endothelial cells; 4. differentiation; Presenting Author: WENJING LI Additional Authors: HAOXUAN ZHENG, BO JIANG Corresponding Author: BO JIANG Affiliations: Guangdong Provincial key laboratory of Gastroenterology, Department of Gastroenterology, Nanfang Hospital, Southern Medical University Objective: Fas signaling was reported to participate in cell apoptosis. However, this pathway has also been reported to induce epithelial-mesenchymal

transition (EMT). EMT has been reported to be simultaneously associated with cancer stem cell (CSC) generation, leading to the hypothesis that Fas signaling may induce signaling pathway the obtainment of cancer stem cell characteristics. Methods: The effects of Fas-ligand

(FasL) treatment on colon cancer cells were tested using CCK-8 assay, soft agar assay, sphere formation assay, flow cytometry, immunoblot and immunofluorescence analyses. Results: Low-dose of FasL(12.5 ng/ml) didn’t effect the proliferation rate of colon cancer cells SW480. Fas signaling enhanced the clone-forming ability and stem-cell characteristics in colorectal cancer cell line SW480 combined with upregulated expression of stem-cell related surface markers Selleckchem Buparlisib as well as transcriptional factors, all of which indicating enhanced CSC generation. The ERK1/2 pathway was activated by Fas signaling and is required 上海皓元 for FasL-induced CSC generation. Conclusion: Altogether, these data indicate that Fas signaling may induce CSC generation through the activation of ERK1/2 pathway in colorectal cancer cell line SW480. Key Word(s): 1. Fas signaling; 2. cancer stem cell; 3. colorectal cancer; Presenting Author: XIN XU Additional Authors: BANGMAO WANG, QINGXIANG YU Corresponding Author: XIN XU Affiliations: General Hospital of Tianjin Medical university Objective: To compare the expression levels of transient receptor potential channel (TRPC) and cholinergic muscarinic acetylcholine receptor (CHRM) in human gastrointestinal

stromal tumors (GISTs). Methods: Immunohistochemical staining was applied to detect the expression of TRPC and CHRM in clinical specimens of GISTs. Results were evaluated using Pearson’s correlation and a multivariate analysis Results: Expression of TRPC1, TRPC3, CHRM2 and CHRM3 subtypes was determined in GISTs (57.5%, 47.5 %, 22.5%, 55.0%). With the increase of tumor malignancy, the expression levels of TRPC and CHRM decreased respectively (P < 0.05). Conclusion: GISTs express TRPC1, TRPC3, CHRM2 and CHRM3 subtypes, providing a new evidence for the origination of GIST from interstitial cells of Cajal (ICCs) GISTs may maintainpart of structures of ICCs for mediating neurotransmitter functions in gastrointestinal motility. Key Word(s): 1. GIST; 2. ICC; 3. TRPC; 4.

Post LT predictors are use of thymoglobulin and high Clavien score. Moreover, high Clavien score and blood loss during surgery contributed more than delirium on selleck LOS. Disclosures: Eberhard L. Renner – Advisory Committees or Review Panels: Vertex Canada,

Novartis, Astellas Canada, Roche Canada, Gambro, AbbVIe, BMS; Grant/ Research Support: Novartis Canada, Gilead; Speaking and Teaching: Novartis, Astellas Canada, Roche Canada The following people have nothing to disclose: Koki Yamada, Max Marquez, Khalid Mumtaz Background&Aims: The translocation of bacterial antigens into blood of patients with decompensated cirrhosis has been related with poor prognosis and an increased inflammatory outlook. The aim of this study was to evaluate the association between liver transplantation and the systemic bacterial antigen clearance in cirrhotic patients and also to determine the relationship between bacterial antigen translocation in liver transplant donors and recipients. Patients&Methods: Patients with decompensated cirrhosis admitted for liver transplantation at the Digestive Surgery Unit of Hospital General Universitario de Alicante, Spain, were consecutively included. Peripheral blood samples from the recipient were collected at the beggin-ing of surgery and 72 hours after liver transplantation. A blood sample was also collected

from the donor. Bacterial genomic translocation was identified by partial sequencing TAM Receptor inhibitor analysis of amplified 16SrRNA gene of prokariotes. Results:

Forty-nine patients (40 male, mean age 55±9.5 years) were included in the study. Etiology was mainly alcohol (n=18, 37%), HCV (n=13, 26.5%) or alcohol+HCV (n=9, 18%). Twenty-eight patients had hepatic carninoma. Thirteen patients had ascitic fluid. MELD mean score was 18 ±6. Seventeen patients showed blood bacterial DNA before surgery (34.7%). Of those, 14 patients showed blood bacterial DNA 72 hours after liver transplantation (82.3%). Sequencing analysis identified the same bacterial species in 11 out of 14 patients (78.5%). In the group of patients without bacterial antigen translocation before surgery, 10 patients showed blood bacterial genomic fragments MCE (31.2%). On the other hand, bacterial DNA was detected in 19 liver transplant donors (38.7%). Five out of 10 liver recipients (50%) who had not bacterial DNA and 8 out of 17 liver recipients who had bacterial DNA (47%) before surgery and showed it after transplantation received the organ from a bacterial DNA-positive donor. Sequencing analysis identified the same bacterial species as that found after surgery in 7 cases (5 without and 2 with bacterial DNA before surgery). Finally, 4 out of 5 patients with partial portal thrombosis before surgery showed bacterial DNA fragments in blood. No other clinical or analytical correlations were found. Conclusion: Circulating bacterial antigens persist in blood of patients with cirrhosis after liver transplantation.

This study demonstrates the feasibility, safety, and intermediate term effectiveness of endovascular stent reconstruction of spontaneous,

cervico-cranial arterial dissection. “
“Hepatic encephalopathy (HE) is an uncommon complication of total parenteral nutrition (TPN). Cytotoxic edema has not been reported Cilomilast in vitro in children with TPN-related HE. We describe a case of TPN-related HE presenting with diffuse cytotoxic edema which reversed after liver transplantation. “
“Wernicke’s encephalopathy is a metabolic disorder caused by deficiency of thiamine (vitamin B1) seen in alcoholics and even in nonalcoholic patients, classically presenting with a triad of ataxia, ophthalmoplegia, and altered mental status. Typical findings in magnetic resonance imaging are represented by symmetric signal alterations in medial thalami, mamillary bodies, tectal plate, and periaqueductal area and atypical findings involve lesions in cerebellum, midline vermis, red nuclei, dentate, caudate, cranial nerve nuclei, splenium and cerebral cortex. We report here a case of nonalcoholic starvation induced atypical WE showing symmetrical lesions in substantia see more nigra in addition to the classical neuroradiological

findings. J Neuroimaging 2012;22:204-207. “
“An effort to define and validate a Harmonized Protocol for standard hippocampal segmentation is being carried out. We wished to estimate the effect of magnetic resonance image (MRI) spatial orientation on manual hippocampal segmentations to define optimal standard orientation of MRIs for hippocampal volumetry. MCE公司 Three expert tracers segmented twice the hippocampi of 10 ADNI subjects on MRI slices oriented perpendicular to the anterior-posterior commissure (AC-PC) line and the long hippocampal axes plane, following internationally harmonized landmarks. We computed intra and interrater reliability figures for total volumes and similarity coefficients. Total volume reliability was similar for both orientations. Similarity coefficients were significantly higher for

the AC-PC orientation (exact P = 0.002). These data show that AC-PC orientation is slightly more reliable for manual segmentations, possibly due to better visualization of the cerebrospinal fluid spaces separating hippocampal head and amygdala. A Delphi panel of experts has used these data to decide on the optimal orientation for a Harmonized Protocol for hippocampal segmentation. “
“The so-called “crowned dens” is a peculiar manifestation of calcium crystal deposition diseases, either caused by calcium pyrophosphate dihydrate or caused by calcium hydroxiapatite crystals, characterized by the presence of calcific deposits around the odontoid, often showing a crown-like configuration on imaging. It has protean clinical and radiological pictures, and care should be taken to avoid misinterpretation and diagnostic errors.

Quantitative RT-PCR of the cultures in the SC controls versus those in HDM-C indicated that SR messenger RNA (mRNA) more than doubled (P < 0.05). The effect was even more profound in the cells embedded into matrix and given HDM-C, resulting in ramifying and

branching ducts formation, lined by cells with a phenotype of mature cholangiocytes (Fig. 8C). Quantitative RT-PCR indicated significantly higher levels of expression of cholangiocyte-specific genes for GGT, CFTR, and AE-2 (Fig. 7). Formation of islet-like structures increased significantly both in cultures on plastic and in HDM-P and when embedded into matrix and given HDM-P. The monolayers in HDM-P produced dense balls of aggregated cells budding from the edges of the colonies and containing cells expressing C-peptide, PDX1, and insulin. Four to five such aggregate-structures appeared on average in cells on plastic and in HDM-P; FK506 nmr secreted human C-peptide could be detected especially in cultures stimulated with high glucose levels (Fig. 5). In cultures embedded into matrix and given HDM-P, the islet-like clusters occurred at the CP-673451 cell line edges of the hydrogels (pale blue structures) and were positive for dithizone staining, indicating cells with zinc condensed

in insulin granules in the cytoplasm (Fig. 6). Immunohistochemistry indicated that these neoislet-like structures were positive for PDX1, human C-peptide, and insulin as well as for glucagon and somatostatin (data medchemexpress not shown). The quantitative RT-PCR assays (Fig. 7) of these cultures were the most dramatic in the elevation of expression of genes specific for pancreatic endocrine cells. To explore whether biliary tree stem cells have the ability to differentiate into mature liver cell type in vivo, we transplanted isolated biliary tree stem/progenitors directly into the livers of normal SCID mice (n = 3) and checked for their fate(s) 30 days later. The mice were not subjected to any injury process, meaning that the engraftment occurred under quiescent

liver conditions. Human cells were found around injection sites and some were dispersed into the liver sinusoids of periportal and intralobular parenchyma. We estimate that an average of 6.52% ± 2.5% of the total area of the hepatic lobes was occupied by mature human hepatocytes positive for human HepPar-1 and albumin (Fig. 8). Moreover, the bile ducts were lined with a high percentage (average 12.7% ± 5.5%) of mature human cholangiocytes, positive for human CK7 (Fig. 8), meaning that human cholangiocytes coexisted with human hepatocytes within areas of liver parenchyma in the hosts. Human cells were not observed in sham-transplanted animals, and no tumors formed in any of the transplanted animals.

1). Similar risk values for HCC were observed among HBsAg-positive carriers (OR = 1.67) and among

HBsAg-negative participants (OR = 1.82). Additionally, we analyzed possible modified effects of anti-HCV status and XPC genotypes on HCC risk and found similar risk values for HCC among anti-HCV–positive and anti-HCV–negative groups. Likelihood ratio tests for the interaction between the stratified variables, including HBsAg status (negative and positive) and anti-HCV status (negative and positive), and XPC genotypes showed that this was not statistically significant (Pinteraction > 0.05; Supporting Table 2). To study the relationship between the polymorphism of XPC codon 939 and AFB1 exposure years in the risk for HCC, we analyzed the joint effects of AFB1 learn more exposure years and genotypes on HCC risk (Table 3). In this analysis, we used as a reference the lowest risk group: those who had

XPC-LL and short-term AFB1 exposure. The results showed that increasing the number of AFB1 exposure years consistently increased HCC risk; moreover, this effect was more pronounced among the XPC-LG and XPC-GG subjects. Additionally, we evaluated the multiplicatively interactive effects of genotypes and AFB1 exposure years according to the following selleck compound formula (first shown in the Patients and Methods section)24: Interestingly, we found some evidence of interactive effects of genotypes and exposure years on HCC risk (22.33 > 8.69 × 1.88). A similar increased-risk trend was also found in the joint-effects analysis of XPC genotypes and AFB1 DNA adduct levels for the risk of HCC (18.38 > 4.62 × 1.11; Table 3). On the basis of a recent report showing that the dysregulation of XPC is highly related to HCC,28 using immunochemistry, we investigated whether XPC genotypes influenced its expression in the cancerous tissues of 834 HCC cases. Different

expression levels were detected in tumor tissues from cases with different genotypes (r = −0.369; Table 4). Representative photographs exhibit the aforementioned correlation between the genotypes and expression levels medchemexpress (Fig. 1A-C). An association analysis of the risk genotypes [i.e., genotypes of the XPC codon 939 Gln alleles (XPC-LG/GG)] or the nonrisk genotype (XPC-LL) and the clinical characteristics of HCC (including the etiology and severity of liver diseases) was first performed separately. Significant differences in the distributions of the genotypes were observed with respect to different AFB1 expression years or levels but not with respect to age, gender, minority status, HBsAg status, anti-HCV status, tumor size, cirrhosis status, or TNM stage (Supporting Table 3).

prevalence and associated factors Presenting Author: JIN TAO Additional Authors: XIUQING WEI, YANPING LIANG, BIN WU Corresponding Author: JIN TAO Affiliations: 4th Affiliated Hospital of Sun Yat-Sen University, 4th Affiliated Hospital of Sun Yat-Sen University, 3rd Affiliated Hospital high throughput screening assay of Sun Yat-Sen University Objective: To study the effect of biological feedback treatment of the outlet obstructive constipation. Methods: A analysis of the clinical data of 56 cases of biological feedback treatment of the outlet obstructive constipation was made. Results: Among 54 cases who completed the biological feedback treatment, the results of rectal manometer detection

in 35 cases indicated that the rectum sensitivity threshold and the maximum tolerance capacity and recto-anal inhibitory reflex decreased, compared with those before treatment. Paradoxical contraction of pelvic floor disappeared and normal bowel movement was regained;in cases the symptoms were improved, including times of bowel 5-Fluoracil datasheet movement, functional

constipation and anorectic distention. The effective rate of biofeedback treatment was 92.6%. Only 4 cases were ineffective and 2 cases stopped treatment. Conclusion: The short-term effect of biological feedback treatment for the outlet obstructive constipation is satisfactory, and has advantages of low cost and no need for hospital admission. Key Word(s): 1. outlet obstructive constipation; 2. biological feedback treatment; 3. functional constipation Presenting Author: YAN WANG Additional Authors: YAN WANG, HAI TAO SHI, FEN RONG CHEN, JU HUI ZHAO,

HONG LI, JIONG JIANG Corresponding Author: YAN WANG Affiliations: Second Hospital of Xi’An Jiaotong University, Second Hospital of Xi’An Jiaotong University, Second Hospital of Xi’An Jiaotong University, Second Hospital of Xi’An Jiaotong University, Second Hospital of Xi’An Jiaotong University, Second Hospital of Xi’An Jiaotong University 上海皓元 Objective: The central effects and mechanism of ghrelin on the small intestinal motility are not clear. Our study aimed to explore the effects and mechanism of ghrelin after intracerebroventricular (ICV) injection on the interdigestive myoelectric complex (IMC) in rats. Methods: (1) In the electrophysiologic experiment, two pairs of silver electrodes were implanted in the duodenum and jejunum. Rats were received ICV injection of ghrelin (6.4 μg kg −1) during fasting. Some rats were pretreated with intravenous injection of phentolamine, propranolol and atropine respectively. Other groups of rats were received ICV injection of anti-neuropeptide Y (NPY) IgG and (D-Lys3) GHRP-6 before ghrelin injected. (2) The c-Fos activation on the central nervous system (CNS) and enteric nervous system (ENS) through ICV injection of ghrelin was studied by the immunohistochemistry. Results: (1) Ghrelin showed an excitatory effect on the IMC. This effect was inhibited by atropine, anti-NPY IgG and (D-Lys3) GHRP-6, but not by propranolol and phentolamine.

3–93.6% and 94.9%. Negative predictive values were very high (100%, 100% and 98.7% respectively). But positive predictive values were lower, ranging from 62.5 to 71.4%. Conclusion:  All monoclonal fecal tests in this series presented similar performance in the post-treatment setting. A negative test after treatment adequately predicted cure of the infection. However, nearly a third of tests were false positive, showing a poor predictive

yield for persistent infection. “
“Background: Helicobacter pylori-associated disease has led to aggressive diagnostic and eradication protocols that are partially responsible for Ixazomib the decrease in prevalence of H. pylori carriage. Recent evidence indicates that in low-prevalence populations, H. pylori may have protective effects on allergic diseases. The aim of this study was to explore the relationship between pediatric asthma and H. pylori infection in a population with high

prevalence of H. pylori infection. Materials and Methods:  A national referral laboratory was screened for all 13C urea breath tests performed in children aged 5–18 years between 2007 and 2008, for patient demographics and physician-diagnosed asthma. Data concerning asthma-associated medication usage were extracted from electronic medical records and databases. Data were analyzed using a stepwise logistic regression model. Results:  During the study period, 6959 patients underwent urea breath testing (average age 12.4 ± 3.5 years). Of these, 3175/6959 (45.6%) were positive for H. pylori, and 578/6959 (8.3%) had asthma. Rates of asthma in H. pylori-positive and H. pylori-negative Selleck 3Methyladenine children were 7.3 and 9.1%, respectively (odds ratio 0.82; 95% confidence interval

(CI) 0.69–0.98; p = .032). We also confirmed that male gender, urban residence, and age are associated with childhood asthma. Conclusions:  We demonstrate an inverse association between H. pylori and pediatric asthma in a population with a high prevalence of H. pylori. “
“Recent studies found that gastric cancer patients with Helicobacter pylori infection had a better response to chemotherapy and had an improved overall prognosis compared with those without. However, the underlying mechanism remains unknown. Quantitative real-time PCR (qRT-PCR) was utilized to determine the expression profile of miR-141 in H. pylori infected cells and tissues and their medchemexpress respective controls. qRT-PCR and Western blot were used to determine the expression level of KEAP-1. Luciferase reporter assays were used to determine whether KEAP-1 was a direct target of miR-141 in the gastric cancer cells. MTT and apoptosis assay were performed to detect the survival of cells under cisplatin treatment. We found that H. pylori infection can significantly down-regulate miR-141 expression. Knockdown miR-141 expression in 7901/DDP and 7901 cells could significantly improve cisplatin sensitivity. Over-expression of miR-141 resulted in enhanced resistance to cisplatin in both gastric cancer cells.

9–11 The “Out of Africa” hypothesis would be supported if global HBV genotype distributions

matched these anatomically modern human (Homo sapiens) migrations. Crucially, HBV sequences sampled from several isolated indigenous populations belong to separate subgenotypes.12–16 In some cases, such as the Indonesian archipelago, the distribution of HBV genotypes/subgenotypes is associated with Deforolimus cost the ethnic origin of the populations.12 These geographical patterns indicate that HBV diversity might be associated with early waves of human migration, although HBV phylogeny does not match perfectly the evolutionary history of human populations or primates.5 We investigated the controversy about the origin of HBV in humans and systematically searched for patterns in HBV phylogeny related

to modern human history. Based on evidence supporting the coincidence of HBV and human migrations, we investigated the timescale of global HBV dispersal and tested the hypothesis of co-divergence of the virus with modern humans using phylodynamic selleck inhibitor and phylogeographic methods. We also propose a model for the origin of HBV in Old World primates. We suggest, based on multiple lines of evidence, that the “Out of Africa” hypothesis is far more likely than the alternative hypotheses about the HBV origin in humans. HBV, hepatitis B virus; 95% HPD, 95% higher posterior density; ka, thousand years ago; tMRCA, time to most recent common ancestor. If HBV co-diverged with human populations,

we should be able to find distinct patterns relating to ancient human population movements. We systematically searched the literature of HBV epidemiology using the keywords “Amerindians,” “Pacific,” “Aborigines,” “Indigenous,” AND “HBV.” We also downloaded nucleotide sequences isolated from populations using these keywords. The search was completed in August 2010 and updated in May 2012 (Supporting Information). We tested for HBV-human co-divergence using a stepwise calibration-test approach. Briefly, we checked whether the coalescence times of the Amerindian population (13.0-20.0 ka BP), MCE when used to calibrate the ages of the Amerindian-specific genotypes on the HBV tree, were able to estimate the co-migration of HBV and humans in Polynesia. These dates are based on genetic and archaeological evidence for the dispersal times of modern humans in the Americas.17 We then incorporated the Polynesian and the Haitian calibration dates in our molecular clock analyses (6.6 ± 1.5 ka and no earlier than 500 years ago, respectively) to incorporate dates that covered a larger part of the HBV genetic diversity. If HBV had only appeared in the human population a few thousand years ago, we would not expect early and late coalescent dates in the human phylogeny to match with those in the phylogeny of their HBV isolates. We also tested whether historical human population sizes correlated with the inferred effective population sizes of HBV.

After specifying important co-stimulatory interactions required for the re-stimulation of FVIII-specific memory B cells, we were interested to study the potential impact of different concentrations of FVIII on this process. We tested a range of concentrations between 1 pg mL−1 and 100 μg mL−1 of FVIII (Fig. 3a) [18]. Re-stimulation of memory B cells could be detected at concentrations of FVIII that were as small as 100 pg mL−1 (Fig. 3a)

[18]. Optimal re-stimulation was achieved at concentrations of 3–10 ng mL−1, which correspond to about 3–10% of the physiological plasma concentration (Fig. 3a) [18]. When we further increased the concentration of FVIII, inhibition of memory B-cell re-stimulation was observed. The BYL719 in vitro inhibition started at a concentration of FVIII of 100–300 ng mL−1 with an almost complete inhibition at 1 μg mL−1 FVIII (Fig. 3a) [18]. The dose-response relation for T-cell re-stimulation was very different from the dose-response relation for memory B-cell re-stimulation. Optimal stimulation of FVIII-specific

T cells was observed at concentrations of 10–30 μg mL−1 FVIII (Fig. 3b,c). Inhibition of T-cell stimulation was seen at concentrations of 100 μg mL−1 FVIII. Based on these results, we conclude that the concentration of FVIII required for inhibition of memory B-cell PLX-4720 mw re-stimulation and the concentration required for inhibition of T-cell re-stimulation are very different (Fig. 3a–c), which makes it unlikely that the inhibition of memory B-cell re-stimulation is caused by an inhibition of T-cell stimulation. The major T-cell cytokines found in culture supernatants after stimulation of spleen cells with FVIII were IL-10 and IFN-γ (Fig. 3c), which is consistent with findings we reported previously [13,21]. To further support these results,

we analysed the frequency of FVIII-specific T cells by intracellular cytokine staining 3 days after re-stimulation of MCE公司 spleen cells. We compared concentrations of 10 ng mL−1, which re-stimulate, and 20 μg mL−1 FVIII which inhibit memory B-cell differentiation and observed a correlation between the frequency of FVIII-specific T cells producing IL-2, IL-10 or IFN-γ and the concentration of FVIII used for the re-stimulation (data not shown). We did not observe any inhibitory effects of 20 μg mL−1 of FVIII on T-cell stimulation despite the fact that this concentration of FVIII completely blocks the re-stimulation of FVIII-specific memory B cells [18]. Infections, particularly infections from the central venous catheter inserted in patients with haemophilia A and FVIII inhibitors during ITI therapy, commonly cause a rise in anti-FVIII antibody titres [22].

2 ± 3.1 to 8.7 ± 3 kg (−15%) with reduced carbohydrate and from 10.1 ± 3.3 to 8.6 ± 2.9 kg (−15%) with reduced fat (P = n.s. between interventions, P < 0.001 compared with baseline for both). Total body fat% estimated by bioimpedance analysis decreased similarly for both interventions (reduced carbohydrate: 35.6 ± 6.4% before and 33.2 ± 7.2% after, P < 0.01; reduced fat: 36.4 ± 5.5% before and 33.5 Palbociclib ± 5.1% after, P < 0.001). Cardiorespiratory fitness expressed as maximum oxygen uptake did not change with diet in either group. We observed similar changes in fasting insulin and glucose concentration as well as HOMA index in both intervention

groups (Table 2). Triglycerides, free fatty acids, and high-density lipoprotein (HDL)-cholesterol Selleckchem Cilomilast concentrations were also not significantly different

after diet among groups. However, total- and high-density lipoprotein (LDL)-cholesterol decreased more in subjects on a reduced fat diet compared to the reduced carbohydrate diet (Table 2). Liver aminotransferases decreased numerically but not statistically more in the reduced fat group. Adiponectin, fetuin-A, and high sensitive CRP measurements showed similar response in both dietary groups (Table 2). We next analyzed subjects according to their intrahepatic fat content at baseline. We observed a greater intrahepatic fat loss along with a greater reduction of ALT by trend for subgroups with high initial IHL content, irrespective of dietary macronutrient composition (Fig. 5, first and second panels). Furthermore, subjects with high baseline IHL also showed a better relative reduction in IHL (−50 ± 22% versus −31 ± 36 on reduced carbohydrate; −44 ± 20 versus −23 ± 49% on reduced fat; P < 0.05 for both). In contrast, similar responses occurred for visceral fat mass, insulin sensitivity

(Fig. 5, third panel; Fig. 6, first panel) as well as fasting insulin, glucose, and HOMA index between subgroups. To assess influences of insulin sensitivity on the response to macronutrient composition, we stratified subjects into an insulin-sensitive and an insulin-resistant group using a predefined C-ISI cutoff of 4.5.28 The insulin-resistant group was heavier 上海皓元医药股份有限公司 (95.9 ± 15.8 versus 90.1 ± 15.9 kg; P = 0.072) and showed higher IHL values (12.5 ± 11.9 versus 5.8 ± 6.3%; P < 0.01) compared with the insulin-sensitive group. Insulin-resistant subjects lost 7.9 ± 4.6 kg on the reduced carbohydrate and 7.8 ± 4.9 kg on the reduced fat diet (n.s.). Insulin sensitive subjects lost 7.2 ± 4.2 kg on the reduced carbohydrate and 5.2 ± 4.1 kg on the reduced fat diet (P = 0.075). IHL in insulin-resistant subjects decreased 6% ± 6.7% with reduced carbohydrates and 4.9% ± 4.8% with reduced fat (n.s.). In insulin-sensitive subjects, IHL decreased 2.1% ± 2.3% with the reduced carbohydrate and 3.3% ± 5.1% (n.s.) with the reduced fat diet. When stratifying subjects for impaired glucose tolerance before diet those with impaired glucose tolerance had similar bodyweight (94.8 ± 15.