Change in the diagnosis of inflammatory bowel disease: a hospital-based cohort study from Korea

Background/AimsAccurately diagnosing inflammatory bowel disease (IBD) remains a challenge, but is crucial for providing proper management for affected patients. The aim of the present study was to evaluate the frequency of change in diagnosis in Korean patients who were referred to our institution with a diagnosis of IBD.MethodsWe enrolled 1,444 patients diagnosed with ulcerative colitis (UC) and 1,452 diagnosed with Crohn's disease (CD), who had been referred to the Asan Medical Center between January 2010 and December 2014. These patients were assessed and subsequently classified as having UC, CD, indeterminate colitis, possible IBD, or non-IBD.ResultsDuring a median follow-up of 15.9 months, 400 of the 2,896 patients (13.8%) analyzed in this study experienced a change in diagnosis. A change in diagnosis from UC to CD, or vice-versa, was made in 24 of 1,444 patients (1.7%) and 23 of 1,452 patients (1.6%), respectively. A change to a non-IBD diagnosis was the most common modification; 7.5% (108 of 1444) and 12.7% (184 of 1452) of the patients with a referral diagnosis of UC and CD, respectively, were reclassified as having non-IBD. Among the 292 patients who were ultimately determined not to have IBD, 135 (55 UC and 80 CD cases) had received IBD-related medication.ConclusionsThere are diagnostic uncertainties and difficulties in relation to IBD. Therefore, precise assessment and systematic follow-up are essential in the management of this condition

Genetic Traceability of Black Pig Meats Using Microsatellite Markers

Pork from Jeju black pig (population J) and Berkshire (population B) has a unique market share in Korea because of their high meat quality. Due to the high demand of this pork, traceability of the pork to its origin is becoming an important part of the consumer demand. To examine the feasibility of such a system, we aim to provide basic genetic information of the two black pig populations and assess the possibility of genetically distinguishing between the two breeds. Muscle samples were collected from slaughter houses in Jeju Island and Namwon, Chonbuk province, Korea, for populations J and B, respectively. In total 800 Jeju black pigs and 351 Berkshires were genotyped at thirteen microsatellite (MS) markers. Analyses on the genetic diversity of the two populations were carried out in the programs MS toolkit and FSTAT. The population structure of the two breeds was determined by a Bayesian clustering method implemented in structure and by a phylogenetic analysis in Phylip. Population J exhibited higher mean number of alleles, expected heterozygosity and observed heterozygosity value, and polymorphism information content, compared to population B. The FIS values of population J and population B were 0.03 and −0.005, respectively, indicating that little or no inbreeding has occurred. In addition, genetic structure analysis revealed the possibility of gene flow from population B to population J. The expected probability of identify value of the 13 MS markers was 9.87×10−14 in population J, 3.17×10−9 in population B, and 1.03×10−12 in the two populations. The results of this study are useful in distinguishing between the two black pig breeds and can be used as a foundation for further development of DNA markers

The Relation of Menarcheal Age to Anthropometric Profiles in Korean Girls

The aim of this study was to represent the trend of early menarche and to assess the association of age at menarche with anthropometric profiles of Korean children and adolescents. A cross sectional survey was conducted with 13,371 girls aged 10 to 18 yr, recruited nationwide from April, 2005 to March, 2006. Height, weight and waist circumference of the subjects were measured; and the subjects self-reported their ages at menarche. We found that the menarcheal girls were taller (P<0.05 for the girls between 10 and 14 yr) and heavier (P<0.05 for the girls between 10 and 18 yr) than non-menarcheal ones. Menarcheal girls also showed higher body mass index (BMI), and greater waist circumference than non-menarcheal ones. Significant differences were represented according to the age at menarche in terms of BMI, waist circumference, % body fat mass, waist hip ratio and neck circumference as well as height and weight (P<0.05). In conclusion, girls who matured early were taller and heavier in early adolescence than those who matured later

Overexpression of Glucose-6-Phosphate Dehydrogenase Is Associated with Lipid Dysregulation and Insulin Resistance in Obesity

Glucose-6-phosphate dehydrogenase (G6PD) produces cellular NADPH, which is required for the biosynthesis of fatty acids and cholesterol. Although G6PD is required for lipogenesis, it is poorly understood whether G6PD in adipocytes is involved in energy homeostasis, such as lipid and glucose metabolism. We report here that G6PD plays a role in adipogenesis and that its increase is tightly associated with the dysregulation of lipid metabolism and insulin resistance in obesity. We observed that the enzymatic activity and expression levels of G6PD were significantly elevated in white adipose tissues of obese models, including db/db, ob/ob, and diet-induced obesity mice. In 3T3-L1 cells, G6PD overexpression stimulated the expression of most adipocyte marker genes and elevated the levels of cellular free fatty acids, triglyceride, and FFA release. Consistently, G6PD knockdown via small interfering RNA attenuated adipocyte differentiation with less lipid droplet accumulation. Surprisingly, the expression of certain adipocytokines such as tumor necrosis factor alpha and resistin was increased, whereas that of adiponectin was decreased in G6PD overexpressed adipocytes. In accordance with these results, overexpression of G6PD impaired insulin signaling and suppressed insulin-dependent glucose uptake in adipocytes. Taken together, these data strongly suggest that aberrant increase of G6PD in obese and/or diabetic subjects would alter lipid metabolism and adipocytokine expression, thereby resulting in failure of lipid homeostasis and insulin resistance in adipocytes

Molecular Mechanisms for Ketone Body Metabolism, Signaling Functions, and Therapeutic Potential in Cancer

The ketone bodies (KBs) β-hydroxybutyrate and acetoacetate are important alternative energy sources for glucose during nutrient deprivation. KBs synthesized by hepatic ketogenesis are catabolized to acetyl-CoA through ketolysis in extrahepatic tissues, followed by the tricarboxylic acid cycle and electron transport chain for ATP production. Ketogenesis and ketolysis are regulated by the key rate-limiting enzymes, 3-hydroxy-3-methylglutaryl-CoA synthase 2 and succinyl-CoA:3-oxoacid-CoA transferase, respectively. KBs participate in various cellular processes as signaling molecules. KBs bind to G protein-coupled receptors. The most abundant KB, β-hydroxybutyrate, regulates gene expression and other cellular functions by inducing post-translational modifications. KBs protect tissues by regulating inflammation and oxidative stress. Recently, interest in KBs has been increasing due to their potential for treatment of various diseases such as neurological and cardiovascular diseases and cancer. Cancer cells reprogram their metabolism to maintain rapid cell growth and proliferation. Dysregulation of KB metabolism also plays a role in tumorigenesis in various types of cancer. Targeting metabolic changes through dietary interventions, including fasting and ketogenic diets, has shown beneficial effects in cancer therapy. Here, we review current knowledge of the molecular mechanisms involved in the regulation of KB metabolism and cellular signaling functions, and the therapeutic potential of KBs and ketogenic diets in cancer

Endoplasmic reticulum stress induces hepatic steatosis via increased expression of the hepatic very low-density lipoprotein receptor

Recent evidence suggests that obese animals exhibit increased endoplasmic reticulum (ER) stress in the liver and adipose tissue. Although ER stress is closely associated with lipid homeostasis, it is largely unknown how ER stress contributes to hepatic steatosis. In this study, we demonstrate that the induction of ER stress stimulates hepatic steatosis through increased expression of the hepatic very low-density lipoprotein receptor (VLDLR). Among the unfolded protein response sensors, the protein kinase RNA-like ER kinaseactivating transcription factor 4 signaling pathway was required for hepatic VLDLR up-regulation. In primary hepatocytes, ER stressdependent VLDLR expression induced intracellular triglyceride accumulation in the presence of very low-density lipoprotein. Moreover, ER stressdependent hepatic steatosis was diminished in the livers of VLDLR-deficient and apolipoprotein Edeficient mice compared with wild-type mice. In addition, the VLDLR-deficient mice exhibited decreased hepatic steatosis upon high-fat diet feeding. Conclusion: These data suggest that ER stressdependent expression of hepatic VLDLR leads to hepatic steatosis by increasing lipoprotein delivery to the liver, which might be a novel mechanism explaining ER stressinduced hepatic steatosis. (HEPATOLOGY 2013;57:13661377)N