Assessment of subclinical left ventricular systolic dysfunction in patients with type 2 diabetes: Relationship with HbA1c and microvascular complications.

Background: We aimed to examine the association between glycated hemoglobin (HbA1c), microvascular complications, and subclinical left ventricular (LV) systolic dysfunction, and to determine the strength of the correlation in asymptomatic patients with type 2 diabetes mellitus (T2DM).

Methods: Global longitudinal strain (GLS) was employed to assess the subclinical LV function of 152 enrolled T2DM patients with preserved LV ejection fraction, with the cutoff for subclinical LV systolic dysfunction predefined as GLS < 18%.

Results: According to univariate analysis, the reduced GLS exhibited association with the clinical features including HbA1c, triglyceride, systolic blood pressure, fasting glucose, heart rate, diabetic retinopathy, and urinary albumin creatinine ratio (UACR) (all p < .

Association of peripheral neuropathy with subclinical left ventricular dysfunction in patients with type 2 diabetes.

Objectives: The impacts of diabetic peripheral neuropathy (DPN) on clinical manifestations of left ventricular (LV) function in patients suffering from type 2 diabetes mellitus (T2DM) and the preserved LV ejection fraction (LVEF) lack a full evaluation. This study was carried out to investigate the correlation of peripheral neuropathy with subclinical LV systolic dysfunction, accompanied by the exploration of the relevant clinical features of peripheral neuropathy in these patients.

Methods: A retrospective analysis was conducted depending on the data of 101 consecutive inpatients with T2DM and preserved LVEF (all ≥ 50 %), without coronary artery disease and other histories of heart disease.

SIRT1 rs10823108 and FOXO1 rs17446614 responsible for genetic susceptibility to diabetic nephropathy.

SIRT1 and FOXO1 play an important role in the pathogenesis of diabetic nephropathy (DN). However, the association between genetic polymorphisms and susceptibility to type 2 DN (T2DN) has not been explored. In this study, a total of 1066 patients with type 2 diabetes mellitus (T2DM) (413 without and 653 with DN) were enrolled.

Effects of FoxO1 on podocyte injury in diabetic rats.

Objective: This study was designed to investigate the protective effect of forkhead transcription factor O1 (FoxO1) on podocyte injury in rats with diabetic nephropathy.

Methods: Streptozotocin-induced diabetic rats were served as DM group, while DM rats transfected with blank lentiviral vectors (LV-pSC-GFP) or lentiviral vectors carrying constitutively active FoxO1 (LV-CA-FoxO1) were served as LV-NC group or LV-CA group, respectively. The control group (NG) consisted of uninduced rats that received an injection of diluent buffer.

Activation of FoxO1/ PGC-1α prevents mitochondrial dysfunction and ameliorates mesangial cell injury in diabetic rats.

The generation of hyperglycemia-induced mitochondrial reactive oxygen species (ROS) is a key event in diabetic nephropathy development. The forkhead-box class O1 (FoxO1) and peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α) proteins are implicated in oxidative stress. We investigated the in vivo association of FoxO1 and PGC-1α in renal cortices from streptozotocin-induced diabetic rats and in rat kidney mesangial cells (MCs) treated with high glucose, in vitro.

Lentiviral Vector-Mediated FoxO1 Overexpression Inhibits Extracellular Matrix Protein Secretion Under High Glucose Conditions in Mesangial Cells.

Diabetic nephropathy is characterized by inordinate secretion of extracellular matrix (ECM) proteins from mesangial cells (MCs), which is tightly associated with excessive activation of TGF-β signaling. The forkhead transcription factor O1 (FoxO1) protects mesangial cells from hyperglycemia-induced oxidative stress, which may be involved in ameliorating the redundant secretion of ECM proteins under high glucose conditions. Here, we reported that high glucose elevated the level of p-Akt to attenuate endogenous FoxO1 bioactivities in MCs, accompanied with decreases in the mRNA expressions of catalase (CAT) and superoxide dismutase 2 (SOD2).

Overexpression of the FoxO1 Ameliorates Mesangial Cell Dysfunction in Male Diabetic Rats.

The dysfunction of mesangial cells (MCs) in high-glucose (HG) conditions plays pivotal role in inducing glomerular sclerosis by causing the imbalance between generation and degradation of extracellular matrix (ECM) proteins, which ultimately leads to diabetic nephropathy. This study was designed to determine the function of forkhead box protein O1 (FoxO1), an important transcription factors in regulating cell metabolism and oxidative stress, in MCs in HG conditions. Up-regulation of fibronectin, collagen type IV, and plasminogen activator inhibitor (PAI-1) was observed under HG conditions in vivo and in vitro, accompanied with elevation of protein kinase B (Akt) phosphorylation and reduction of FoxO1 bioactivity.

[Effects of over-expressed forkhead transcription factor O1 on high glucose induced extracellular matrix secretion in rat mesangial cells].

Objective: To explore the role and molecular mechanism of forkhead transcription factor O1 (FoxO1) for extracellular matrix (ECM) protein accumulation in rat mesangial cells (MCs) cultured under high-glucose conditions.

Methods: The MCs were transfected with either lentiviral vectors containing the sequences of constitutively active FoxO1 (LV-CA-FoxO1) or empty vectors (LV-NC-GFP). The MCs were divided into 4 groups of normal glucose (5.

Nesfatin-1 correlates with hypertension in overweight or obese Han Chinese population.

We investigated blood nesfatin-1 levels in hypertension patients. We found that fasting plasma nesfatin-1 levels were significantly higher in hypertension patients than in control groups, especially in overweight/obese hypertension patients (4.5 ± 2.