Enhancing Pd Catalytic Activity by Amine Group Modification for Efficient Direct Synthesis of H2O2.

A great deal of research has been carried out on the design of Pd-based catalysts in the direct synthesis of H2O2, mainly for the purpose of improving the H2O2 selectivity by weakening the activation energy on the Pd active site and thus inhibiting the dissociation of the O-O bonds in O2*, OOH*, and HOOH*. However, this often results in insufficient activation energy for the reaction between H2 and O2 on Pd, leading to difficulties in improving both the selectivity and productivity of H2O2 simultaneously. Based on this, this study reports an efficient catalyst composed of amine-functionalized SBA-15-supported Pd. The strong metal-support interaction not only makes the PdNPs highly dispersed with more Pd active sites but also improves the stability of the catalyst. The amine group modification increases the proportion of Pd0, further enhancing Pd activity and promoting the adsorption and conversion of H2 and O2 on Pd, thereby significantly increasing H2O2 productivity. Additionally, the density-functional theory simulation results showed that due to the hydrogen-bonding force between the amine group and H2O2, this particular anchoring effect would make the hydrogenation and decomposition of H2O2 effectively suppressed. Ultimately, both the selectivity and productivity of H2O2 are improved simultaneously.

High fat diet-induced downregulation of TRPV2 mediates hepatic steatosis via p21 signalling

The global prevalence and incidence of non-alcoholic fatty liver disease (NAFLD) are exhibiting an increasing trend. NAFLD is characterized by a significant accumulation of lipids, though its underlying mechanism is still unknown. Here we report that high-fat diet (HFD) feeding induced hepatic steatosis in mice, which was accompanied by a reduction in the expression and function of hepatic TRPV2. Moreover, conditional knockout of TRPV2 in hepatocytes exacerbated HFD-induced hepatic steatosis. In an in vitro model of NAFLD, TRPV2 regulated lipid accumulation in HepG2 cells, and TRPV2 activation inhibited the expression of the cellular senescence markers p21 and p16, all of which were mediated by AMPK phosphorylation. Finally, we found that administration of probenecid, a TRPV2 agonist, impaired HFD-induced hepatic steatosis and suppressed HFD-induced elevation in p21 and p16. Collectively, our findings imply that hepatic TRPV2 protects against the accumulation of lipids by modulating p21 signalling. (AU)

High fat diet-induced downregulation of TRPV2 mediates hepatic steatosis via p21 signalling

The global prevalence and incidence of non-alcoholic fatty liver disease (NAFLD) are exhibiting an increasing trend. NAFLD is characterized by a significant accumulation of lipids, though its underlying mechanism is still unknown. Here we report that high-fat diet (HFD) feeding induced hepatic steatosis in mice, which was accompanied by a reduction in the expression and function of hepatic TRPV2. Moreover, conditional knockout of TRPV2 in hepatocytes exacerbated HFD-induced hepatic steatosis. In an in vitro model of NAFLD, TRPV2 regulated lipid accumulation in HepG2 cells, and TRPV2 activation inhibited the expression of the cellular senescence markers p21 and p16, all of which were mediated by AMPK phosphorylation. Finally, we found that administration of probenecid, a TRPV2 agonist, impaired HFD-induced hepatic steatosis and suppressed HFD-induced elevation in p21 and p16. Collectively, our findings imply that hepatic TRPV2 protects against the accumulation of lipids by modulating p21 signalling. (AU)

The ultramicropore biochar derived from waste distiller's grains for wet-process phosphoric acid purification: Removal performance and mechanisms of Cr(VI).

Solid waste and heavy metal pollution are long-term and challenging subjects in the field of environmental engineering. In this study, we propose a sustainable approach to "treating waste with waste" by utilizing the ultramicropore biochar derived from solid waste distiller's grains as a means to remove Cr(VI) from simulated wastewater and wet phosphoric acid. The biochar prepared in this research exhibit extremely high specific surface areas (up to 2973 m2/g) and a well-developed pore structure, resulting in a maximum Cr(VI) adsorption capacity of 426.0 mg/g and over 99% removal efficiency of Cr(VI). Furthermore, the adsorbent can be reused for up to eight cycles without significant reduction in its Cr(VI) adsorption performance. Mechanistic investigations suggest that the exceptional Cr(VI) adsorption capacity can be attributed to the synergistic effect of electrostatic interaction and reduction adsorption. This study offers an alternative approach for the resource utilization of solid waste distiller's grains, and the prepared biochar holds promise for the removal of Cr(VI) from wastewater and wet-process phosphoric acid.

High fat diet-induced downregulation of TRPV2 mediates hepatic steatosis via p21 signalling.

The global prevalence and incidence of non-alcoholic fatty liver disease (NAFLD) are exhibiting an increasing trend. NAFLD is characterized by a significant accumulation of lipids, though its underlying mechanism is still unknown. Here we report that high-fat diet (HFD) feeding induced hepatic steatosis in mice, which was accompanied by a reduction in the expression and function of hepatic TRPV2. Moreover, conditional knockout of TRPV2 in hepatocytes exacerbated HFD-induced hepatic steatosis. In an in vitro model of NAFLD, TRPV2 regulated lipid accumulation in HepG2 cells, and TRPV2 activation inhibited the expression of the cellular senescence markers p21 and p16, all of which were mediated by AMPK phosphorylation. Finally, we found that administration of probenecid, a TRPV2 agonist, impaired HFD-induced hepatic steatosis and suppressed HFD-induced elevation in p21 and p16. Collectively, our findings imply that hepatic TRPV2 protects against the accumulation of lipids by modulating p21 signalling.

Localization diagnosis of adrenocorticotrophic hormone-dependent Cushing's syndrome: two case reports and literature review.

BACKGROUND: The common causes of adrenocorticotrophic hormone (ACTH)-dependent Cushing's syndrome (CS) include Cushing's disease (CD) and ectopic ACTH syndrome (EAS). The differential diagnosis and lesion location of CD and EAS often bring great difficulties to clinical diagnosis and treatment. This article reports the localization diagnosis, treatment, and follow-up results of two patients with ACTH-dependent CS with different causes and reviews the literature. CASE DESCRIPTION: Case 1: a 29-year-old female patient attended the clinic because of irregular menstruation, weight gain, and violaceous striae. The low dose dexamethasone suppression test (LDDST) was not suppressed, and the high dose dexamethasone suppression test (HDDST) suggested the results of serum cortisol and 24-h urine free cortisol were contradictory. Magnetic resonance imaging (MRI) indicated pituitary microadenoma, and bilateral inferior petrosal sinus sampling (BIPSS) indicated ACTH was centrally secreted. CD was diagnosed. The patient underwent transsphenoidal surgery, and the symptoms of CS were improved after the operation. A natural pregnancy occurred more than half a year after the surgery, and a healthy baby boy was delivered 9 months later. Case 2: a 29-year-old female patient complained of facial redness and elevated blood pressure. Examination showed refractory hypokalemia and abnormally elevated serum cortisol and ACTH. Androgens also increased. Neither LDDST nor HDDST was inhibited. Chest-to-pelvis computed tomography (CT) scan revealed a soft tissue mass in the anterior mediastinum, considered as a possible thymoma. EAS and thymoma were diagnosed. An anterior mediastinal mass resection was performed, and pathological results suggested thymic carcinoid weakly positive for ACTH. After the operation, hypertension and hypokalemia were relieved, and cortisol, ACTH and androgens returned to normal levels. CONCLUSIONS: The differentiation between CD and EAS should be comprehensively evaluated in combination with the medical history, function tests, pituitary MRI, and other tests. If the function test results are discordant or pituitary MRI shows the lesion diameter is less than 6 mm, BIPSS should be further performed to confirm the diagnosis. The lesions of EAS are complex and diverse, and it is necessary to pay attention to imaging examinations of the neck-to-pelvis to locate lesion and provide direction for subsequent treatment.

Preparation and pore-forming mechanism of hydrogen bond and ionic bond double-driven chitosan-based mesoporous carbon.

Using chitosan as the carbon source, F127 as the template, and sodium tripolyphosphate as cross-linking agent, a hydrogen bond and ionic bond double-driven mesoporous carbon material was prepared via the sol-hydrothermal method and its formation mechanism was discussed. According to the results from FTIR, Raman, XPS, physical adsorption analyzer, SEM, TEM, and TG-IR, the mesoporous carbon material was formed under the synergistic effect of hydrogen bond and ionic bond has a mesoporous volume of 0.44 cm3/g, a BET surface area of 262 m2/g, and possesses the ideal unimodal distribution around 2.20 nm. The mesopores are originated from the degradation of hydrophobic segment PPO of F127, and the micropores come from the gases CO2, CO, NH3, CH4, tetraethylene glycol dimethyl ether, and 2,6-diisopropylphenyl isocyanate produced during the degradation of prepolymers. The maximum adsorption capacity of this mesoporous carbon for tannic acid (Sips model) at 30 °C is 70.4 mg/g.

Oxidation modification of chitosan-based mesoporous carbon by soft template method and the adsorption and release properties of hydroxycamptothecin.

Spray drying and a direct carbonization technology were coupled to prepare nitrogen-doped mesoporous carbon nanoparticles (NMCs) using chitosan as a carbon source and nitrogen source precursor and a triblock amphiphilic copolymer (F127) as a soft template, then oxidative modification was performed by ammonium persulfate (APS) to prepare oxidized mesoporous carbon nanoparticles (O-NMCs). The pore structure, chemical composition and wettability of the mesoporous materials were studied before and after oxidative modification, the microscopic morphology, structure, composition and wetting performance of the mesoporous carbon were characterized by transmission electron microscopy (TEM), an X-ray diffractometer (XRD), N2 adsorption-desorption instrument, X-ray photoelectron spectroscopy (XPS), contact angle tests and other analyses, meanwhile influences of the mesoporous carbon material on adsorption and release performance of a poorly-soluble antitumor drug hydroxycamptothecin (HCPT) were investigated. It was demonstrated from results that the surface wettability of the oxidatively-modified mesoporous carbon material was improved, the contact angle of the mesoporous carbon materials was reduced from 133.4° to 58.2° and the saturated adsorption capacity of HCPT was 676.97 mg/g and 647.20 mg/g respectively. The dissolution rate of the raw material hydroxycamptothecin was improved due to the nanopore structure of the mesoporous carbon material, the dissolution rate of mesoporous carbon material-loaded hydroxycamptothecin was increased from 22.7% to respective 83.40% and 81.11%.

Study on the preparation and mechanism of chitosan-based nano-mesoporous carbons by hydrothermal method.

In this paper, the hydrothermal method to synthesize and characterize nano-mesoporous carbons and their synthesis mechanism are reported. Using tri-block Pluronic F127 as a structuring agent and chitosan (CS) as a carbon source, the nano-mesoporous carbons were synthesized by a one-step sol polymerization and hydrothermal process, followed by carbonization at high temperature. The pore structure of the carbon materials was characterized by physical adsorption analyzer, and the morphology was characterized by SEM and TEM. Fourier-transform infrared, Raman and x-ray photoelectron spectroscopy were used to study the synthesis mechanism. The results showed that the self-assembly polymerization reaction between CS and F127 in a weakly acidic system was only implemented driven by the hydrogen bond auxiliary electrostatic interactions initiated by protonated amino groups. The nitrogen from amino groups and acetylamino groups, the oxygen in acetylamino groups, hydroxyl groups and the glycosidic bonds of CS, and the oxygen from the hydrophilic segments of F127 were the main active sites. The mesoporous material possesses a high Brunauer-Emmett-Teller surface area (163 m2/g) and large pore volume (0.462 cm3/g) with pore diameter around 2.1 nm. The nitrogen content was 1.08% and existed in the pore wall as the form of pyridine, pyrrole and quaternary nitrogen.

Identification of key sites determining the cofactor specificity and improvement of catalytic activity of a steroid 5ß-reductase from Capsella rubella.

Progesterone 5ß-reductases (P5ßRs) are involved in 5ß-cardenolide formation by stereo-specific reduction of the △4,5 double bond of steroid precursors. In this study a steroid 5ß-reductase was identified in Capsella rubella (CrSt5ßR1) and its function in steroid 5ß-reduction was validated experimentally. CrSt5ßR1 is capable of enantioselectively reducing the activated CC bond of broad substrates such as steroids and enones by using NADPH as a cofactor and therefore has the potential as a biocatalyst in organic synthesis. However, for industrial purposes the cheaper NADH is the preferred cofactor. By applying rational design based on literature and complementary mutagenesis strategies, we successfully identified two key amino acid residues determining the cofactor specificity of the enzyme. The R63 K mutation enables the enzyme to convert progesterone to 5ß-pregnane-3,20-dione with NADH as cofactor, whereas the wild-type CrSt5ßR1 is strictly NADPH-dependent. By further introducing the R64H mutation, the double mutant R63K_R64H of CrSt5ßR1 was shown to increase enzymatic activity by13.8-fold with NADH as a cofactor and to increase the NADH/NADPH conversion ratio by 10.9-fold over the R63 K single mutant. This finding was successfully applied to change the cofactor specificity and to improve activity of other members of the same enzyme family, AtP5ßR and DlP5ßR. CrSt5ßR1 mutants are expected to have the potential for biotechnological applications in combination with the well-established NADH regeneration systems.

One-Step Synthesis of Nitrogen-Doped Hydrophilic Mesoporous Carbons from Chitosan-Based Triconstituent System for Drug Release.

In situ nitrogen-doped hydrophilic mesoporous carbon spheres with different carbon-to-silicon (C/Si) ratios (NMCs-x/3, x = 5, 6, 7, and 8) were prepared by one-step method coupled with a spray drying and carbonizing technique, in which triblock copolymer (F127) and tetraethyl orthosilicate (TEOS) were used as template agents, and biocompatible chitosan (CS) was used as the carbon source and nitrogen source. These carbon materials were characterized by TG, BET, XRD, Raman, FTIR, TEM, XPS, and contact angle measuring device. The adsorption and release properties of mesoporous carbon materials for the poorly soluble antitumor drug hydroxycamptothecin (HCPT) were investigated. Results showed that nanospherical mesoporous carbon materials were successfully prepared with high specific surface area (2061.6 m2/g), narrowly pore size distribution (2.01-3.65 nm), and high nitrogen content (4.75-6.04%). Those NMCs-x showed a satisfactory hydrophilicity, which gradually increased with the increasing of surface N content. And the better hydrophilicity of NMCs-x was, the larger adsorption capacity for HCPT. The absorption capacity of NMCs-x towards HCPT was in the following orders: qNMCs-5/3 > qNMCs-6/3 > qNMCs-7/3 > qNMCs-8/3. NMCs-5/3 had the largest saturated adsorption capacity of HCPT (1013.51 mg g-1) and higher dissolution rate (93.75%).

The role of myocardin-related transcription factor-A in Aß25-35 induced neuron apoptosis and synapse injury.

Myocardin-related transcription factor-A (MRTF-A) highly expressed in brain has been demonstrated to promote neuronal survival via regulating the transcription of related target genes as a powerful co-activator of serum response factor (SRF). However, the role of MRTF-A in Alzheimer's disease (AD) is still unclear. Here, we showed that MRTF-A was significantly downregulated in cortex of the Aß25-35-induced AD rats, which played a key role in Aß25-35 induced cerebral neuronal degeneration in vitro. Bilateral intracerebroventricular injection of Aß25-35 caused significantly MRTF-A expression decline in cortex of rats, along with significant neuron apoptosis and plasticity damage. In vitro, transfection of MRTF-A into primary cultured cortical neurons prevented Aß25-35 induced neuronal apoptosis and synapses injury. And luciferase reporter assay determined that MRTF-A could bind to and enhance the transactivity of the Mcl-1 (Myeloid cell leukemia-1) and Arc (activity-regulated cytoskeletal-associated protein) promoters by activating the key CArG box element. These data demonstrated that the decreasing of endogenous MRTF-A expression might contribute to the development of AD, whereas the upregulation MRTF-A in neurons could effectively reduce Aß25-35 induced synapse injury and cell apoptosis. And the underlying mechanism might be partially due to MRTF-A-mediated the transcription and expression of Mcl-1 and Arc by triggering the CArG box.

[Determination of 35 antibiotic residues of tetracyclines, sulfonamides, penicillins, macrolides and amphenicols in milk by liquid chromatography-tandem mass spectromtery].

A liquid chromatography-tandem mass spectrometry (LC-MS/MS) method was established for the simultaneous determination of 35 antibiotic residues of tetracyclines, sulfonamides, penicillins, macrolides and amphenicols in milk. The samples were extracted with alkaline acetonitrile and McIlvaine buffer solution under ultrasonication. The separation of target compounds was performed on an Eclipse XDB-C, column (150 mm x 2.1 mm, 3.5 µm) with gradient elution at a flow rate of 0.25 mL/min, and with an injection volume of 10 µL. The identification and quantification of the compounds were completed by liquid chromatography-tandem mass spectrometry in multiple reaction monitoring ( MRM) mode. The limits of detection were all below 10.0 µg/kg. The average spiked recoveries of the method ranged from 70. 1% to 109. 9% with relative standard deviations (RSDs) of 2.89%-9.99%. After validation, the method was applied to the analysis of antibiotic residues in milk products in China. Fifty samples were screened under the well defined methodology, and the results showed that chloramphenicol, only in one sample, was monitored with the content of 0.48 µg/kg. A risk of contamination of milk with chloramphenicol has been determined to exist. Therefore this method is convenient, rapid, sensitive and reliable, and can be successfully applied to the simultaneous detection of the 35 antibiotic residues of tetracyclines, sulfonamides, penicillins, macrolides and amphenicols in milk.

Antioxidant and antigenotoxic activity of bioactive extracts from corn tassel.

This study is designed to evaluate antioxidant and antigenotoxic activities of corn tassel extracts (CTTs). The major bioactive components of CTTs include flavonoid, saponin and polysaccharide. The antioxidant properties of the three bioactive components of CTTs were investigated by Ferric Reducing Antioxidant Property (FRAP) and 1, 1-diphenyl-2-picrylhydrazyl (DPPH) assays. The activities of the extracts were determined by assessing the inhibition of mutagenicity of the direct-acting mutagen fenaminosulf, sodium azide, and indirect-acting mutagen 2-aminofluorene using the Ames test (strains TA98 and TA100). The results showed that the extraction rates of flavonoid, saponin, and polysaccharide from the dried corn tassels were 1.67%, 2.41% and 4.76% respectively. DPPH and FRAP assay strongly demonstrated that CTTs had antioxidant properties. CTTs at doses of 625, 1250 and 2500 µg per plate reduced 2-aminofluorene mutagenicity by 12.52%, 28.76% and 36.49% in Salmonella typhimurium TA98 strain assay respectively and by 10.98%, 25.27% and 37.83%, at the same doses in Salmonella typhimurium TA100 assay system, respectively. 3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide (MTT) assay showed that the different concentrations of CTTs inhibited the proliferation of MGC80-3 cells in a dose-dependent manner (P<0.01). It is concluded that these integrated approaches to antioxidant and antigenotoxicity assessment may be useful to study corn tassel as a natural herbal material.

Baicalin protects PC-12 cells from oxidative stress induced by hydrogen peroxide via anti-apoptotic effects.

PRIMARY OBJECTIVE: To examine the neuroprotection of baicalin, a flavonoid compound derived from the dried root of Scutellaria baicalensis Georgi, on neurons. RESEARCH DESIGN: A rat PC12 cell line was used to study the neuroprotection and possible mechanisms of baicalin on H2O2-induced neuron damage. METHODS: Three anti- and one pro-apoptosis genes in PC12 cells were examined. Cell apoptosis was induced by H2O2 and apoptotic rate was obtained by flow cytometry. MTT for cell viability, immunofluorescence microscopy for promoter activity and western blot for gene expression were also employed. RESULTS: Data of MTT reduction assay and flow cytometry revealed that viability loss and apoptotic rate were reduced by pre-treatment of PC12 cells with baicalin for 24 hours. Baicalin was also found to increase SOD, GSH-Px activities and to decrease MDA level. Results from Western blot and immunofluorescence microscopy showed baicalin increased the expressions of survivin, Bcl-2 and p-STAT3 and decreased caspase-3 expression which were attenuated by AG-490. CONCLUSIONS: The results point to the possibility of the neuroprotective effects of baicalin on neuronal apoptosis induced by oxidative stress and indicate that activation of the JAK/STAT signalling pathway might involve the anti-apoptotic effect of baicalin.

Antioxidant activity of ginseng cultivated under mountainous forest with different growing years.

Ginseng cultivated and grown naturally under mountainous forest is formally called "Lin-Xia-Shan-Shen" (LXSS) and grown in manual condition is called garden ginseng (GG) according to Chinese pharmacopoeia (2010 edition). Usually the growing condition of LXSS is similar to wild ginseng and mostly used in Chinese folks in ancient times. The antioxidant properties of LXSS with different growing years were evaluated by their inhibitions of thiobarbituric acid-reactive substance (TBA-RS) formation in liver homogenate and 2, 2-diphenyl-1-picrylhydrazyl (DPPH)-radical scavenging activity comparing with those of GG. The inhibitions of different polar extracts (n-butanol and water) of LXSS and GG on TBA-RS formation were also evaluated. The results showed that the antioxidant effects of LXSS were higher than those of GG and the TBARS formation inhibition of LXSS with longer growing years were stronger than those with shorter growing years, while the DPPH-radical scavenging activity of LXSS did not show significant difference with the change of the growing year. The results indicated that the inhibitory effect of TBA-RS formation and the DPPH-radical scavenging of LXSS were correlated with the contents of ginsenosides. In adddition, the starch contents of LXSS and GG were determined by micro-amount method with spectrophotometer. It showed that the starch content in GG was higher than that of LXSS whose starch decreased gradually with the growing year.

High genetic diversity and structured populations of the oriental fruit moth in its range of origin.

The oriental fruit moth Grapholita ( = Cydia) molesta is a key fruit pest globally. Despite its economic importance, little is known about its population genetics in its putative native range that includes China. We used five polymorphic microsatellite loci and two mitochondrial gene sequences to characterize the population genetic diversity and genetic structure of G. molesta from nine sublocations in three regions of a major fruit growing area of China. Larval samples were collected throughout the season from peach, and in late season, after host switch by the moth to pome fruit, also from apple and pear. We found high numbers of microsatellite alleles and mitochondrial DNA haplotypes in all regions, together with a high number of private alleles and of haplotypes at all sublocations, providing strong evidence that the sampled area belongs to the origin of this species. Samples collected from peach at all sublocations were geographically structured, and a significant albeit weak pattern of isolation-by-distance was found among populations, likely reflecting the low flight capacity of this moth. Interestingly, populations sampled from apple and pear in the late season showed a structure differing from that of populations sampled from peach throughout the season, indicating a selective host switch of a certain part of the population only. The recently detected various olfactory genotypes in G. molesta may underly this selective host switch. These genetic data yield, for the first time, an understanding of population dynamics of G. molesta in its native range, and of a selective host switch from peach to pome fruit, which may have a broad applicability to other global fruit production areas for designing suitable pest management strategies.

catena-Poly[[dichloridocopper(II)]-µ-4,4'-bis-(benzimidazol-1-yl)biphen-yl].

In the title compound, [CuCl(2)(C(26)H(18)N(4))](n), the Cu(II) ion is four-coordinated by two N atoms from two 4,4'-bis-(benzo-imidazol-1-yl)biphenyl ligands and two chloride anions, in a slightly distorted tetra-hedral environment. The biphenyl ligand acts as a linear bidentate ligand, connecting the metal atoms into an infinite chain parallel to [101]. In the biphenyl ligand, the two benzene rings make a dihedral angle of 33.19 (7)°.

Changes of serum omentin-1 levels in normal subjects and in patients with impaired glucose regulation and with newly diagnosed and untreated type 2 diabetes.

AIMS: To assay the levels of serum omentin-1 in subjects with different levels of glucose regulation and to analyze the relationship between serum omentin-1 levels and body mass index (BMI), glycoslated hemoglobin (HbA1c), plasma glucose, insulin resistance index (HOMA-IR), TNF-alpha and IL-6 levels. METHODS: Forty-six patients with impaired glucose regulation (IGR), 55 patients with newly diagnosed and untreated type 2 diabetes mellitus (T2DM), and 50 subjects with normal glucose tolerance (NGT) were enrolled in this study. The levels of serum omentin-1 and plasma glucose at fasting and at 2h after glucose load and fasting serum levels of TNF-alpha, IL-6, insulin, and HbA1c were measured. HOMA-IR was calculated. RESULTS: The levels of serum omentin-1 were lower in the IGR and T2DM groups than in the NGT group. Within groups, omentin-1 levels were no significant difference before and after glucose load. The level of serum omentin-1 was negatively correlated to BMI, HOMA-IR, fasting insulin, TNF-alpha, IL-6, plasma glucose. HOMA-IR and BMI were independent related factors that influenced the levels of serum omentin-1. CONCLUSIONS: Serum omentin-1 levels were decreased in impaired glucose regulation subjects. Lack of omentin-1 may contribute to the development of insulin resistance and T2DM.

Apelin inhibits insulin secretion in pancreatic beta-cells by activation of PI3-kinase-phosphodiesterase 3B.

AIMS: Apelin is secreted by adipocytes acting on APJ receptor and plays an important role in control of feeding behavior, energy expenditure, and the regulation of body fluid homeostasis. The adipokine is regulated by insulin and tumor necrosis factor-alpha in adipose tissue, suggesting apelin is involved in the regulation of pancreatic function. In this study, we incubated rat insulinoma INS-1 cells producing insulin for 60 min and examined the effects of pyr(1)-apelin-13 on insulin secretion and the mechanism. MAIN METHODS: INS-1 cells were incubated in the presence of various concentrations of glucose and/or apelin, glucagon-like peptide-1 (GLP-1), phosphoinositide 3-kinase (PI3-kinase) inhibitor, phosphodiesterase 3B (PDE3B) inhibitor, and cAMP analogues. We examined the effect of apelin on insulin secretion and the pathway of the action. Insulin concentrations were measured by radioimmunoassay. KEY FINDINGS: We found that apelin over the concentration range of 1-10(4) nmol/L inhibited the insulin response to glucose and GLP-1 and the concentration effect was biphasic. The effect of apelin was abolished when insulin secretion was induced with cAMP analogues that cannot be hydrolyzed by cyclic nucleotide PDE3B. Selective inhibitors of PDE3B and PI3-kinase completely prevent the apelin effect on insulin secretion and cAMP accumulation. SIGNIFICANCE: These findings suggest that apelin exerts direct inhibitory actions on the pancreatic beta-cells by activating PI3-kinase-dependent PDE3B and subsequently suppressing of cAMP levels.