HI is common among Chinese patients undergoing surgery for pheochromocytoma. Our study identified three predictive factors for intraoperative HI: a large tumour diameter, diabetes/prediabetes and a great preoperative systolic blood pressure fluctuation. Furthermore, patients are more likely to suffer from HI when they have more predictive risk factors. Identification of these risk factors can help to improve perioperative management.
Resistin is a 12.5-KDa cysteine-rich peptide that has been implicated in the impairment of glucose homeostasis via the AMP-activated protein kinase (AMPK) pathway in a rodent model. However, the role resistin plays in humans is controversial. This study investigated the effect of resistin on glucose metabolism and insulin signaling using human recombinant resistin and small interfering RNA (siRNA) against AMPKalpha2 to treat the human liver HepG2 cells. The mRNA of key genes involved in glucose metabolism and the insulin-signaling pathway were detected by real-time RT-PCR. Phosphorylation levels of Akt and AMPK were measured by western blot. The incorporation of D-[U-(14)C] glucose into glycogen was quantitated by liquid scintillation counting. The results demonstrate that resistin stimulated expressions of glucose-6-phosphatase (G6Pase), phosphoenolypyruvate carboxykinase (PEPCK), and suppressor of cytokine signaling 3 (SOCS-3), repressed the expressions of insulin receptor substrate 2(IRS-2) and glucose transporter 2(GLUT2). In addition, resistin inhibited the insulin-induced phosphorylation of Akt independent of AMPK. In conclusion, our findings suggest that resistin induces insulin resistance in HepG2 cells at least partly via induction of SOCS-3 expression and reduction of Akt phosphorylation through an AMPK-independent mechanism. Resistin also increases glucose production via AMPK-mediated upregulated expression of the genes encoding hepatic gluconeogenic enzymes, G6Pase, and PEPCK.
Lipid-induced insulin resistance is associated with inflammatory state in epidemiological studies. However, it is still unclear whether the activation of NF-κB, a pivotal transcription factor of inflammation, plays a crucial role in mediating skeletal muscle insulin resistance. This study addressed what was the role of NF-κB in lipid-induced insulin resistance and whether NF-κB activation was sufficient to cause insulin resistance in C2C12 myotubes. A 16 h exposure of myotubes to palmitate reduced net insulin-stimulated glucose uptake by 48%, GLUT4 translocation by 52%, Akt phosphorylation by 54%, induced a 1.8-fold increase in insulin-stimulated insulin receptor substrate (IRS) phosphorylation, and doubled NF-κB activation. Myotubes transfected with NF-κB p65 siRNA for 24 h and followed by a treatment with palmitate for 16 h efficiently blocked NF-κB activation, and prevented the detrimental effects of palmitate on the metabolic actions of insulin. Transfection of myotubes with I-κBα siRNA for 24 h also led to a twofold induction of NF-κB activation, and reduced net insulin-stimulated glucose uptake by 30%, GLUT4 translocation by 35%, Akt phosphorylation by 31%, induced a 0.7-fold increase in insulin-stimulated IRS phosphorylation. These findings suggest that NF-κB overexpression per se is sufficient to impair insulin sensitivity and palmitate-induced insulin resistance is mediated by NF-κB in skeletal muscle cells.
Symptomatic isolated dissection of the superior mesenteric artery (SIDSMA) represents an extremely rare condition. Although various treatments including conservative treatment, endovascular stenting (ES), and surgical repair are currently available, consensus treatment guideline is absent due to scarce of SIDSMA cases. Thus, we present our experience in the treatment of SIDSMA at our single center.Fourteen cases of SIDSMA were treated with conservative treatment, catheter-directed thrombolysis (CDT), endovascular stenting (ES), or surgical repair at our center between January 2008 and January 2014. Demographics, clinical manifestations, coexisting medical conditions, imaging feature, treatments, and follow-up outcome of these patients were retrospectively collected and analyzed.For 13 patients without peritonitis, conservative treatment was given for 4 to 6 days initially. After the first observation cycle, symptoms and signs were alleviated in 8 patients, and conservative treatments were continued. The remaining 5 patients received technically and clinically successful ES (in 4) or CDT (in 1) due to worsening symptoms and signs during conservative treatment. One patient with peritonitis underwent emergency surgery, with the necrotic small intestine resected. However, the abdominal pain was not alleviated 17 days postoperatively, ES was thus performed and symptoms relieved immediately. Two weeks after ES, a new aneurysm and partial thrombosis in the distal part of the stent were found by computed tomography angiography in this patient. No intestinal infarction or mortality developed during hospitalization. Follow-up was accomplished in 11 cases, ranging from 4 to 74 months (23.5 ± 21.3). Except that one complained with mild abdominal pain, the other 10 achieved complete remission. All patients were free from new aneurysmal formation of SMA and all stents remained patent.For SIDSMA without peritonitis, conservative treatment can be provided with reasonable success rate, while ES may serve as an effective alternative once conservative treatment fails. For SIDSMA with peritonitis, open surgery remains the treatment of choice by resection of necrotic intestine and revasculization.
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