Acute pancreatitis in intraductal papillary mucinous neoplasm: a single-center retrospective cohort study with systematic review and meta-analysis.

Background: Intraductal papillary mucinous neoplasm (IPMN) is a cystic tumor of the pancreas arising from abnormal papillary proliferation of ductal epithelial cells, and is a precancerous lesion of pancreatic malignancy. This study aimed to evaluate associations between acute pancreatitis (AP) and histologic subtypes of IPMN.

Methods: In the clinical study, patients with IPMN confirmed by surgical resection specimens at our institute between 2009 and 2021 were eligible for inclusion.

Correlation between High Incidence of Colorectal Neoplastic Polyps and High-risk Adenomas in Patients with Diabetes Mellitus: A Retrospective Study.

Background: Early detection and resection of colorectal polyps by routine colonoscopy screening can be effective in reducing the risk of colorectal cancer (CRC).

Objective: This study aimed to determine the association between diabetes mellitus (DM) and different types of colorectal polyps in the Chinese population.

Methods: A retrospective analysis was performed on inpatients admitted to the Gastroenterology Department of our hospital from January to December 2019.

Effects of hemicellulose on intestinal mucosal barrier integrity, gut microbiota, and metabolomics in a mouse model of type 2 diabetes mellitus.

Background And Objective: Impaired gut barrier contributes to the progression of type 2 diabetes mellitus (T2DM), and the gut microbiota and metabolome play an important role in it. Hemicellulose, a potential prebiotics, how its supplementation impacted the glucose level, the impaired gut barrier, and the gut microbiota and metabolome in T2DM remained unclear.

Methods: In this study, some mice were arranged randomly into four groups: db/db mice fed by a compositionally defined diet (CDD), db/db mice fed by a CDD with 10% and 20% hemicellulose supplementation, and control mice fed by a CDD.

LncRNA DICER1-AS1 promotes colorectal cancer progression by activating the MAPK/ERK signaling pathway through sponging miR-650.

Background: Colorectal cancer (CRC) is a disease with high morbidity and mortality rates globally. Long noncoding RNAs (lncRNAs) play a fundamental role in tumor progression, and increasing attention has been paid to their role in CRC. This study aimed to determine the function of lncRNA DICER1 antisense RNA 1 (DICER1-AS1) in CRC and confirm its potential regulatory mechanisms in CRC.

Pancreatic-Like Cells Derived From Mouse Embryonic Stem Cells Are Regulated by Pdx1 Involving the Notch Pathway.

Objectives: Embryonic stem cells (ESCs)-derived pancreatic precursor cells have great potential for pancreas repair. Expression of pancreatic duodenal homeobox 1 (Pdx1) in definitive endoderm (DE) cells is the premise that DE cells differentiate into pancreatic cells. To achieve the required number of Pdx1-expressing DE cells for cell transplantation therapy, a valid model must be established.

Impaired intestinal barrier function in type 2 diabetic patients measured by serum LPS, Zonulin, and IFABP.

Introduction: The epithelial tight junctions of intestine were impaired in murine model of type 2 diabetes mellitus (T2DM). The aim of this work was to investigate the alteration of intestinal barrier in T2DM patients.

Methods: 90 patients with T2DM and 28 healthy controls were recruited.

m6A methyltransferase METTL3 maintains colon cancer tumorigenicity by suppressing SOCS2 to promote cell proliferation.

N6‑methyladenosine (m6A) RNA modification maintained by N6‑methyltransferases and demethylases is involved in multiple biological functions. Methyltransferase like 3 (METTL3) is a major N6‑methyltransferase. However, the role of METTL3 and its installed m6A modification in colorectal tumorigenesis remains to be fully elucidated.

Effects of berberine and metformin on intestinal inflammation and gut microbiome composition in db/db mice.

Berberine and metformin, both established pharmaceutical agents with herbal origins, have incidental beneficial effects on multiple diseases, including diabetes. These effects have been speculated to occur via the gut microbiome. In this study, we administered either berberine or metformin to db/db mice and investigated changes in body weight, food intake, and blood glucose levels.

Faecalibacterium prausnitzii-derived microbial anti-inflammatory molecule regulates intestinal integrity in diabetes mellitus mice via modulating tight junction protein expression.

Background: Impaired intestinal barrier structure and function have been validated as an important pathogenic process in type 2 diabetes mellitus (T2DM). Gut dysbiosis is thought to be the critical factor in diabetic intestinal pathogenesis. As the most abundant commensal bacteria, Faecalibacterium prausnitzii (F.

Musashi 1-positive cells derived from mouse embryonic stem cells treated with LY294002 are prone to differentiate into intestinal epithelial-like tissues.

The majority of Musashi 1 (Msi1)‑positive cells derived from mouse embryonic stem cells (mESCs) are prone to differentiate into neural epithelial‑like cells, and only a small proportion of Msi1‑positive cells differentiate into intestinal epithelial‑like cells. Whether inhibiting the phosphatidylinositol 3‑kinase (PI3K) signaling of mESCs can promote the differentiation of Msi1‑positive cells into intestinal epithelial‑like cells remains to be fully elucidated. In the present study, to inhibit PI3K signaling, mESCs were treated with LY294002.

Butyrate suppresses abnormal proliferation in colonic epithelial cells under diabetic state by targeting HMGB1.

Butyrate is widely accepted as a proliferation inhibitor in colon cancer but less thoroughly characterized in the colonic epithelium of objects with type 2 diabetes mellitus. The present study investigated the regulatory effect of butyrate on proliferation, the related molecule high-mobility group box 1 (HMGB1) and the receptor for advanced glycation end products (RAGE) in the colon of db/db type 2 diabetic model mice and non-cancerous NCM460 colon cells. Proliferation and the expression of HMGB1 and RAGE were increased and could be partially reversed by butyrate treatment in the colon of db/db mice, which were consistent in NCM460 cells under a high glucose state.

Butyrate ameliorated-NLRC3 protects the intestinal barrier in a GPR43-dependent manner.

Background: Intestinal barrier dysfunctions are related to dysbacteriosis and chronic gut inflammation in type 2 diabetes. Although there is emerging evidence that the chronic gut inflammatory response is stimulated by nucleotide-binding oligomerization domain-like receptors (NLRs), the relationship and precise mechanism between NLRC3 and the colonic epithelial barrier remains largely elusive.

Methods: We investigated the function and mechanism of NLRC3 in the colonic tissues of diabetic mice and colonic epithelial cell lines.

Infection Is Associated with Type 2 Diabetes, Not Type 1 Diabetes: An Updated Meta-Analysis.

Background: Extragastric manifestations of () infection have been reported in many diseases. However, there are still controversies about whether infection is associated with diabetes mellitus (DM). This study was aimed at answering the question.

Certain Dietary Habits Contribute to the Functional Dyspepsia in South China Rural Area.

BACKGROUND Functional dyspepsia (FD) refers to a group of upper gastrointestinal syndromes, subdivided into two types: postprandial distress syndrome (PDS) and epigastric pain syndrome (EPS). The etiology of FD remains unclear; however, unhealthy dietary habit is one potential underlying cause. We aim to explore the association of poor dietary habits with FD and its subtypes.

Wip1 gene silencing enhances the chemosensitivity of human colon cancer cells.

Colon cancer is one of the most common cancers in the world. Multidrug resistance is one of the main reasons for failure of therapy in patients with advanced colon cancer. In previous studies, multiple methods were investigated to reverse the multidrug resistance of colon cancer cells.

Epigenetic modification of TLE1 induce abnormal differentiation in diabetic mice intestinal epithelium.

The intestinal epithelium cells (IECs) in diabetes mellitus (DM) patients have been proven to be abnormally differentiated. During the differentiation of IECs, epigenetic modification acts as an important regulator. In this study, we aimed to examine the epigenetic alteration of Transducin-like Enhancer of Split 1 (TLE1), a multitask transcriptional co-repressor, contributing to the differentiation homeostasis in IECs of DM mice.

Sox9 transcriptionally regulates Wnt signaling in intestinal epithelial stem cells in hypomethylated crypts in the diabetic state.

Background: Distinctive structures called crypts harbor intestinal epithelial stem cells (IESCs) which generate progenitor and terminally differentiated cells in the intestinal epithelium. Mammalian IESCs and their daughter cells require the participation of DNA methylation and the transcription factor Sox9 for proliferation and differentiation. However, the association between Sox9 and DNA methylation in this process remains elusive.

Overexpression of miR-429 impairs intestinal barrier function in diabetic mice by down-regulating occludin expression.

Diabetes mellitus (DM) is a group of metabolic diseases characterised by insulin deficiency/resistance and hyperglycaemia. We previously reported the presence of an impaired tight junction and decreased expression of occludin (Ocln) and zonula occludens-1 (ZO-1) in the intestinal epithelial cells (IECs) of type 1 DM mice, but the exact mechanism remains unclear. In this study, we investigated the role of microRNAs (miRNAs) in impairing the tight junction in IECs of DM mice.

Association of Bactericidal Dysfunction of Paneth Cells in Streptozocin-Induced Diabetic Mice with Insulin Deficiency.

BACKGROUND Type 1 diabetes mellitus (T1DM) is associated with increased risks of enteric infection. Paneth cells constitute the first line of the gut defense. Little is known about the impact of T1DM on the bactericidal function of intestinal Paneth cells.

Transgelin increases metastatic potential of colorectal cancer cells in vivo and alters expression of genes involved in cell motility.

Background: Transgelin is an actin-binding protein that promotes motility in normal cells. Although the role of transgelin in cancer is controversial, a number of studies have shown that elevated levels correlate with aggressive tumor behavior, advanced stage, and poor prognosis. Here we sought to determine the role of transgelin more directly by determining whether experimental manipulation of transgelin levels in colorectal cancer (CRC) cells led to changes in metastatic potential in vivo.

miRNA-30e regulates abnormal differentiation of small intestinal epithelial cells in diabetic mice by downregulating Dll4 expression.

Objectives: Depression of the Notch/Hes1 pathway has been reported to play a role in abnormal differentiation of intestinal epithelial cells (IECs) in diabetes mellitus (DM). However, the mechanism by which this pathway influences IEC differentiation has remained unclear. In this study, we have investigated the role of microRNAs (miRNAs) in regulating the Notch/Hes1 pathway in IECs of DM mice.

MEK/ERK pathway activation by insulin receptor isoform alteration is associated with the abnormal proliferation and differentiation of intestinal epithelial cells in diabetic mice.

In previous studies, we have reported the abnormal proliferation and differentiation of intestinal epithelial cells (IECs) in diabetes mellitus (DM) mice. The insulin receptor (IR) and its downstream mitogen-activated protein kinase kinase (MAPKK also known as MEK)/extracellular-regulated protein kinase (ERK) pathway is a classic pathway associated with cell proliferation and differentiation. The purpose of the present study is to investigate the role of the MEK/ERK pathway in abnormal proliferation and differentiation of IECs in DM mice.