Genetic Reduction of Glucose Metabolism Preserves Functional β-Cell Mass in KATP-Induced Neonatal Diabetes.

β-Cell failure and loss of β-cell mass are key events in diabetes progression. Although insulin hypersecretion in early stages has been implicated in β-cell exhaustion/failure, loss of β-cell mass still occurs in KATP gain-of-function (GOF) mouse models of human neonatal diabetes in the absence of insulin secretion. Thus, we hypothesize that hyperglycemia-induced increased β-cell metabolism is responsible for β-cell failure and that reducing glucose metabolism will prevent loss of β-cell mass.

Stranger Months: How SARS-CoV-2, Fear of Contagion, and Lockdown Measures Impacted Attendance and Clinical Activity During February and March 2020 at an Urban Emergency Department in Milan.

Objectives: An unprecedented wave of patients with acute respiratory failure due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease 2019 (COVID-19) hit emergency departments (EDs) in Lombardy, starting in the second half of February 2020. This study describes the direct and indirect impacts of the SARS-CoV-2 outbreak on an urban major-hospital ED.

Methods: Data regarding all patients diagnosed with COVID-19 presenting from February 1 to March 31, 2020, were prospectively collected, while data regarding non-COVID patients presenting within the same period in 2019 were retrospectively retrieved.

High-fat-diet-induced remission of diabetes in a subset of K -GOF insulin-secretory-deficient mice.

Aims: To examine the effects of a high-fat-diet (HFD) on monogenic neonatal diabetes, without the confounding effects of compensatory hyperinsulinaemia.

Methods: Mice expressing K channel gain-of-function (K -GOF) mutations, which models human neonatal diabetes, were fed an HFD.

Results: Surprisingly, K -GOF mice exhibited resistance to HFD-induced obesity, accompanied by markedly divergent blood glucose control, with some K -GOF mice showing persistent diabetes (K -GOF-non-remitter [NR] mice) and others showing remission of diabetes (K -GOF-remitter [R] mice).

N-cadherin Regulation of Bone Growth and Homeostasis Is Osteolineage Stage-Specific.

N-cadherin inhibits osteogenic cell differentiation and canonical Wnt/β-catenin signaling in vitro. However, in vivo both conditional Cdh2 ablation and overexpression in osteoblasts lead to low bone mass. We tested the hypothesis that N-cadherin has different effects on osteolineage cells depending upon their differentiation stage.