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Background: Sudomotor dysfunction is one of the earliest manifestations of small fiber neuropathy (SFN), reflecting the alteration of sympathetic C fiber innervation of the sweat glands. Among other techniques, such innervation can be assessed by measuring electrochemical skin conductance (ESC) in microsiemens (µS). In this study, ESC was measured at the feet to detect distal SFN. For this objective, the performance of a new device, the Body Scan® (Withings, France), intended for home use, was compared with that of a reference device, the Sudoscan® (Impeto Medical, France), which requires a hospital setting. Methods: In patients with diabetes with or without neuropathy or non-diabetic patients with lower-limb neuropathy, the diagnostic performance of the Body Scan® measurement was assessed by calculating its sensitivity (Se) and specificity (Sp) to detect at least moderate SFN (Se70 and Sp70), defined by a value of feet ESC ≤ 70 µS and > 50 µS on the Sudoscan® measure, or severe SFN (Se50 and Sp50), defined by a value of feet ESC ≤ 50 µS on the Sudoscan® measure. The agreement between the two devices was assessed with the analysis of Bland-Altman plots, mean absolute error (MAE), and root mean squared error (RMSE) calculations. The repeatability of the measurements was also compared between the two devices. Results: A total of 147 patients (52% men, mean age 59 years old, 76% diabetic) were included in the analysis. The sensitivity and specificity to detect at least moderate or severe SFN were: Se70 = 0.91 ([0.83, 0.96]), Sp70 = 0.97 ([0.88, 0.99]), Se50 = 0.91 ([0.80, 0.98]), and Sp50 = 0.99 ([0.94, 1]), respectively. The bias and 95% limits of agreement were 1.5 [-5.4, 8.4]. The MAE was 2.9 and the RMSE 3.8. The intra-sample variability was 2.0 for the Body Scan® and 2.3 for the Sudoscan®. Conclusion: The ESC measurements provided by the Body Scan® were in almost perfect agreement with those provided by the reference device, the Sudoscan®, which validates the accuracy of the Body Scan® for the detection of SFN. By enabling simple, rapid, and autonomous use by the patient at home, this new technique will facilitate screening and monitoring of SFN in daily practice. [ABSTRACT FROM AUTHOR]

A significant number of studies invoked diabetes as a risk factor for virus infections, but the issue remains controversial. We aimed to examine whether non-autoimmune diabetes mellitus enhances the risk of virus infections compared with the risk in healthy individuals without non-autoimmune diabetes mellitus. In this systematic review and meta-analysis, we assessed case-control and cohort studies on the association between non-autoimmune diabetes and viruses. We searched PubMed, Embase, Cochrane Database of Systematic Reviews, Cochrane Central Register of Controlled Trials, and Web of Science with no language restriction, to identify articles published until February 15, 2021. The main outcome assessment was the risk of virus infection in individuals with non-autoimmune diabetes. We used a random-effects model to pool individual studies and assessed heterogeneity (I2) using the χ2 test on Cochrane's Q statistic. This study is registered with PROSPERO, number CRD42019134142. Out of 3136 articles identified, we included 68 articles (90 studies, as the number of virus and or diabetes phenotype varied between included articles). The summary OR between non-autoimmune diabetes and virus infections risk were, 10.8(95% CI: 10.3–11.4; 1-study) for SARS-CoV-2; 3.6(95%CI: 2.7–4.9, I2 = 91.7%; 43-studies) for HCV; 2.7(95% CI: 1.3–5.4, I2 = 89.9%, 8-studies;) for HHV8; 2.1(95% CI: 1.7–2.5; 1-study) for H1N1 virus; 1.6(95% CI: 1.2–2.13, I2 = 98.3%, 27-studies) for HBV; 1.5(95% CI: 1.1–2.0; 1-study) for HSV1; 3.5(95% CI: 0.6–18.3 , I2 = 83.9%, 5-studies) for CMV; 2.9(95% CI: 1–8.7, 1-study) for TTV; 2.6(95% CI: 0.7–9.1, 1-study) for Parvovirus B19; 0.7(95% CI: 0.3–1.5 , 1-study) for coxsackie B virus; and 0.2(95% CI: 0–6.2; 1-study) for HGV. Our findings suggest that, non-autoimmune diabetes is associated with increased susceptibility to viruses especially SARS-CoV-2, HCV, HHV8, H1N1 virus, HBV and HSV1. Thus, these viruses deserve more attention from diabetes health-care providers, researchers, policy makers, and stakeholders for improved detection, overall proper management, and efficient control of viruses in people with non-autoimmune diabetes. [ABSTRACT FROM AUTHOR]

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OBJECTIVE -- To evaluate day-to-day variations of insulin needs in type 2 diabetic patients with end-stage renal disease (ESRD) on maintenance hemodialysis. RESEARCH DESIGN AND METHODS -- We developed a 24-h euglycemic clamp in patients who received an average of 2,200 calories in a standardized three-meal and two-snack regimen per day, adjusted to body size and sex. Intravenous insulin was adjusted every 30 min to achieve 5.5 ± 1.1 mmol/l glycemia over 24 h prehemodialysis, during hemodialysis session, and 24 h posthemodialysis in 10 type 2 diabetic patients, aged 55.7 ± 8.7 years with 11.9 ± 4.5 years diabetes duration, undergoing maintenance hemodialysis for 2.3 ± 2.3 years. Insulin requirements were derived from the dose of insulin administered to maintain euglycemia per period of time and day-to-day comparisons performed. RESULTS -- Mean capillary glycemia was 5.5 ± 0.3 mmol/l prehemodialysis and 5.3 ± 0.2 mmol/l posthemodialysis (P = 0.39). Pre- and posthemodialysis areas under the glucose curve were comparable. This was achieved by infusing 23.6 ± 7.7 IU/24 h prehemodialysis vs. 19.9 ± 4.9 IU/24 h posthemodialysis, indicating a 15.3% decrease posthemodialysis (P = 0.09). Basal insulin needs decreased from 0.4 ± 0.1/h prehemodialysis to 0.3 ± 0.1/h posthemodialysis (P = 0.01). Total boluses were decreased by 2.2 ± 3.1 IU (P =0.15). Changes in blood urea did not correlate with changes in insulin needs (r = 0.1, P = 0.79). CONCLUSIONS--The present study has demonstrated a significant 25% reduction in basal insulin requirements the day after dialysis compared with the day before. No significant change in boluses was observed, and overall the reduction of total insulin requirements was -15% equivalent to -4 IU/day posthemodialysis of marginal statistical significance. [ABSTRACT FROM AUTHOR]

OBJECTIVE--The clinical expression of maturity-onset diabetes of the young (MODY)-3 is highly variable. This may be due to environmental and/or genetic factors, including molecular characteristics of the hepatocyte nuclear factor 1-α (HNF1A) gene mutation. RESEARCH DESIGN AND METHODS--We analyzed the mutations identified in 356 unrelated MODY3 patients, including 118 novel mutations, and searched for correlations between the genotype and age at diagnosis of diabetes. RESULTS--Missense mutations prevailed in the dimerization and DNA-binding domains (74%), while truncating mutations were predominant in the transactivation domain (62%). The majority (83%) of the mutations were located in exons 1- 6, thus affecting the three HNF1A isoforms. Age at diagnosis of diabetes was lower in patients with truncating mutations than in those with missense mutations (18 vs. 22 years, P = 0.005). Missense mutations affecting the dimerization/DNA-binding domains were associated with a lower age at diagnosis than those affecting the transactivation domain (20 vs. 30 years, P = 10-4). Patients with missense mutations affecting the three isoforms were younger at diagnosis than those with missense mutations involving one or two isoforms (P = 0.03). CONCLUSIONS--These data show that part of the variability of the clinical expression in MODY3 patients may be explained by the type and the location of HNF1A mutations. These findings should be considered in studies for the search of additional modifier genetic factors. Diabetes 57:503-508, 2008 [ABSTRACT FROM AUTHOR]

Summary: Background: Type 2 diabetes is affected by genetics and environmental factors. We aimed to assess the effect of an in-utero diabetic environment independently of the genetic background for type 2 diabetes. Methods: We measured insulin sensitivity and insulin secretion in response to oral and intravenous glucose in 15 non-diabetic adult offspring of mothers with type 1 diabetes (exposed participants) and 16 offspring of type 1 diabetic fathers (controls). No participants had type 1 diabetes-associated autoantibodies. We also measured pancreatic polypeptide, a marker of parasympathetic drive to the pancreas. Findings: There was no difference between the groups with respect to percent body fat and insulin sensitivity. Five of the 15 exposed participants, but none of the controls had impaired glucose tolerance (p=0.02). Early insulin secretion after an oral glucose tolerance test was lower in exposed participants than in controls: 8.6 IU/mmol (SD 5.4) in exposed participants with impaired glucose tolerance, 14.2 IU/mmol (6.5) in those with normal glucose tolerance and 17.7 IU/mmol (10.9) in controls (p=0.04). Mean insulin secretion rate during glucose infusion study was 4.7 pmol/kg per min (3.6) in people with impaired glucose tolerance, 5.5 pmol/kg per min (4.5) in exposed participants with normal glucose tolerance and 7.5 pmol/kg per min (6.1) in controls (p<0.0001). The area under the curve of pancreatic polypeptide 120 min after oral glucose ingestion was 1007 (429) in people with impaired glucose tolerance, 2829 (1701) in those with normal glucose tolerance, and 3224 (1352) in controls (p=0.04). Interpretation: Exposure to a diabetic environment in utero is associated with increased occurrence of impaired glucose tolerance and a defective insulin secretory response in adult offspring, independent of genetic predisposition to type 2 diabetes. This insulin secretory defect could be related to low parasympathetic tone. Epidemiological studies are needed... [ABSTRACT FROM AUTHOR]