Intermedin Alleviates Diabetic Cardiomyopathy by Up-Regulating CPT-1β through Activation of the Phosphatidyl Inositol 3 Kinase/Protein Kinase B Signaling Pathway.

Diabetic cardiomyopathy (DCM), one of the most serious long-term consequences of diabetes, is closely associated with myocardial fatty acid metabolism. Carnitine palmitoyltransferase-1β (CPT-1β) is the rate-limiting enzyme responsible for β-oxidation of long-chain fatty acids. Intermedin (IMD) is a pivotal bioactive small molecule peptide, participating in the protection of various cardiovascular diseases.

Intermedin alleviates diabetic vascular calcification by inhibiting GLUT1 through activation of the cAMP/PKA signaling pathway.

Background And Aims: Vascular calcification (VC) is regarded as an independent risk factor for cardiovascular events in type 2 diabetic patients. Glucose transporter 1 (GLUT1) involves VC. Intermedin/Adrenomedullin-2 (IMD/ADM2) is a cardiovascular protective peptide that can inhibit multiple disease-associated VC.

Intermedin Inhibits NLRP3 Inflammasome Activation by Targeting IRE1α in Cardiac Fibrosis.

Intermedin (IMD), a paracrine/autocrine peptide, protects against cardiac fibrosis. However, the underlying mechanism remains poorly understood. Previous study reports that activation of nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain containing 3 (NLRP3) inflammasome contributes to cardiac fibrosis.

Positive Association of Leptin and Artery Calcification of Lower Extremity in Patients With Type 2 Diabetes Mellitus: A Pilot Study.

Objective: We aimed to explore the role and possible mechanism of leptin in lower-extremity artery calcification in patients with type 2 diabetes mellitus (T2DM).

Methods: We recruited 59 male patients with T2DM and 39 non-diabetic male participants. All participants underwent computed tomography scan of lower-extremity arteries.

Effects of Incretin-based Therapies on Weight-related Indicators among Patients with Type 2 Diabetes: A Network Meta-analysis.

Objective: To evaluate the effects of incretin-based therapies on body weight as the primary outcome, as well as on body mass index (BMI) and waist circumference (WC) as secondary outcomes.

Methods: Databases including Medline, Embase, the Cochrane Library, and clinicaltrials.gov (www.

Intermedin Ameliorates Homocysteine-Promoted Atherosclerotic Calcification by Inhibiting Endoplasmic Reticulum Stress.

Aim: Vascular calcification (VC) is thought to be an independent predictor of cardiovascular morbidity and mortality. Intermedin (IMD) is a cardiovascular protective peptide and can inhibit vascular medial calcification in rats. In this study, we investigated the effect of IMD on atherosclerotic calcification induced by a high-fat diet plus homocysteine (Hcy) and the potential mechanisms.

Leptin knockout attenuates hypoxia-induced pulmonary arterial hypertension by inhibiting proliferation of pulmonary arterial smooth muscle cells.

Pulmonary arterial hypertension (PAH) is a fatal disease characterized by excessive vascular smooth muscle cells proliferation in small pulmonary arteries, leading to elevation of pulmonary vascular resistance with consequent right ventricular (RV) failure and death. Recently, emerging evidence has shown that leptin signaling is involved in different cardiac pathologies; however, the role of leptin remains limited in the setting of PAH. Thus, in this study, we tested the hypothesis of direct involvement of leptin in the development of PAH.

Leptin and coronary heart disease: a systematic review and meta-analysis.

Introduction: Leptin, an adipose tissue-derived hormone, plays a central role in regulating human energy homeostasis. The role of leptin in regulating blood pressure, activating the sympathetic nervous system, insulin resistance, platelet aggregation, arterial thrombosis, angiogenesis, and inflammatory vascular responses suggests that leptin may have a close relationship with the development of coronary heart disease (CHD). However, no conclusive data are available to determine the association between leptin and CHD.

[Research advances on leptin and respiratory diseases].

Leptin is a product of the obese (ob) gene and acts through its receptor Ob-R. Leptin is primarily known for its role as a hypothalamic modulator of food, especially in intake, energy balance, fat stores and body weight. Recent studies have shown that leptin may be involved in the development of respiratory diseases such as pulmonary artery hypertension, chronic obstructive pulmonary disease, lung neoplasms and asthma.

Increased plasma levels of endothelin-1 and urotensin-II in patients with coronary heart disease.

Research has identified the vasoconstrictors endothelin-1 (ET-1) and urotensin-II (U-II) as having a role in the development of atherosclerotic cardiovascular disease. We aimed to observe alterations in plasma levels of both ET-1 and U-II in patients with coronary heart disease (CHD) undergoing percutaneous transluminal coronary angioplasty (PTCA) and stent therapy from November 2006 through May 2007. We examined plasma levels of ET-1 and U-II in 40 patients with CHD and 40 age-matched healthy subjects by radioimmunoassay (RIA).

Plasma levels of copeptin in patients with coronary heart disease.

The present study was undertaken to investigate alteration in plasma levels of copeptin, a stable fragment derived from provasopressin, in patients with coronary heart disease. We measured plasma level of copeptin in 21 patients with coronary heart disease (CHD) and 12 age-matched healthy subjects by radioimmunoassay (RIA). Chi-square test, Student's t-test and one-way analysis of variance were used for statistical analyses.

Plasma level of mitochondrial coupling factor 6 increases in patients with coronary heart disease.

Background: The aim of the present study was to investigate alterations in the plasma level of coupling factor 6 (CF6), a novel endogenous inhibitor of prostacyclin, in patients with coronary heart disease.

Methods And Results: In total, 35 patients with coronary heart disease and 20 age-matched healthy subjects were examined. Plasma levels of CF6 and 6-keto-prostaglandin (PG)F(1a) (a stable metabolite of prostacyclin) were measured using radioimmunoassay.

[Change of mitogen-activated protein kinase phosphatase-1 in heart and aorta of SHR and its effect on proliferation of vascular smooth muscle cells stimulated by angiotensin II].

Aim And Methods: To investigate the role of mitogen-activated protein kinase phosphatase-1 (MKP-1) in the regulation of cells proliferation, the expression of MKP-1 and extracellular signal-regulated kinase-1 (ERK-1) in heart and aorta of spontaneous hypertensive rat (SHR) and WKY were studied. We also investigated the effect of MKP-1 genes,which were transfected into vascular smooth muscle cells (VSMC) using the classical calcium phosphate coprecipitation technique, on the incorporation of 3H-TdR in VSMC stimulated by angiotensin II (Ang II).

Results: (1) Compared with that of WKY, MKP-1 expression in heart and aorta were significantly decreased by 53% (P < 0.