Effects of Sodium Glucose Co-Transporter 2 Inhibitors in Type 1 Diabetes Mellitus on Body Composition and Glucose Variabilities: Single-Arm, Exploratory Trial.

Introduction: Sodium glucose co-transporter 2 (SGLT2) inhibitors are widely used in the management of type 2 diabetes mellitus; they prevent cardiovascular events and reduce fat mass. However, little is known about the effects of SGLT2 inhibitors on type 1 diabetes mellitus as an adjuvant to insulin therapy. Therefore, we aimed to elucidate the effects of SGLT2 inhibitors on body composition of patients with type 1 diabetes mellitus and assess blood glucose variability.

Assessing Patient Satisfaction Following Sodium Glucose Co-Transporter 2 Inhibitor Treatment for Type 1 Diabetes Mellitus: A Prospective Study in Japan.

Introduction: In Japan, several sodium glucose co-transporter 2 (SGLT2) inhibitors have been used for type 1 diabetes mellitus as an adjuvant therapy to insulin therapy; however, there are no clinical reports regarding the satisfaction of its use. Therefore, we conducted a survey among patients with type 1 diabetes undergoing treatment using an SGLT2 inhibitor.

Methods: This is a single-arm open-label prospective study including 24 patients with type 1 diabetes who were to be initiated on ipragliflozin treatment between March and August 2019.

Effects of ipragliflozin versus metformin in combination with sitagliptin on bone and muscle in Japanese patients with type 2 diabetes mellitus: Subanalysis of a prospective, randomized, controlled study (PRIME-V study).

Aims/introduction: Recent randomized clinical trials have suggested that sodium-glucose cotransporter 2 inhibitors might reduce cardiovascular events and heart failure, and have renal protective effects. Despite these remarkable benefits, the effects of sodium-glucose cotransporter 2 inhibitors on bone and muscle are unclear.

Materials And Methods: A subanalysis of a randomized controlled study was carried out to evaluate the effects of the sodium-glucose cotransporter 2 inhibitor, ipragliflozin, versus metformin on bone and muscle in Japanese patients with type 2 diabetes mellitus (baseline body mass index ≥22 kg/m and hemoglobin A1c 7-10%) who were already receiving sitagliptin.

Comparing the effects of ipragliflozin versus metformin on visceral fat reduction and metabolic dysfunction in Japanese patients with type 2 diabetes treated with sitagliptin: A prospective, multicentre, open-label, blinded-endpoint, randomized controlled study (PRIME-V study).

A prospective, multicentre, open-label, blinded-endpoint, randomized controlled study was conducted to evaluate the efficacy of treatment with ipragliflozin (sodium-dependent glucose transporter-2 inhibitor) versus metformin for visceral fat reduction and glycaemic control among Japanese patients with type 2 diabetes treated with sitagliptin, HbA1c levels of 7%-10%, and body mass index (BMI) ≥ 22 kg/m . Patients were randomly assigned (1:1) to receive ipragliflozin 50 mg or metformin 1000-1500 mg daily. The primary outcome was change in visceral fat area as measured by computed tomography after 24 weeks of therapy.

Helicobacter cinaedi infection in patients with diabetes: a case report.

Background: Helicobacter cinaedi causes bacteremia without characteristic clinical symptoms and is firstly isolated from human immunodeficiency virus (HIV)-positive homosexual men.

Findings: Here we describe, for the first time case report, two female patients with diabetes who had H. cinaedi bacteremia.

Distinct regions of Galpha13 participate in its regulatory interactions with RGS homology domain-containing RhoGEFs.

Galpha12 and Galpha13 transduce signals from G protein-coupled receptors to RhoA through RhoGEFs containing an RGS homology (RH) domain, such as p115 RhoGEF or leukemia-associated RhoGEF (LARG). The RH domain of p115 RhoGEF or LARG binds with high affinity to active forms of Galpha12 and Galpha13 and confers specific GTPase-activating protein (GAP) activity, with faster GAP responses detected in Galpha13 than in Galpha12. At the same time, Galpha13, but not Galpha12, directly stimulates the RhoGEF activity of p115 RhoGEF or nonphosphorylated LARG in reconstitution assays.

Genetically unique microsporidian Encephalitozoon cuniculi strain type III isolated from squirrel monkeys.

Microsporidian spores were isolated from two squirrel monkeys (Saimiri sciureus) that had been bred at an animal-breeding colony in Japan. The spores were identified as Encephalitozoon cuniculi on the basis of nucleotide sequence analysis of the small-subunit (SSU) rRNA gene. The internal transcribed spacer (ITS) gene sequence revealed that these isolates were classified into genotype III because it contained tetrarepeats of 5'-GTTT-3'.

Critical role of lysine 204 in switch I region of Galpha13 for regulation of p115RhoGEF and leukemia-associated RhoGEF.

Heterotrimeric G proteins of the G12 family regulate the Rho GTPase through RhoGEFs that contain an amino-terminal regulator of G protein signaling (RGS) domain (RGS-RhoGEFs). Direct regulation of the activity of RGS-RhoGEFs p115 or leukemia-associated RhoGEF (LARG) by Galpha13 has previously been demonstrated. However, the precise biochemical mechanism by which Galpha13 stimulates the RhoGEF activity of these proteins has not yet been well understood.

Rat cerebral endothelial cells express trk C and are regulated by neurotrophin-3.

Cerebral endothelial cells (CEC) are critical for formation of the vascular system in the mammalian central nervous system (CNS). We focused on the neurotrophin (NT) for its possible involvement in signaling for the regulation of CEC to control formation and maintenance of the vascular system in CNS in comparison of rat cerebral endothelial cells (RCEC) with rat aortic endothelial cells (RAEC). We found that (1) trk C, a receptor for neurotrophin-3 (NT-3), is dominantly expressed in RCEC, but trk B, a receptor for brain-derived neurotrophic factor, is dominantly expressed in RAEC; (2) NT-3 inhibited the proliferation of RCEC; and (3) NT-3 stimulated the production of nitric oxide (NO) with increases in protein expression of endothelial NO synthase.

Galpha 12 activates Rho GTPase through tyrosine-phosphorylated leukemia-associated RhoGEF.

Heterotrimeric G proteins, G12 and G13, have been shown to transduce signals from G protein-coupled receptors to activate Rho GTPase in cells. Recently, we identified p115RhoGEF, one of the guanine nucleotide exchange factors (GEFs) for Rho, as a direct link between Galpha13 and Rho [Kozasa, T., et al.