A5024864404- Digestive system and related health
- Diet and metabolism studies
- Helicobacter pylori-related gastroenterology studies
- Gastrointestinal motility and disorders
- Diet, Metabolism, and Disease
- MicroRNA in disease regulation
- Dietary Effects on Health
- Cholesterol and Lipid Metabolism
- Peptidase Inhibition and Analysis
- Reproductive System and Pregnancy
- Galectins and Cancer Biology
- Kruppel-like factors research
- Nutrition and Health in Aging
- Genetic factors in colorectal cancer
- Gut microbiota and health
- Tissue Engineering and Regenerative Medicine
- Cannabis and Cannabinoid Research
- Infant Nutrition and Health
- Pancreatic function and diabetes
- Biochemical Analysis and Sensing Techniques
- Microbial Inactivation Methods
- Pancreatic and Hepatic Oncology Research
- Regulation of Appetite and Obesity
- COVID-19 Clinical Research Studies
- Gastrointestinal Tumor Research and Treatment
University of Nevada, Reno
2019-2024
Massachusetts General Hospital
2023-2024
Abstract Background/Aim Diabetes has substantive co‐occurrence with disorders of gut‐brain interactions (DGBIs). The pathophysiological and molecular mechanisms linking diabetes DGBIs are unclear. MicroRNAs (miRNAs) key regulators gut dysmotility. We investigated whether impaired barrier function is regulated by a miRNA, miR‐10b‐5p, Methods created new mouse line using the Mb3Cas12a/Mb3Cpf1 endonuclease to delete mir‐10b globally. Loss studies in knockout (KO) mice were conducted...
Gender and biological sex have distinct impacts on the pathogenesis of type 2 diabetes (T2D). Estrogen deficiency is known to predispose female mice T2D. In our previous study, we found that high-fat, high-sucrose diet (HFHSD) induces T2D in male through miR-10b-5p/KLF11/KIT pathway, but not females, highlighting hormonal disparities susceptibility. However, underlying molecular mechanisms this protection females remain elusive. To address knowledge gap, utilized ovariectomized,...
Gender and biological sex have distinct impacts on the pathogenesis of type 2 diabetes (T2D). Estrogen deficiency is known to predispose female mice T2D. In our previous study, we found that a high-fat, high-sucrose diet (HFHSD) induces T2D in male through miR-10b-5p/KLF11/KIT pathway, but not females, highlighting hormonal disparities susceptibility. However, underlying molecular mechanisms this protection females remain elusive. To address knowledge gap, utilized ovariectomized,...
Transcriptome data on the quantitative numbers of transcriptional variants expressed in primary cells offer essential clues into specific cellular functions and biological processes. We have previously collected transcriptomes from smooth muscle (SMC), interstitial Cajal (ICC), PDGFRα+ (fibroblast-like cells) isolated murine jejunal colonic and/or mucosal tissues as well associated (jejunal muscle, mucosa). In this study, we built Smooth Muscle Browser (SMTB),...
Metalloendopeptidase ADAM-Like Decysin 1 (ADAMDEC1) is an anti-inflammatory peptidase that almost exclusively expressed in the gastrointestinal (GI) tract. We have recently found abundant and selective expression of Adamdec1 colonic mucosal PDGFRα+ cells. However, cellular origin for this gene controversial as it also known to be intestinal macrophages. mRNAs were selectively subepithelial ADAMDEC1 protein was mainly released from cells accumulated layer lamina propria space near epithelial...
Subepithelial platelet-derived growth factor receptor alpha (PDGFRα) + cells found in the colonic mucosal tissue come close contact with epithelial cells, immune neurons, capillaries, and lymphatic networks. Mucosal subepithelial PDGFRα (MuPαC) are important regulators various intestinal diseases including fibrosis inflammation. However, transcriptome of MuPαC has not yet been elucidated. Using Pdgfra-eGFP mice flow cytometry, we isolated obtained their data. In analyzing transcriptome,...
Abstract Citrin Deficiency (CD) is caused by inactivation of SLC25A13, a mitochondrial membrane protein required to move electrons from cytosolic NADH the matrix in hepatocytes. People with CD do not like sweets. We discovered that SLC25A13 loss causes accumulation glycerol-3-phosphate (G3P), which activates carbohydrate response element binding (ChREBP) transcribe FGF21, acts brain restrain intake sweets and alcohol, key genes de novo lipogenesis. Mouse human data establish G3P-ChREBP as...