Joo-hun Oh
Yonsei University · Medicine
About the Lab
Professor Joo-hun Oh's research lab focuses on the molecular mechanisms underlying metabolic regulation, particularly in type 2 diabetes and obesity, with an emphasis on gut-brain axis signaling, intestinal glucose metabolism, and the role of gut hormones such as GLP-1 and PYY. The lab investigates novel therapeutic targets and molecules—including natural compounds like 4-HBA and investigational drugs like BIM23B065—for metabolic and endocrine disorders. Using integrated approaches combining in vivo animal models, in vitro cell systems, organoids, and advanced imaging techniques such as 18F-FDG PET, the lab explores how bariatric surgery and pharmacological agents modulate glucose homeostasis and tissue metabolism. A key focus is on understanding the role of non-olfactory G protein-coupled receptors, such as OR51E1, in metabolic hormone secretion and intestinal function.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
154-Hydroxybenzaldehyde (4-HBA) is a naturally occurring benzaldehyde and the major active constituent of Gastrodia elata. While recent studies have demonstrated metabolic effects of 4-HBA, little is known about the physiological role of 4-HBA in acute wound healing. Here, we investigated the effects and mechanisms of 4-HBA on acute wound healing. Using an in vitro approach, we found that 4-HBA significantly promoted keratinocyte cell migration and invasion by increasing focal adhesion kinase and
Glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), produced by intestinal enteroendocrine L cells, are important gut hormones that coordinate gastrointestinal physiology, metabolism, and appetite. We aimed to investigate the role of olfactory receptor (OR) OR51E1 in GLP-1 and PYY secretion. We analyzed the expression of olfactory marker protein (OMP), an indicator of OR-mediated events in nonolfactory systems, in human intestinal L cells. Furthermore, we analyzed OMP and OR51E1 expression in
Objective The mechanisms underlying type 2 diabetes resolution after Roux-en-Y gastric bypass (RYGB) are unclear. We suspected that glucose excretion may occur in the small bowel based on observations in humans. The aim of this study was to evaluate the mechanisms underlying serum glucose excretion in the small intestine and its contribution to glucose homeostasis after bariatric surgery. Design 2-Deoxy-2-[ 18 F]-fluoro-D-glucose (FDG) was measured in RYGB-operated or sham-operated obese diabeti
The Roux-en-Y gastric bypass (RYGB) is highly effective in the remission of obesity and associated diabetes. The mechanisms underlying obesity and type 2 diabetes mellitus remission after RYGB remain unclear. This study aimed to evaluate the changes in continuous dynamic FDG uptake patterns after RYGB and examine the correlation between glucose metabolism and its transporters in variable endocrine organs using 18 F-fluoro-2-deoxyglucose positron emission tomography images. Increased glucose meta
BACKGROUND: Acromegaly is a rare disease primarily caused by growth hormone (GH)-secreting pituitary adenomas, and its treatment is costly. Moreover, some patients are unresponsive to treatment. Hence, there are increasing efforts to develop new drugs with improved effectiveness for this disease. BIM23B065 is a novel chimeric molecule that acts on both somatostatin and dopamine receptors. This study aimed to investigate the effects of BIM23B065 compared with those of a somatostatin receptor anal
Abstract The olfactory marker protein (OMP), which is also expressed in nonolfactory tissues, plays a role in regulating the kinetics and termination of olfactory transduction. Thus, we hypothesized that OMP may play a similar role in modulating the secretion of hormones involved in Ca 2+ and cAMP signaling, such as glucagon. In the present study, we confirmed nonolfactory α-cell-specific OMP expression in human and mouse pancreatic islets as well as in the murine α-cell line αTC1.9. Glucagon an
Metformin is widely used as a first-line therapy for type 2 diabetes mellitus. However, the molecular mechanisms by which it modulates intestinal glucose metabolism remain incompletely defined. Here metformin was orally administered to male C57BL/6 mice, followed by intraperitoneal glucose tolerance testing and fluorine-18 fluorodeoxyglucose tracing to evaluate glucose homeostasis. To investigate changes in intestinal glucose metabolism, IEC6 and Caco-2 cell lines were used for in vitro analysis
Pituitary adenoma-induced excess endocrine growth hormone (GH) secretion can lead to breast cancer development and metastasis. Herein, we used an acromegaly mouse model to investigate the role of excess endocrine GH on triple-negative breast cancer (TNBC) growth and metastasis. Additionally, we aimed to elucidate the molecular mechanism of transcription factor 20 (TCF20)/nuclear factor erythroid 2-related factor 2 (NRF2) signaling-mediated aggressiveness and metastasis of TNBC. Excess endocrine
Obesity causes chronic diseases such as diabetes, hyperlipidemia, and stroke, which increase the mortality rate. Among the various studies on obesity, the role of the olfactory system to regulate energy homeostasis has been recently studied. Olfactory marker protein (OMP) is a cytoplasmic protein expressed primarily in mature chemosensory neurons in the main olfactory epithelium and involved in the olfactory receptor (OR)-mediated signal transduction cascade with olfactory canonical signaling co
Olfactory marker protein (OMP) regulates olfactory transduction and is also expressed in adipose tissue. Since it serves as a regulatory buffer for cyclic AMP (cAMP) levels, we hypothesized that it plays a role in modulating adipocyte differentiation. To determine the role of OMP in adipogenesis, we examined the differences in body weight, adipose tissue mass, and adipogenic or thermogenic gene expression between high-fat diet-fed control and Omp-knockout (KO) mice. cAMP production, adipogenic g
Abstract Disclosure: J. Nam: None. C. Kang: None. J. Oh: None. E. Wang: None. S. Lee: None. J. Hong: None. E. Lee: None. C. Ku: None. Object: Although the effect of metformin is widely known, little research has been performed on clinical significance and potential mechanism of increased intestinal glucose uptake which is commonly found in [18F]-fluoro-D-glucose (FDG) positron emission tomography. The aim of this study is to assess the altered glucose metabolism in the combined colon and termina
Objective We aimed to compare the molecular mechanisms and metabolic outcomes of Roux‐en‐Y gastric bypass (RYGB) and single anastomosis duodeno–ileal bypass with sleeve gastrectomy (SADI‐S) using a preclinical model. Methods Otsuka Long‐Evans Tokushima Fatty rats with diet‐induced obesity underwent RYGB, SADI‐S, or sham surgery. Metabolic parameters, including glucose tolerance, body weight, and 18F‐fluorodeoxyglucose biodistribution, were assessed at 1‐ and 2‐month postsurgery. The expression o
Abstract Disclosure: C. Kang: None. J. Oh: None. E. Wang: None. S. Lee: None. J. Nam: None. J. Hong: None. E. Lee: None. C. Ku: None. Background: Rosiglitazone, a synthetic peroxisome proliferator-activated receptor γ (PPAR γ) ligand, are used to treat type II diabetes. Over the last few years, PPAR γ has received much attention for its ability to exert variable tumors. Objective: The aim of this study is to investigate the anti-tumor effect of rosiglitazone on prolactin secreting pituitary aden
Intestinal glucose excretion, defined as increased intestinal serum glucose uptake and secretion into the lumen, influences bariatric surgery-associated glycaemic control. Here, we investigate molecular mechanisms that activate intestinal glucose excretion. We evaluate altered transcriptomes in variable intestinal glucose excretion models and big data-based drug discovery systems. We show that protein kinase C (PKC) activation mimics transcriptome alterations observed during intestinal glucose e
Research Areas
Dive deeper into Joo-hun Oh's research on Nubint
Open this lab's papers in the app to read with AI, summarize, and cite in your writing.