Marked Increase in Urinary C-peptide Levels after Treatment with Sacubitril/Valsartan in Patients with Type 2 Diabetes Mellitus and Hypertension.

Sacubitril/valsartan, a novel therapy in chronic heart failure (CHF), inhibits the breakdown of various peptides. However, whether or not sacubitril/valsartan administration affects urinary C-peptide levels is unclear. We herein report a 70-year-old man with type 2 diabetes mellitus (T2DM) and hypertension coexisting with CHF and nephrotic syndrome.

Impact of COVID-19 pandemic on glycemic control among outpatients with type 2 diabetes in Japan: A hospital-based survey from a country without lockdown.

Aims: Some studies have reported changes in glycemic control of patients with diabetes mellitus under lockdown. However, no previous study examined the impact of the pandemic on glycemic control in patients with diabetes in countries that did not introduce a lockdown such as Japan. This study aimed to assess changes in glycemic control during the pandemic in patients with type 2 diabetes treated at a Japanese clinic.

[Present Execution of and Problems with Clinical Lipid Examination and Application of "the Japan Atherosclerotic Society (JAS) Guidelines for Prevention of Atherosclerotic Cardiovascular Diseases 2012"].

It is well known that dyslipidemia is one of the most crucial risk factors for atherosclerosis, including cardiovascular diseases (ASCVD). In order to prevent the onset of ASCVD, the Japan Atherosclerotic Society (JAS) published the JAS Guidelines in 2012 for appropriate lipid examination and treatment. However, it is unknown how the guidelines are practically used by Japanese clinicians.

Atf6α-null mice are glucose intolerant due to pancreatic β-cell failure on a high-fat diet but partially resistant to diet-induced insulin resistance.

Activating transcription factor 6α (ATF6α) is essential for the endoplasmic reticulum (ER) stress response. Since recent studies suggested that ER stress is involved in the pathogenesis of type 2 diabetes mellitus, we have analyzed Atf6α-null (Atf6α(-/-)) mice challenged with metabolic overload or genetic manipulations. Atf6α(-/-) mice were fed a high-fat diet to create diet-induced obese (DO) mice, and were subjected to examination of glucose homeostasis with biochemical and morphological analysis of the pancreatic β-cell and liver tissues.

The JNK pathway modulates expression and phosphorylation of 4E-BP1 in MIN6 pancreatic beta-cells under oxidative stress conditions.

Stress-mediated apoptosis may play a crucial role in loss of pancreatic beta-cell mass, contributing to the development of diabetes. We have recently identified that translational control involving the translational suppressor eIF4E binding protein-1 (4E-BP1) which is important for beta-cell survival under endoplasmic reticulum (ER) stress. The Eif4ebp1 gene, encoding 4E-BP1, is a direct target of a transcription factor activating transcription factor-4 (ATF4), a master regulator of gene expression in stress responses.