About

Dr. Jack Odle has spent his career in agri-medical research, exploring nutritional and metabolic interventions to improve the health of domestic animals and humans. He has worked over 30 years to develop and utilize the young pig as a pediatric nutrition and metabolism model. The piglet research model developed in his laboratories is considered the premier model for pediatric pre-clinical research. His basic science research on piglets can apply broadly to all mammalian neonates. Specific elements of his research have investigated the developmental regulation of lipid metabolism and nutritional variables impacting the intestinal health of the neonate. He serves as Editor-in-chief of the journal Current Developments in Nutrition, published by the American Society for Nutrition.

Research topics

• Biology
• Medicine
• Internal medicine
• Microbiology
• Biochemistry
• Immunology
• Cell biology
• Genetics
• Chemistry
• Physiology
• Biotechnology
• Animal science
• Endocrinology

Selected publications

• Establishment of a broiler jejunal organoid model based on optimized activators or optimized two-step media and its assessment

  Poultry Science · 2026-04-13 · 1 citations

  articleOpen access

  Intestinal organoids (IOs), as a novel three-dimensional (3D) in vitro model, have been widely applied for studying intestinal physiology, metabolism and health in human, rodents and farm animals. However, the culture methods for poultry, especially for broiler IOs, need to be improved due to their low differentiation to form complex, self-organized 3D structures and intact barrier functions. This study aimed to establish the broiler jejunal organoid (JO) model by optimizing the culture conditions of JOs and evaluating the cellular components and barrier integrity of JOs via a two-step media [TSM, including both JO growth medium and JO differentiation medium (JODM)]. The results showed that JODM containing 50 or 100 ng/mL of R-spondin 1 and 2.5 μM of Chiron 99021 increased (P < 0.001) the budding percentage of the JOs up to about 80% and maintained their passaging and cryopreservation capabilities. Furthermore, a variety of intestinal functional cells differentiated into JOs as evidenced by the expressions of different marker proteins, and JOs displayed evidence of barrier integrity. Compared with conditioned medium-dependent medium (CMDM) and IntestiCult™ Organoid Growth Medium (IOGM), TSM increased (P < 0.001) the budding percentage of JOs up to about 80%. Moreover, IOGM and TSM up-regulated (P < 0.001) marker genes expression of different intestinal functional cells compared with CMDM, and jejunal crypts sourced from broilers of different ages had no effect (P = 0.792) on the differentiation and budding percentage of JOs. In conclusion, the broiler JOs model established using the TSM-culture protocol developed in this study has the advantages of high differentiation, enriched budding structures and stable passaging and cryopreservation, providing a superior experimental model for studying the physiological responses of the broiler intestine to nutrients, feed additives, pathogens, drugs and their mechanisms.

  PublisherDOI

• The Involvement of the PI3K/AKT Pathway in Zn Alleviation of Heat Stress-Induced Damage to Broiler Jejunal Organoids

  Animals · 2026-05-13

  articleOpen access

  The direct involvement of the phosphatidylinositol 3-kinase (PI3K)/serine threonine kinase (AKT) signaling pathway in the alleviation of the heat stress (HS)-induced damage to the integrity and barrier function of broiler jejunal organoids (JOs) by supplemental zinc (Zn) has not been confirmed. To verify it, two experiments were conducted in the present study. In experiment 1, the optimal concentrations of PI3K/AKT inhibitor (PI3K-IN-1) or agonist (YS-49) were screened. In experiment 2, the role of PI3K/AKT in Zn alleviation of HS-induced damage to JOs was evaluated with three JO types as control groups under baseline incubation temperature (40 °C) plus a 3 (JOs types) × 3 (Zn sources) factorial design under high temperature (44 °C). The results showed that the optimal concentrations of the PI3K-IN-1 and YS-49 for effectively inhibiting and promoting (p &lt; 0.001) phosphorylation of PI3K and AKT were 16 μmol/L and 9 μmol/L, respectively. Adding Zn, especially Zn proteinate with moderate chelation strength (Zn-Prot M), alleviated (p &lt; 0.001) the HS-induced increases in diamine oxidase content and lactate dehydrogenase activity in the media and the HS-induced decreases in JOs budding percentage, proportions of 5-ethynyl-2′-deoxyuridine and proliferating cell nuclear antigen positive cells, and the phosphorylation of PI3K and AKT. PI3K/AKT inhibition or activation reduced or enhanced (p &lt; 0.05) the above alleviating effect of Zn, especially Zn-Prot M. These results indicate that the PI3K/AKT signaling pathway mediated the alleviation of HS-induced damage to integrity and barrier function of broiler JOs by supplemental Zn, particularly Zn-Prot M via promotion of cell proliferation.

  PublisherDOI

• Single-cell transcriptomics predict novel potential regulators of acute epithelial restitution in the ischemia-injured intestine

  UNC Libraries · 2026-05-06

  articleOpen access

  Intestinal ischemic injury damages the epithelial barrier predisposes patients to life-threatening sepsis unless that barrier is rapidly restored. There is an age-dependency of intestinal recovery in that neonates are the most susceptible to succumb to disease of the intestinal barrier versus older patients. We have developed a pig model that demonstrates age-dependent failure of intestinal barrier restitution in neonatal pigs which can be rescued by the direct application of juvenile pig mucosal tissue, but the mechanisms of rescue remain undefined. We hypothesized that by identifying a subpopulation of restituting enterocytes by their expression of cell migration transcriptional pathways, we can then predict novel upstream regulators of age-dependent restitution response programs. Superficial mucosal epithelial cells from recovering ischemic jejunum of juvenile pigs underwent single cell transcriptomics and predicted upstream regulator CSF-1 was interrogated in our model. A subcluster of absorptive enterocytes expressed several cell migration pathways key to restitution. Differentially expressed genes in this subcluster predicted their upstream regulation by colony stimulating factor-1 (CSF-1). We validated age-dependent induction of <em>CSF-1</em> by ischemia and documented that CSF-1 and CSF1R co-localized in ischemic juvenile, but not neonatal, wound-adjacent epithelial cells and in the restituted epithelium of juveniles and rescued neonates. Further, the CSF-1 blockade reduced restitution <em>in vitro</em>, and CSF-1 improved barrier function in injured neonatal pig in preliminary <em>ex vivo</em> experiments. These studies validate an approach to inform potential novel therapeutic targets, such as CSF-1, to improve outcomes in neonates with intestinal injury in a unique pig model.

  PublisherDOI

• 122. Hormone-responsive Porcine Endometrial Epithelial Organoids: Establishment, Validation, and Transcriptomic Characterization

  Journal of Animal Science · 2026-04-01

  articleOpen access

  Abstract The endometrium, composed of luminal and glandular epithelial cells (EECs) and stromal cells (ESCs), plays a central role in integrating maternal hormonal signals and conceptus-derived cues to establish and sustain pregnancy in mammals. While endometrial epithelial organoids (EEOs) have advanced mechanistic studies in humans and mice. a comparable model in pigs has been lacking, limiting opportunities to investigate peri-implantation events in this agriculturally and biomedically relevant species. Here, we report the first establishment of porcine endometrial epithelial organoids (pEEOs) from postnatal day-10 uteri. Epithelial sheets were isolated, dissociated, embedded in growth factor-reduced Matrigel, and maintained in stem cell-supportive medium. The pEEOs demonstrated long-term viability ( &amp;gt; 10 passages) and maintained epithelial identity, confirmed by cytokeratin 8 expression and lack of mesenchymal contamination (vimentin-negative). Importantly, pEEOs displayed robust hormone responsiveness: estradiol (E2) alone or in combination with progesterone analog plus cAMP (EPC treatment) significantly induced expression of steroid-responsive genes critical for endometrial receptivity (PGR, HSD17B2, OLFM4, ESR2, SPP1; P &amp;lt; 0.05). Bulk RNA-seq analysis revealed that EPC-treated pEEOs exhibited a distinct transcriptomic landscape, with 1,078 genes upregulated and 1,257 genes downregulated relative to vehicle controls. Gene ontology enrichment highlighted pathways central to early pregnancy establishment, including transmembrane transport, cilium assembly, lipid transport, and regulation of cell communication and receptor signaling pathway (FDR &amp;lt; 0.05). Notably, transcriptomic profiles of hormone-treated pEEOs showed strong similarity to in vivo uterine luminal epithelial transcriptomes during early pregnancy, demonstrating their physiological relevance. Collectively, this work provides the first validated porcine endometrial epithelial organoid system, offering a powerful new platform for investigating endometrial biology conceptus-uterus interactions, and mechanisms regulating early pregnancy in pigs. This model holds broad potential for advancing both reproductive biology research and the improvement of swine reproductive efficiency.

  PublisherOA PDFDOI

• PSI-22 Effects of modifying PPAR activity on carnitine uptake in swine mammary organoids.

  Journal of Animal Science · 2025-10-01

  articleOpen access

  Abstract Carnitine is essential in growth and development of newborn pigs due to its role in energy production and detoxification via removing acyl-residues. The primary source of carnitine after birth is sow’s milk because newborn pigs have a limited capacity to synthesize carnitine. The carnitine concentration in sow milk varies with dietary carnitine and lactation stage in which the expression of mammary organic cation transporter (OCTN) may play a decisive role as the mediator of carnitine homeostasis. Regulation of peroxisome proliferator–activated receptor (PPAR) influences expression of genes associated with carnitine synthesis and OCTN activity in liver, kidney and enterocyte, but the regulatory role in mammary tissue is not clear especially as lactation leads to down-regulation of PPARα. In this study, the effects of altering PPARα and PPARγ expression on carnitine uptake was examined in vitro in organoids cultured from mammary tissue of pregnant sows. The organoids were incubated with PPARα agonist clofibrate (10 µM), PPARγ agonist thiazolidinedione (TDZ, 10 µM) and antagonist GW9662 (5 µM) in a 3-dimentional environment. The expression of genes PPARα and PPARγ, and genes associated with carnitine uptake OCTN1 (SLC22A4) and OCTN2 (SLC22A5), and genes associated with fatty acid oxidation, carnitine palmitoyltransferase (CPTIα), CPTIβ and acyl-CoA oxidase (ACOX) were determined after 48 hours using RT-PCR. Carnitine uptake rate was measured by adding 16 μM of 3H-labeled carnitine (1µCi/µmol) to cultures for 30 minutes. Clofibrate stimulated expression of PPARα, SLC22A4, SLC22A5 and CPTIβ (p &amp;lt; 0.05) with no significant changes in PPARγ, CPTIα and ACOX (p &amp;gt; 0.1). However, the stimulation did not change carnitine uptake. TDZ had no impact on the expression of all examined genes but GW-9662 significantly increased CPTIα expression by 4-fold. Consistent with CPTIα expression, carnitine transfer rate increased by 70%. Correlation analysis between the gene expression and carnitine uptake rate indicated that the elevation of carnitine uptake was correlated with CPTIα expression (p &amp;lt; 0.005, Corr=0.97) or the ratio of CPTIα/CPTIβ, (p &amp;lt; 0.005, Corr=0.99). We conclude that up-regulation of PPARα expression increases expression of genes associated with mammary carnitine transporters and fatty acid oxidation, but carnitine uptake is subject to the metabolic status of mammary tissue. Supported by Animal Health and Production and Animal Products (grant no. 2023-67015-39663/1030033) from the USDA National Institute of Food and Agriculture, and by the North Carolina Agricultural Research Hatch projects 1016618 and 02780. Keyword: carnitine, mammary, organoids

  PublisherOA PDFDOI

• Effects of Maternal Clofibrate Supplementation During Gestation and Lactation on Intestinal Fatty Acid Oxidation of Suckling Piglets

  Preprints.org · 2025-06-26 · 1 citations

  preprintOpen accessSenior author

  To accelerate maturation of intestinal function and promote growth and development, the effect of maternal clofibrate on intestinal fatty acid metabolism was investigated in postnatal piglets. 27 pregnant sows were fed either 0, 0.25, or 0.5% clofibrate during late gestation and early lactation. [1-14C]-Oleic acid metabolism was measured in vitro in intestinal mucosa of piglets with/without L-carnitine and/or malonate. Clofibrate increased oleic acid metabolism on d1, and the increase was higher from 0.5 than 0.25% of maternal clofibrate (p &amp;amp;lt; 0.005). Flux to CO2 increased with age while flux to acid soluble products (ASP) remained constant after d1. Flux to esterified products (ESP) increased on d7, but the increase was dampened by clofibrate (p &amp;amp;lt; 0.0001). Carnitine increased flux to CO2 and malonate decreased it (p &amp;amp;lt; 0.0001), but neither affected ASP or ESP. Intestinal NEFA and TG levels decreased linearly, and CPT activity increased quadratically with age. Clofibrate increased ACOX abundance but decreased the ratio of CPT1A and CPT1B on d1. Postnatal age increased FABP2 but decreased PPARα and RXRα. In conclusion, maternal supplementation of clofibrate promotes intestinal energy generation from fat oxidation in postnatal piglets, but the promotion is influenced by age, in which ACOX, FABP2 and CPT1 might play modulatory roles.

  PublisherOA PDFDOI

• Evaluation of Carnitine Status in Postnatal Piglets from Sows Fed Clofibrate

  Current Issues in Molecular Biology · 2025-11-29

  articleOpen access

  Milk carnitine content decreases quickly with lactation days and is accompanied by PPARα downregulation. This study aimed to investigate the effects of the maternal supplementation of the PPARα agonist, clofibrate, on milk carnitine content and carnitine status in neonates during lactation. Pregnant sows (n = 27) were fed diets containing either 0, 0.25, or 0.5% clofibrate from d107 gestation to d7 of lactation. Carnitines were determined in milk on d1, 3, 5, 7, 10, 14, and 19 post farrowing and in the plasma, intestine, and liver of piglets on d1, 7, 14, and 19. Milk carnitine decreased quadratically with lactation days (p &lt; 0.0001). Hepatic and intestinal carnitines increased with postnatal age (p &lt; 0.05). Correlations between levels were detected between milk and plasma (R2 = 0.5, p &lt; 0.0001) and milk and intestine (R2 = 0.23; p &lt; 0.05). Clofibrate increased BBH expression (p &lt; 0.05) and tended to increase OCTN2 expression (p = 0.055) in intestine and TMLH in liver (p = 0.059). Hepatic ALD and TMLH increased (p &lt; 0.0005) with postnatal age. However, gene modification had no effect on plasma and mucosa carnitine concentrations. We conclude that changes in carnitines within plasma and mucosa are mostly driven by milk carnitines during postnatal development.

  PublisherDOI

• Dietary Zn proteinate alleviates heat stress-induced intestinal integrity disruption possibly by promoting cell proliferation via related signaling pathways in the jejunum of broilers

  Journal of Integrative Agriculture · 2025-05-01 · 4 citations

  articleOpen access

  Heat stress (HS) can induce the disruption of small intestinal integrity in broilers. Here we examined the efficacies and possible mechanisms of zinc proteinate with moderate chelation strength (Zn-Prot M) compared to ZnSO 4 .7H 2 O (ZnSO 4 ) in alleviating HS-induced disruption of small intestinal integrity in broilers. The experiment included 7 treatments. Twenty two-d-old birds were randomly allotted into 1 of 5 treatments under high temperature (HT, 9:00-17:00: 34±1°C, 8 h d -1 ; 17:00–9:00: 28±1°C) with 1 control (HT-CON) plus 2 [dietary Zn sources, Zn-Prot M and ZnSO 4 ] × 2 [added Zn levels, 30 and 60 mg kg -1 ] factorial arrangement, and 1 of 2 treatments under normal temperature (NT) with the control (NT-CON) and pair-feeding matched to HT-CON (NT-PF). The results showed that HS dramatically reduced ( P <0.05) small intestinal villus height (VH), VH/crypt depth (CD) and villus surface area (VSA), the amount of proliferating cell nuclear antigen (PCNA) positive cells, mRNA or protein expression levels of phosphatidylinositol 3-kinase (PI3K), serine threonine kinase (AKT), extracellular regulated protein kinase (ERK), protein kinase C (PKC), G protein-coupled receptor 39 (GPR39), phosphorylated PI3K (p-PI3K)/PI3K, p-AKT/AKT, p-ERK/ERK and phospholipase C (PLC) β1/2, and PLC activity. HS also remarkably increased ( P <0.05) small intestinal CD and mRNA or protein levels of P38 mitogen activated protein kinase (P38 MAPK), C-jun N-terminal kinase (JNK)1/2 and p-JNK/JNK in the jejunum of heat stressed (HS) broilers. However, dietary supplementation with Zn, especially organic Zn as Zn-Prot M at 60 mg kg -1 , significantly increased ( P <0.05) small intestinal VH, VH/CD and VSA, as well as the amount of PCNA positive cells, PLC activity, mRNA expression levels of PI3K , AKT , GPR39 and PLC β1 , protein expression levels of p-PI3K/PI3K, p-AKT/AKT, p-ERK/ERK, GPR39 and PLC β1, and decreased ( P <0.05) small intestinal CD, JNK2 mRNA expression level and p-JNK/JNK protein expression level in the jejunum of HS broilers. These results suggest that dietary supplemental Zn, especially 60 mg Zn kg -1 as Zn-Prot M, can effectively alleviate HS-induced small intestinal injury possibly by promoting cellular proliferation via the GPR39/PLC β1-mediated PI3K/AKT or MAPK pathways in the jejunum of HS broilers.

  PublisherDOI

• 207. Effects of intestinal carnitine transporter expression on carnitine status and fatty acid oxidation in suckling piglets

  Animal - science proceedings · 2025-08-01

  article
  PublisherDOI

• Single-cell transcriptomics predict novel potential regulators of acute epithelial restitution in the ischemia-injured intestine

  American Journal of Physiology-Gastrointestinal and Liver Physiology · 2025-01-24

  articleOpen access

  These studies validate an approach to identify and predict upstream regulation of restituting epithelium in a unique pig intestinal ischemic injury model. Identification of potential molecular mediators of restitution, such as CSF-1, will inform the development of targeted therapeutic interventions for the medical management of patients with ischemia-mediated intestinal injury.

  PublisherOA PDFDOI

Recent grants

• Post-natal development of enteric glial cell-epithelial interactions in repair of ischemic-injured intestine

  NIH · $1.8M · 2019–2025

Frequent coauthors

• Xi Lin

  108 shared

• Sheila K. Jacobi

  The Ohio State University

  40 shared

• Anthony T. Blikslager

  North Carolina State University

  35 shared

• R. T. Zijlstra

  University of Alberta

  25 shared

• R. J. Harrell

  Institute for Bioscience and Biotechnology Research

  23 shared

• Amanda L. Ziegler

  North Carolina State University

  23 shared

• Yongwen Zhu

  South China Agricultural University

  21 shared

• Sharon M. Donovan

  University of Illinois Urbana-Champaign

  20 shared

Education

• PhD, Nutrition

  University of Wisconsin Madison

  1989

• MS, Meat and Animal Science

  University of Wisconsin Madison

  1985

• BS, Animal Science

  Purdue University

  1982

Awards & honors

• William Neal Reynolds Distinguished Professor