Visfatin and apelin are two novel adipocyte- secreted hormone proposed to link obesity with insulin resistance. In this study we investigated whether plasma visfatin and apelin levels were altered in normal, impaired glucose tolerance, and type 2 diabetic subjects. We also assessed the association between plasma visfatin, or apelin and body composition, metabolic parameters, and resistin concentrations in these subjects. The visfatin levels of fasting and 2-h post-glucose load were found to be significantly decreased in diabetics compared with the controls ( P<0.05). In contrast, basal apelin levels were significantly increased in the IGT and diabetic subjects compared with the controls ( P<0.05 and P<0.01). The apelin levels of 2-h post-glucose load were significantly higher than the basal levels in every group (all P<0.05). Fasting plasma visfatin was found to correlate positively and significantly with BMI, WHR, and fasting plasma resistin, but negatively with HbA1c and 2 h OGTT glucose. Multiple regression analysis showed that WHR, HbA1c, 2 h OGTT glucose were independent related factors influencing plasma visfatin levels. Fasting plasma apelin levels correlated positively with HOMA-IR, BMI, TC, LDL-C, FBG and Fasting plasma insulin. Multiple regression analysis also showed that HOMA-IR, BMI, and TC were independent related factors influencing plasma apelin levels. The present work indicates the potential link of visfatin and apelin with the pathogenesis of insulin resistance and T2DM.
Glycerol-3-phosphate acyltransferase (GPAT) is the rate-limiting enzyme in the de novo pathway of glycerolipid synthesis. It catalyzes the conversion of glycerol-3-phosphate and long-chain acyl-CoA to lysophosphatidic acid. In mammals, four isoforms of GPATs have been identified based on subcellular localization, substrate preferences, and NEM sensitivity, and they have been classified into two groups, one including GPAT1 and GPAT2, which are localized in the mitochondrial outer membrane, and the other including GPAT3 and GPAT4, which are localized in the endoplasmic reticulum membrane. GPATs play a pivotal role in the regulation of triglyceride and phospholipid synthesis. Through gain-of-function and loss-of-function experiments, it has been confirmed that GPATs play a critical role in the development of obesity, hepatic steatosis, and insulin resistance. In line with this, the role of GPATs in metabolism was supported by studies using a GPAT inhibitor, FSG67. Additionally, the functional characteristics of GPATs and the relation between three isoforms (GPAT1, 3, and 4) and insulin resistance has been described in this review.
These findings provide a strong case for population-level risk reduction initiatives to be undertaken, especially among people with lower income, a lower level of knowledge on Alzheimer's disease and with chronic diseases.
BackgroundRecent studies have demonstrated that the coracohumeral ligament (CHL) is shortened and thickened in a frozen shoulder. We analyzed the rate in CHL visualization between patients with frozen shoulder and normal volunteers using Magnetic Resonance Imaging (MRI) to determine the CHL thickness in the patients with a frozen shoulder.Methods and FindingsThere were 72 shoulder joints in 72 patients (50 femles and 22 males with a mean age of 53.5 years) with clinical evidence and MR imaging evidence of frozen shoulder. These were prospectively analyzed to identify and measure the maximum thickness of the CHL. The control group, which included 120 shoulder joints in 60 normal volunteer individuals (30 females and 30 males with a mean age of 50.5 years) was also referred for MR imaging. A chi-square test was used to analyze the data of the rate of CHL visualization between the patients with frozen shoulder and the control group. A two-way ANOVA was used to analyze the mean maximal thickness of CHL. The CHL was visualized in 110 out of 120 shoulders in the control group (91.7%), and in 57 out of 72 shoulders for the frozen shoulder group (79.2%), there was significant difference, using a chi-square test (P<0.05). The CHL was not visualized in 10 out of 120 shoulders in the control group (8.3%), and 15 out of 72 shoulders in the frozen shoulder group (20.8%), there was a significant difference (P<0.05). The CHL thickness (3.99±1.68 mm) in the patients with frozen shoulder was significantly greater than that thickness (3.08±1.32 mm) in the control group, using a two-way ANOVA (P<0.001). The CHL thickness (3.52±1.52 mm, n = 97) in the female shoulders was no significantly greater than that thickness (3.22±1.49 mm, n = 70) in the male shoulders, using a two-way ANOVA (P>0.05).ConclusionsMR Imaging is a satisfactory method for CHL depiction, and a thickened CHL is highly suggestive of frozen shoulder.
We investigated in conscious rats the role of capsaicin-sensitive neurons and alpha-calcitonin gene-related peptide (CGRP), the form preferentially expressed in capsaicin sensory neurons, in mediating intracisternal thyrotropin-releasing hormone (TRH) analogue-induced vagal muscarinic gastroprotection against ethanol lesions. The TRH analogue RX-77368 (1.5 ng ic) reduced by 78 and 66% gastric hemorrhagic lesions induced by intragastric intubation of 60 and 80% ethanol, respectively. alpha-CGRP (1 nmol/kg iv) inhibited by 88% gastric lesions induced by 60% ethanol, and this peptide action was blocked by the CGRP antagonist, CGRP-(8-37) (128 nmol/kg iv). The protective effect of RX-77368 against 60% ethanol was completely abolished by the CGRP monoclonal antibody 4901 (4.8 mg/kg iv), CGRP-(8-37) (128 nmol/kg iv), and capsaicin pretreatment (125 mg/kg). Gastric lesions induced by 60% ethanol were not altered by the CGRP antagonist or antibody alone but were enhanced by capsaicin pretreatment. These results suggest that the gastroprotection induced by intracisternal TRH analogue involves an interaction between central vagal efferent pathways and splanchnic sensory afferent terminals containing CGRP.
To assess the vaginal microbiome throughout full-term uncomplicated pregnancy, a longitudinal study was designed for 12 healthy women who had prepared to become pregnant and then delivered at term (38–42 weeks) without complications. The vaginal microbial community was studied at pre-pregnancy, 8–12, 24–28, 37–38 weeks of gestation, and puerperium, using hypervariable tag sequencing of the V3–V4 region of the 16S rRNA gene. Sequencing produced approximately 10 million reads on the Illumina MiSeq. Members of the Firmicutes phyla were prevailing before and during pregnancy periods, and the proportion was quite as Proteobacteria until puerperium. Lactobacillus genus was abundant before and during pregnancy, but post-delivery vaginal microflora variety turned diverse. The species-level analysis revealed that a healthy vaginal microbiome before or during pregnancy was prominently dominated by Lactobacillus crispatus. Furthermore, PCoA analysis revealed for differences in the bacterial community composition between the two levels of Lactobacillus species in pre-pregnancy and pregnancy period (PC1 contribution of 58.46%, PC3 contribution of 8.64%). Based on the taxonomic and PCoA analysis, we found that L. crispatus was dominant in the vaginal microflora of healthy women before or during pregnancy, but at the puerperium, the status changed leading to decreased abundance of protective Lactobacillus species that made vaginal micro-ecological barrier vulnerable to diseases. Additionally, vaginal pH was an important environmental property affecting the vaginal microbial community.
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