%. The insulin-induced decrease in plasma glucose at 30 min was inversely related to the extent of glycation (r=0.99). Glycated insulin (10–8 and 10–6 M) also exhibited a significantly reduced (P<0.05) ability to stimulate glucose oxidation in isolated mouse diaphragm muscle compared with non-glycated insulin. These data indicate that glycated insulin exhibits impaired biological activity which may contribute to glucose intolerance in diabetes. Further studies are required to determine if glycation of insulin occurs in man and if this process contributes to the pathogenesis of diabetes.

In this study, we aimed to demonstrate the effectiveness of serum amino-terminal proCNP (NT-proCNP) levels in predicting coronary heart disease (CHD) and cardiovascular risk in type 2 diabetes mellitus (T2DM) patients. We recruited 73 patients with T2DM in the study. Additionally, we grouped the patients according to their status of diabetic retinopathy (DR) as no DR, non-proliferative DR, or proliferative DR. Serum NT-proCNP levels of the patients were measured and their atherosclerotic cardiovascular disease (ASCVD) risk scores were calculated. There was no significant difference in terms of NT-proCNP levels between the groups (p = 0.3) and in terms of CHD and ASCVD risk scores (p = 0.4 and p = 0.4, respectively). In the correlation analysis, a significant correlation was observed between the NT-proCNP levels and the ASCVD risk score (r = 0.373; p = 0.008 among the entire cohort and r = 0.555; p = 0.01 in the non-proliferative-DR group), smoking status (r = 0.280; p = 0.03 among the entire cohort and r = 0.362; p = 0.035 in the non-proliferative-DR group), sBP (r = 0.278; p = 0.038 among the entire cohort), and dBP (r = 0.284; p = 0.034 among the entire cohort and r = 0.482; p = 0.004 in the proliferative-DR group). In the ROC analysis, we found that the NT-proCNP level predicted a high ASCVD risk score with 83.3% sensitivity and 70.8% specificity and a very high ASCVD risk score with 100% sensitivity and 69.2% specificity among the proliferative-DR patients. No cut-off value was calculated for the prediction of high and very-high ASCVD risk scores in patients with non-proliferative DR. Similarly, no cut-off value was revealed for the prediction of established coronary artery disease in all groups. Our study revealed a significant association between NT-proCNP levels and high ASCVD risk scores in patients with proliferative DR.

Acute insulin deficiency was produced in rabbits treated with anti-insulin guinea pig serum. The changes in the levels of blood sugar, free fatty acids, aceto-acetate, SGOT, SGPT, liver glutamicoxaloacetic and glutamic-pyruvic transaminases, and liver lactate dehydrogenase were examined. A significant increase of the blood glucose level and the free fatty acids as well as glycosuria was observed. The other examined parameters remained unchanged. The results confirm the statement that acute insulin deficiency causes a prompt impairment of glucose and fat metabolism.

Aerobic capacity, as indicated by maximal oxygen uptake (VO2 max) has an important role in contrasting the traditional cardiovascular risk factors and preventing cardiovascular morbidity and mortality. It is known that endothelial function, measured as flow-mediated dilation (FMD) of the brachial artery, is strictly linked to atherogenesis and cardiovascular risk. However, the relationship between VO2 max and FMD has not been fully investigated especially in healthy non-obese subjects. This preliminary study cross-sectionally investigated the relationship between VO2 max and FMD in 22 non-obese, healthy sedentary male subjects. Dividing the cohort in two subgroups of 11 subjects each according to the median value of VO2 max, the FMD was significantly lower in the subgroup with lower VO2 max (mean ± sem: 7.1 ± 0.7 vs. 9.5 ± 0.8 %; P = 0.035). Absolute VO2 max (mL min−1) was significantly and independently correlated with body fat mass (r = −0.50; P = 0.018) and with FMD (r = 0.44; P = 0.039). This preliminary study suggests that maximal oxygen uptake is independently correlated with endothelial function in healthy non-obese adults. These results are also in agreement with the possibility that improving maximal oxygen uptake may have a favorable effect on endothelial function and vice versa.

The effect of propranolol on adrenaline- and insulin-induced changes in blood glucose pyruvate, lactate, phosphorus and potassium were examined in 29 apparently healthy volunteers. A slight, but significant reduction in adrenaline-induced hyperglycaemia was noted, along with suppression of both the increase in pyruvate and lactate and the decrease in phosphorus and potassium attributable to this catecholamine. There was no significant change in the blood glucose curve after insulin whereas insulin-induced increases in pyruvate and lactate were reduced by 44%±17.7 (mean±SEM) and 78%±5.4 respectively, and the fall in phosphorus by 48%±3.1; the decrease in potassium, however, was not significantly modified. These findings suggest that changes in plasma pyruvate, lactate and inorganic phosphates induced by insulin, and regarded as espressions of its peripheral metabolism, are greatly dependent on the β-adrenergic effect of the endogenous catecholamines released during the time when blood glucose values are low.