Experimental and Clinical Endocrinology & Diabetes最新文献

Background: Type 2 diabetes mellitus (T2DM) provokes executive function and long-term memory decrements, and aerobic plus resistance training (combined training) may alleviate this T2DM-related cognitive impairment. Brain-derived neurotrophic factor (BDNF) levels have been found to be related to cognitive performance.

Aim: To analyze the effects of 8-week combined training on executive functions and circulating BDNF levels of subjects with T2DM and verify the association between BDNF levels and combined training-induced changes in executive functions and long-term memory.

Methods: Thirty-five (63±8 years old) subjects of both sexes were allocated to combined training (n=17, thrice weekly for 8 weeks) or the control group (n=18). Executive functions (evaluated through Trail making test, Stroop color task, and Digit Span), long-term memory (evaluated through the Taylor Complex Figure Test simplified), and plasma samples were compared pre- and post-intervention.

Results: Combined training improved executive function z-score compared to control (d=1.31). Otherwise, BDNF levels were not statistically altered (combined training group: 179±88 pg/mL vs. 148±108 pg/mL; control group: 163±71 pg/mL vs. 141±84 pg/mL, p>0.05). However, pre-training BDNF levels explained 50.4% of the longitudinal improvements in composite executive function z-score (r=0.71, p<0.01), 33.6% of inhibitory control (r=0.58; p=0.02), and 31.4% of cognitive flexibility (r=0.56, p=0.04) in the combined training group.

Conclusion: Combined training improved executive functions independently of alterations in resting BDNF levels after 8 weeks. Furthermore, pre-training BDNF levels explained one-half of the variance in combined training-induced improvements in executive functions.

Objective: Previous studies have shown inconsistent associations between niacin supplementation and diabetes, and little is known about the relationship between dietary niacin intake and the risk of diabetes in the general population. Our study aimed to explore the association between dietary niacin intake and the risk of diabetes in the adult population in the United States.

Methods: Data from the 2005-2016 National Health and Nutrition Examination Surveys were analyzed. Diabetes was diagnosed according to the American Diabetes Association criteria. Multivariate logistic regression models were used to estimate the association between dietary niacin intake and diabetes. Covariates included age, sex, race, family income, educational level, drinking status, smoking status, marital status, and physical activity.

Results: This study included 24494 participants, of which 13.63% had diabetes. In the fully adjusted model, a high niacin intake was significantly associated with a reduced risk of diabetes in a dose-dependent manner. When extreme quintiles of niacin intake were compared, the multivariable-adjusted odds ratio was 0.66 (95% confidence interval: 0.49, 0.88) for diabetes, and per ten-unit increment in dietary niacin intake was associated with a 14% lower risk of diabetes. When niacin intake was less than 15.01 mg/d, a ten-unit increment in niacin intake was associated with a 24% higher risk of diabetes. However, the effect was not statistically significant.

Conclusions: Our results suggest that the consumption of adequate amounts of niacin can reduce the risk of diabetes. Furthermore, this protective effect disappeared when the niacin intake was insufficient (less than 15.01 mg/d).

Introduction: Aldosterone excess is linked to cardiovascular events and mortality as well as to low-grade inflammation in the context of metabolic diseases. Whether mildly elevated aldosterone levels in the general population promote cardiovascular risk is still under debate. We analyzed the association of plasma aldosterone concentrations with incident cardiovascular events, cardiovascular and all-cause mortality as well as with biomarkers of subclinical inflammation in the population-based KORA F4 study.

Methods: Plasma aldosterone concentrations were measured with an in-house immunoflurometric assay. The analyses included 2935 participants (n=1076 for selected biomarkers of subclinical inflammation) with a median follow-up of 8.7 (8.2; 9.1) years. The associations were estimated using Cox proportional hazard and linear regression models adjusted for renin, sex, age, body mass index, arterial hypertension, diabetes, estimated glomerular filtration rate, low- and high-density lipoprotein cholesterol, physical activity, smoking, use of angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, beta-blockers, diuretics and calcium channel blockers.

Results: Aldosterone was significantly associated with all-cause mortality (hazard ratio per standard deviation increase: 1.20; 95% confidence interval 1.04-1.37), but not with cardiovascular mortality, incident cardiovascular events, or with biomarkers of subclinical inflammation.

Conclusions: Aldosterone was associated with all-cause mortality in the population-based KORA F4 study, but the previously described associations of excess aldosterone with cardiovascular complications and biomarkers of subclinical inflammation could not be shown.

Objective: To explore the clinical outcomes and establish a predictive model of hypoglycemia during colonoscopy preparation for diabetic patients.

Methods: Three-hundred ninety-four patients with diabetes who received colonoscopy were retrospectively enrolled in this study and assigned to hypoglycemia or non-hypoglycemia groups. Information about clinical characteristics and outcomes during colonoscopy preparation was collected and compared between the two groups. Logistic regression analysis was applied to identify the risk factors of hypoglycemia. These risk factors were used to construct a hypoglycemia predictive model verified by the receiver operating characteristic (ROC) curve and Hosmer-Lemeshow goodness fit test.

Results: Among 394 participants, 66 (16.8%) underwent a total of 88 hypoglycemia attacks during the bowel preparation. Grade 1 hypoglycemia (≤3.9 mmol/L) comprised 90.9% (80/88) of all hypoglycemia attacks and grade 2 hypoglycemia accounted for 9.1% (8/88), signifying that grade 1 hypoglycemia is the most common type. No severe hypoglycemia was identified. The incidence of nocturnal hypoglycemia was 15.9%. Logistic regression analyses revealed that the main risk factors of hypoglycemia during colonoscopy preparation were postprandial C-peptide, serum triglyceride, gender, type of diabetes mellitus, and insulin injection frequencies. The area under the ROC curve of the hypoglycemia prediction model was 0.777 (95% CI: 0.720-0.833).

Conclusion: Diabetic patients are prone to develop mild to moderate hypoglycemia during colonoscopy preparation. This study proposes a predictive model that could provide a reference for identifying patients with a high risk of hypoglycemia during colonoscopy preparation.

Background: Approximately one-fourth of patients treated with sodium-glucose cotransporter 2 inhibitors (SGLT2i) experience an acute estimated glomerular filtration rate (eGFR) reduction of more than 10% ("dippers"). High sodium and protein intake can increase intraglomerular pressure and predispose to a decline in renal function. We investigated whether measured creatinine clearance (CrCl) is a sensitive enough method to detect the initial dip of GFR and if dietary sodium and protein intake might influence the extent of the early change in GFR.

Methods: 28 subjects with type 2 diabetes (T2D) were enrolled. For sodium and urea determination, 24-h urinary samples were collected to estimate sodium and protein intake respectively before and 1, 3 and 6 months after SGLT2i initiation.

Results: Mean CrCl was 83.23±25.52 mL/min/1.73 m² (eGFR 67.32±16.07) and dropped by 19% at month 1 (eGFR by 6%). Dippers were 64 and 40%, according to CrCl and eGFR, respectively. Exploring the potential correlation between changes in renal function and salt intake, ΔCrCl and baseline urinary sodium were inversely related at month 1 (r=-0,61; p<0.01), at month 3 (r=-0.51; p=0.01) and month 6 (r=-0,48; p<0.05). Likewise, an inverse correlation between ΔCrCl and baseline urinary urea was demonstrated at months 1 and 3 (r=-0.46; p<0.05 for both); at month 6, a similar trend was observed (r=-0.47; p=0.054).

Conclusions: The present study suggests that a higher dietary sodium and protein intake may amplify the extent of the early dip in GFR, as detected with measured CrCl, in diabetic patients undergoing SGLT2i treatment.

Introduction: Small case series have reported that diabetic ketoacidosis is associated with an elevated osmolar gap, while no previous studies have assessed the accuracy of calculated osmolarity in the hyperosmolar hyperglycemic state. The aim of this study was to characterize the magnitude of the osmolar gap in these conditions and assess whether this changes over time.

Methods: In this retrospective cohort study, two publicly available intensive care datasets were used: Medical Information Mart of Intensive Care IV and the eICU Collaborative Research Database. We identified adult admissions with diabetic ketoacidosis and the hyperosmolar hyperglycemic state who had measured osmolality results available contemporaneously with sodium, urea and glucose values. Calculated osmolarity was derived using the formula 2Na + glucose + urea (all values in mmol/L).

Results: We identified 995 paired values for measured and calculated osmolarity from 547 admissions (321 diabetic ketoacidosis, 103 hyperosmolar hyperglycemic states and 123 mixed presentations). A wide variation in the osmolar gap was seen, including substantial elevations and low and negative values. There was a greater frequency of raised osmolar gaps at the start of the admission, which tends to normalize by around 12-24 h. Similar results were seen regardless of the admission diagnosis.

Conclusions: The osmolar gap varies widely in diabetic ketoacidosis and the hyperosmolar hyperglycemic state and may be highly elevated, especially at admission. Clinicians should be aware that measured and calculated osmolarity values are not interchangeable in this population. These findings should be confirmed in a prospective study.

The growing amount of evidence suggests the existence of a bidirectional relation between coronavirus disease 2019 (COVID-19) and type 2 diabetes mellitus (T2DM), as these two conditions exacerbate each other, causing a significant healthcare and socioeconomic burden. The alterations in innate and adaptive cellular immunity, adipose tissue, alveolar and endothelial dysfunction, hypercoagulation, the propensity to an increased viral load, and chronic diabetic complications are all associated with glucometabolic perturbations of T2DM patients that predispose them to severe forms of COVID-19 and mortality. Severe acute respiratory syndrome coronavirus 2 infection negatively impacts glucose homeostasis due to its effects on insulin sensitivity and β-cell function, further aggravating the preexisting glucometabolic perturbations in individuals with T2DM. Thus, the most effective ways are urgently needed for countering these glucometabolic disturbances occurring during acute COVID-19 illness in T2DM patients. The novel classes of antidiabetic medications (dipeptidyl peptidase 4 inhibitors (DPP-4is), glucagon-like peptide-1 receptor agonists (GLP-1 RAs), and sodium-glucose co-transporter-2 inhibitors (SGLT-2is) are considered candidate drugs for this purpose. This review article summarizes current knowledge regarding glucometabolic disturbances during acute COVID-19 illness in T2DM patients and the potential ways to tackle them using novel antidiabetic medications. Recent observational data suggest that preadmission use of GLP-1 RAs and SGLT-2is are associated with decreased patient mortality, while DPP-4is is associated with increased in-hospital mortality of T2DM patients with COVID-19. Although these results provide further evidence for the widespread use of these two classes of medications in this COVID-19 era, dedicated randomized controlled trials analyzing the effects of in-hospital use of novel antidiabetic agents in T2DM patients with COVID-19 are needed.

Aims: Gastrointestinal disorders, including constipation and fecal incontinence, are common in type 2 diabetes mellitus (T2DM) and may derive from diabetic autonomic neuropathy, severe intestinal bacterial overgrowth, or a dysfunctional anorectal sphincter. The present study aims to characterize the correlation between these conditions.

Methods: Patients with T2DM, prediabetes, and normal glucose tolerance (NGT) were included. The anorectal function was assessed with high-resolution anorectal manometry. Patients were screened for autonomic neuropathy by measuring olfactory, sweat, and erectile dysfunction as well as heart rate variability. Constipation and fecal (in-)continence were evaluated using validated questionnaires. Breath tests were used to assess severe intestinal bacterial overgrowth.

Results: We included 59 participants (32 (54.2%) with T2DM, 9 (15.3%) with prediabetes, and 18 (30.5%) NGT). The presence of autonomic neuropathy, severe bacterial overgrowth, and symptoms of constipation and incontinence were comparable. HbA_1c was correlated with an increased anorectal resting sphincter pressure (r=0.31, P=0.019) and constipation symptoms (r=0.30, P=0.031). In patients with a long-standing diagnosis of T2DM, significantly higher values for maximum anorectal resting pressure (Δ=+27.81±7.84 mmHg, P=0.0015) and baseline pressure (Δ=20.50±9.74 mmHg, P=0.046) were found compared with NGT, but not with prediabetes.

Conclusions: Long-standing T2DM increases anorectal sphincter activity, and constipation symptoms are associated with higher HbA_1c levels. The lack of an association of symptoms with autonomic neuropathy suggests glucotoxicity as the primary mechanism.

Background: In type 2 diabetes, insulin resistance is observed, and β-cells are incapable of responding to glycemia demands, leading to hyperglycemia. Although the nature of β-cells dysfunction in this disease is not fully understood, a link between the induction of pancreatic β-cell premature senescence and its metabolic implications has been proposed. This study aimed to understand the relationship between diabetes and pancreatic senescence, particularly at the beginning of the disease.

Methods: C57Bl/6 J mice were fed two different diets, a normal diet and a high-fat diet, for 16 weeks. Pancreatic histomorphology analysis, insulin quantification, inflammation parameters, and senescence biomarkers for the experimental animals were assessed at weeks 12 and 16.

Results: The results proved that diabetes onset occurred at week 16 in the High Fat Diet group, supported by glycaemia, weight and blood lipid levels. Increased β-cells size and number accompanied by increased insulin expression were observed. Also, an inflammatory status of the diabetic group was noted by increased levels of systemic IL-1β and increased pancreatic fibrosis. Finally, the expression of galactosidase-beta 1 (GLB1) was significantly increased in pancreatic β-cells.

Conclusion: The study findings indicate that senescence, as revealed by an increase in GLB1 expression, is a key factor in the initial stage of diabetes.