bluuebunny/crossref_metadata_2025 huggingface dataset:
Test‐retest reliability of questions assessing physical activity levels among low‐income women
Authors: Li Cheng , Palmer‐Keenan Debra
Published: June 2021

Self‐reported surveys are used to assess dietary and physical activity (PA) behavior changes among low‐income Expanded Food and Nutrition Education Program (EFNEP) adult participants. A multi‐state research project (NC2169) has been established to create a new EFNEP survey that is consistent with America's most recent dietary and physical activity guidelines. The aim of this portion of the project's work was to examine the test‐retest reliability for the survey's PA questions, for which face validity had previously been verified via cognitive interviews. Due to pragmatic concerns (i.e. literacy levels, participant burden and time constraints), questions used for EFNEP evaluation need to be relatively quick and easy to complete. Thus, a single item was used to address each of three PA concepts: Item 1: moderate to vigorous aerobic PA; Item 2: muscle strengthening/resistance training; and Item 3: bodily exertion to intentionally develop and maintain fitness via everyday activities (e.g., taking the stairs instead of the elevator, parking far from a destination to walk more, etc.). Items 1 and 2 were measured on a 7‐point scale, (“0” to “7” days); Item 3 was assessed using a 5‐point Likert‐type scale (“Never” to “Always”). Sixty‐eight low‐income women from Colorado, New Jersey, and Nevada were asked to respond to the questions on two separate occasions, 7–10 days apart. Care was taken to administer questions during periods for which consistent weather patterns had been predicted, as inconsistent weather has been correlated with changes in individuals' activity patterns. Spearman's correlation coefficient, intra‐class correlation coefficient (ICC) and paired t‐test were used to examine test‐retest reliability using SAS (version 9.3). Demographic information was also collected, and analyzed using descriptive statistics (frequencies, means and standard deviations). Of the 68 participant recruited, 64 completed both the test and retest; most were Black (56.3%), had a high school degree or lower (51.5%), and received SNAP benefit (68.0%). Neither test nor retest responses differed significantly by age, race or education levels. Spearman correlation coefficients ranged from 0.60 (Item 3) to 0.88 (Item 2), suggesting a “strong” (0.60–0.79) to “very strong” (0.80–1.00) correlation between the test and retest responses. ICC for Items 1–3 were 0.71, 0.77, 0.64, respectively, which also indicated “good” reliability (ICC= 0.61 to 0.80). Paired t‐tests showed no significant differences between test and retest responses, which, in the absence of external influences, reflected their reliability. In conclusion, these PA questions demonstrated satisfactory test‐retest reliability for assessing low‐income women's physical activity levels. Research to examine the questions' validity remains necessary.

Support or Funding Information

Funding resource: United States Department of Agriculture, New Jersey Agricultural Experiment Station Grant Number: NJ 14211; (Multi‐State Project NC‐2169)
The Impact of a Western Diet on Ossabaw Pig Tissue Transcriptome and Intestinal Microbiome Composition
Authors: Solano‐Aguilar Gloria I , Lakshman Sukla , Molokin Aleksey , Jang Saebyeol , Beshah Ethiopia , Xie Yue , Urban Joseph F , Vinyard Bryan , Escalante Mariana , Walker Maura , Goldbaum Audrey , Meng Huicui , Lamon‐Fava Stefania , Lichtenstein Alice , Matthan Nirupa
Published: June 2021

To determine the impact of dietary patterns on cardiovascular risk factors, tissue transcriptome and intestinal microbiome, we designed a study to compare the effect of feeding Ossabaw pigs two isocaloric diets with 38% energy from fat designed to represent a 1) “Western diet” rich in saturated fatty acids, refined carbohydrates, low fiber and high cholesterol versus 2) a “Heart Healthy Diet” rich in monounsaturated and polyunsaturated fatty acids, unrefined carbohydrates, fruits/vegetables and fiber with low cholesterol content. Half of the pigs fed each diet were also given atorvastatin (Lipitor®) starting at three months of age. Thirty two pigs were randomly allocated in a 2 × 2 factorial design (n=8/group) and fed for six months a 1) Western diet [WD]; 2) Western Diet+ atorvastatin [WD+ S]; 3) Heart‐Healthy Diet [HHD] and a 4) Heart‐Healthy Diet+ atorvastatin [HHD+S]. Compared to HHD, pigs on the WD had higher plasma total cholesterol (C), LDL‐C, non‐HDL‐C, HDL‐C and triglyceride concentrations(p<0.05), and developed early stage atherosclerotic lesions in the aorta and coronary arteries, with reduced damage in WD groups in the presence of Atorvastatin therapy (p<0.1). No significant differences were observed in inflammatory biomarker tumor necrosis factor (TNFα), liver enzymes, DEXA‐body fat distribution and visceral adipocyte morphometry. Liver transcriptome analysis indicated a reduction in the cholesterol and sterol molecular pathways in liver and a small increase in LDLR gene expression in pigsfed HHD independent of statin intervention, and no change in adipose tissue derived stromal cell transcriptome compared to WD. Analysis of fecal microbiota composition by Illumina16S RNA sequencing indicated a significant five to six‐fold reduction of bacterial taxa abundance within Firmicutes phylum including Lachnospiraceae, Lactobacillaceae, and Ruminococcaceae with a five‐fold increase in taxa within Actinobacteria, and two‐fold within Tenericutes and Proteobacteria in WD‐fed pigs compared to baseline levels. Pigs fed the HHD showed a two‐ to four‐fold reduction in Lachnospiraceae, Lactobacillaceae and Ruminococcaceae with a two‐ to three‐fold increase in Bacteroidales, Aeromonadales and Deferribacterales (P<0.05). Statin treatment only induced a two‐fold increase in Deferribacteraceae in pigs fed HHD+S. This study demonstrated that a Heart Healthy Diet combined with statin therapy may prophylactically reduce clinical expression of diet‐induced cardiovascular disease.

Support or Funding Information

HNRCA Research Cluster Initiative and the U.S. Department of Agriculture, under agreement No. 58‐1950‐4‐401 and USDA‐appropriated CRIS 8040‐51530‐056‐00D
Identification of activation of tryptophan‐NAD+ pathway as a central metabolic response to chemical stress from feeding thermally‐oxidized soybean oil in mouse through metabolomics‐based biochemical analysis
Authors: Wang Lei , Yao Dan , Urriola Pedro , Saqui‐Salces Milena , Shurson Gerald , Chen Chi
Published: June 2021

Consumption of thermally‐oxidized lipids is associated with metabolic disorders and cardiovascular disease. However, the specific metabolic events induced by thermally‐oxidized lipids and their underlying mechanisms are not well defined. In this study, the metabolic responses to consuming thermally‐oxidized vegetable oil were examined through metabolomics‐guided biochemical analysis. The control diet containing 7% (w/w) fresh soybean oil diet (CSO) and the treatment diet containing 7% (w/w) heated soybean oil (HSO) were fed to two groups of C57BL/6 mice for 4 weeks, respectively. Liquid chromatography‐mass spectrometry (LC‐MS)‐based metabolomic analysis indicated that HSO greatly altered the composition of metabolomes in serum, urine, and liver samples. A group of hydroxylalkenoic acids in urine were identified as newly formed metabolites from HSO treatment. HSO altered the lipidome, which was indicated by the increases of phospholipids containing saturated fatty acids and the decrease of phospholipids containing polyunsaturated fatty acids in the liver and serum. In the liver, HSO‐induced disruption of redox balance was reflected by the decrease of glutathione (GSH) and ascorbic acid and the upregulation of detoxifying gene expression. Moreover, the levels of several microbial metabolites in urine were affected by HSO, suggesting the changes in microflora. Above all, the most prominent metabolic changes induced by HSO occurred in the tryptophan‐NAD+ pathway since multiple metabolites in this pathway were affected, including the decrease of serum tryptophan, the increases of NAD+ and adenosine metabolites in the liver, and the increases of kynurenic acid, nicotinamide, and nicotinamide N‐oxide in urine. The activation of tryptophan‐NAD+ pathway was confirmed by observing the upregulation of tryptophan 2,3‐dioxygenase, kynureninase, and quinolinate phosphoribosyl transferase expression in this pathway, likely contributed by the activation of peroxisome proliferator‐activated receptor α (PPARα), as suggested by the upregulation of PPARα target genes in the liver and the decreases of triacylglycerols in both serum and liver. Since NAD+ and its metabolites are the indispensable cofactors or substrates of major metabolic events induced by HSO, including the detoxification of reactive aldehydes through aldehyde dehydrogenase, sustaining redox balance and DNA repair activities, and PPARα–mediated metabolic reactions, such as fatty acid β‐oxidation, the activation of tryptophan‐NAD+ pathway is deemed to be a central metabolic event induced by thermally‐oxidized lipids.

Support or Funding Information

NIFA project MIN‐18‐092
The Ratio of HDL to LDL in Serum Is Related to Macular Pigment Density and Cognitive Function in Older Adults: Potential Insights into Lutein Transport to Neural Tissue
Authors: Mohn Emily S , Scott Tammy M , Johnson Elizabeth J
Published: June 2021

The dietary carotenoid, lutein, is selectively taken up into neural tissue. Neural lutein is related to better cognition. However, serum lutein concentrations may not accurately reflect neural levels. Lutein is mainly transported on high‐density lipoprotein (HDL) followed by low‐density lipoprotein (LDL). HDL may play a significant role in delivery of lipophilic nutrients to neural tissue. Therefore, lutein content on HDL may better reflect neural levels. However, this has yet to be investigated in humans. The relative amounts of HDL and LDL (HDL/LDL) is an indicator of the distribution of lutein in the circulation. The aim of this study was to determine the relationship between changes in lipoprotein profiles, neural lutein concentration (measured by macular pigment density, MPD), and cognitive performance in older adults (n=31) using a previously conducted study in which participants were followed for 6 months. Serum collection, MPD (using heterochromatic flicker photometry), and cognitive testing (computerized cognitive assessment battery, CANTAB) were performed at baseline, 3 months, and 6 months. Serum lipoproteins and carotenoids were determined using an enzymatic colorimetric method and HPLC, respectively. There was a group of individuals who had MPD increases >0.10 optical density (OD) over the study period (n=17). These subjects were classified as “MPD responders”. In these subjects, adjusting for age, change in HDL/LDL was positively associated with change in MPD (r=0.66, p=0.006) and the strength of this association was greater in a subset of MPD responders who also had increases in serum lutein (n=10, r=0.77, p=0.01). The association between change in HDL/LDL and MPD was not significant in MPD responders without increases in serum lutein. In all MPD responders, change in both HDL/LDL and MPD were positively associated with change in spatial working memory and increased spatial planning, while change in serum lutein was positively related to spatial planning only (adjusted for age and education, P<0.05). Associations between HDL/LDL and cognition were stronger in the subset of MPD responders who also had increases in serum lutein (P<0.05). In MPD non‐responders (ΔMPD ≤0.05 OD), HDL/LDL was not related to MPD, but was associated with spatial planning. Collectively, these findings lend support to the hypothesis that lutein carried on HDL is targeted to neural tissue and may be important for cognition.

Support or Funding Information

This work was supported by the Hass Avocado Board and USDA (1950‐51000‐087)
Chemical discovery in the microbial world
Authors: Balskus Emily P.
Published: June 2021

Microorganisms like bacteria, archaea, and fungi have amazing chemical capabilities, performing challenging transformations and producing complex, biologically active molecules not easily accessed via any other means. However, we do not yet have an understanding of the enzymatic chemistry responsible for the full diversity of reactions performed by these organisms. Recent advances in DNA sequencing technologies have delivered a wealth of microbial genomes, providing an unprecedented opportunity to discover enzymes that have the potential to change the way chemists make molecules. My lab is identifying new enzymatic transformations by studying the biosynthesis of secondary metabolites with atypical structures or chemical functionality. This talk will discuss our recent progress deciphering the enzymatic chemistry that mediates unusual C–C and C–Cl bond‐forming reactions in several biosynthetic pathways. Functional and mechanistic characterization of these biosynthetic enzymes is revealing new reactivity with potential applications in biocatalysis and metabolic engineering.

Support or Funding Information

This work is supported by the NSF (CAREER Award # 1454007), the Searle Scholars Program, and the Cottrell Scholar Award.
Using the Wilder Collaboration Factors Inventory to Assess SNAP‐Ed Coalitions in Arizona: Results from Four Counties
Authors: McCullough Lauren , Jacobs Laurel , Orzech Kathryn , Farrell Vanessa , McDonald Dan , Florian Traci Armstrong , Zilliox Patricia , Martinez Cathy , Misner Scottie
Published: June 2021

Background

In 2014, the Supplemental Nutrition Assistance Program ‐ Education (SNAP‐Ed) incorporated Policy, Systems and Environmental (PSE) approaches to reinforce obesity prevention efforts. This expansion included engagement in multi‐sectoral coalitions which provide community‐level supports for healthy eating and active living. Coalition success depends on creating well‐defined collaborations that share authority, accountability, resources, and achievements. Arizona's SNAP‐Ed utilized the Wilder Collaboration Factors Inventory (WCFI) to evaluate coalitions' effectiveness in supporting food systems and active living PSE goals at the community level.

Methods

The University of Arizona Nutrition Network (UANN), part of the SNAP‐Ed program in Arizona, used the WCFI to assess six coalitions in four counties (Maricopa, Mohave, Pima, and Pinal).

The WCFI uses a 40‐question Likert scale (1.0–5.0) questionnaire to evaluate collaborations on 20 success factors. The WCFI identifies areas of collaboration strength (4.0–5.0) and weakness (1.0–3.9). Coalition members were invited to complete the WCFI online or in‐person. Of the 117 surveys distributed, 64 were returned, and 61 provided complete responses. The results (N=61) were aggregated to identify similar factor scores across coalitions.

Results

Four out of six coalitions (66%) scored highly in the same success factor: members see collaboration in their self‐interest (average score: 4.5). Half of the coalitions identified unique purpose as a stronger success factor within their collaboration (average score: 4.2).

All coalitions identified the same weaker success factor: lack of sufficient funds, staff, materials, and time (average score: 2.8). Three coalitions had the development of clear roles and policy guidelines as a weak success factor within their coalition (average score: 3.0).

Conclusion

The WCFI results suggest that community coalitions in which SNAP‐Ed staff participate in Arizona reflect an invested membership and a unique purpose in their communities, yet sufficient resources and clear goals are areas that should be strengthened. By providing timely and actionable WCFI data and recommendations to these active living and food systems coalitions in Arizona, capacity can be strengthened to achieve the goals of the collaborations in which SNAP‐Ed participates. The coalitions that use the WCFI results to encourage the strengthening of their coalition's capacity will be more likely to succeed in achieving PSE changes in their communities.

Support or Funding Information

USDA HI050073
Identification of p‐cresol sulfate and secondary bile salts in human urine as sensitive biomarkers of fecal microbiota transplantation in R‐CDI patients
Authors: Bi Zheting , Lu Yuwei , Weigarden Alexa R , Yao Dan , Wang Lei , Khoruts Alexander , Sadowsky Michael J , Chen Chi
Published: June 2021

Fecal microbiota transplantation (FMT) has become an effective therapy for recurrent Clostridium difficile infection (R‐CDI). Besides reestablishing a normal intestinal microbiome that offers better resistance to R‐CDI, the introduction of microflora from healthy donors through FMT is also expected to change the metabolomes in the intestine and the whole body due to diverse metabolic activities of transplanted microbiota. Therefore, monitoring the metabolic changes in biofluids and excretes provides the opportunities for identifying noninvasive biomarkers of microbial recolonization and understanding the metabolic influences of FMT on host and microflora. In this study, FMT‐induced metabolic changes were examined by the metabolomic comparison of pre‐FMT and post‐FMT urine samples from 18 R‐CDI patients who had symptoms rapidly resolved after receiving FMT from two donors. After the liquid chromatography‐mass spectrometry (LC‐MS) analysis of urine samples from the patients and the donors, the LC‐MS data were processed by partial‐least squares‐discriminant analysis (PLS‐DA), leading to the establishment of a multivariate model revealing the separation between pre‐ and post‐FMT urine samples as well as the similarity between post‐FMT and donor samples. Among a group of urinary metabolites affected by the FMT, the most prominent biomarkers are p‐cresol sulfate and secondary bile acid conjugates, which were absent in most pre‐FMT samples, but dramatically increased in the post‐FMT samples. The presence of p‐cresol sulfate and secondary bile acid conjugates in urine after FMT reflected the recovery of microfloral metabolism on tyrosine and primary bile acids in R‐CDI patients. Their levels in urine may function as effective and sensitive therapeutic indicators of the readiness of CDI patient for FMT as well as the recolonization of healthy microfloral colonies after FMT.

Support or Funding Information

NIAID grant R21 AI114722 and NIFA project MIN‐18‐092
Analysis of the Primate “Squeeze‐back” Swallowing Mechanism using X‐ray Reconstruction of Moving Morphology and Fluoromicrometry
Authors: Orsbon Courtney P , Gidmark Nicholas J , Ross Callum F
Published: June 2021

The primate hyolingual apparatus is a complex composite of a muscular hydrostat and a floating bone that is essential for feeding. In particular, the characteristic elevation (i.e., the “squeeze‐back” mechanism) and retraction of the tongue base during swallowing may be important in flipping the epiglottis to protect the laryngeal inlet. However, the link between hyolingual muscle behavior and hyolingual kinematics is poorly supported by in vivo data. Tongue base elevation and retraction could be due to one or a combination of three mechanisms thanks to its redundant morphology: intrinsic tongue muscles inducing hydrostatic deformation, extrinsic muscles moving the whole tongue, or hyoid elevation and protraction deforming the tongue. We evaluated these possibilities using a macaque model system. We implanted two rhesus macaques (one male, one female) with tantalum beads and filmed them during feeding using biplanar videofluoroscopy for X‐ray Reconstruction of Moving Morphology and fluoromicrometry workflows to measure hyoid kinematics, tongue deformation, and muscle length change with high spatiotemporal resolution. The results of general linear models demonstrate significant effects of hyoid movement and hydrostatic deformation on tongue base elevation, while all three mechanisms predict tongue base retraction (p < 0.001). Future directions include incorporating electromyography to understand how hyolingual muscle activity, especially active shortening, generates to tongue movement. These findings not only give insight into the biomechanics of the hyolingual apparatus, but they are also relevant for dysphagia rehabilitation as they suggest that more muscles are involved in tongue base retraction‐‐and perhaps epiglottic flipping‐‐than previously thought.

Support or Funding Information

This research was supported by the NIH (R01 DE023816‐03 and T32 HD007009‐41) and the NSF (MRI 1338066).
Incorporation of Dietary n‐3 Fatty Acids into Selective Phosphatidylcholine Lipids in Human Plasma after Salmon Intake
Authors: Zacek Petr , Bukowski Michael , Raatz Susan , Picklo Matthew
Published: June 2021

Elevated intake of n‐3 long chain polyunsaturatedfatty acids (n‐3 LCPUFA) is associated with reduced risk for cardiovascular disease. Intake of n‐3 LCPUFA is often quantified by analysis of plasmaphospholipid fatty acids (PLFA); however, the typical analysis by gaschromatography does not allow for determination of the phospholipid species that are enriched by the n‐3 LCPUFA. In this work, we tested the hypothesis that the n‐3 LCPUFA, namely docosahexaenoic acid (DHA) and eicosapentaenoic acid(EPA), are incorporated into select phosphatidylcholine (PC) species following intake of farm‐raised, Atlantic salmon. Plasma samples were obtained from a randomized, cross‐over designed study in which participants (n = 9) consumed farm‐raised Atlantic salmon at levels of 90 g and 180 g twice weekly for 4 weeks with an 8 week washout between treatments. Plasma lipids were extracted and analyzed using a shotgun MS/MS method with the capability to quantify isobaric PC species. Our data indicate that under basal conditions, EPA and DHA are incorporated into PC species containing palmitic acid (PA), stearic acid (SA), and oleic acid (OA) as the complementary fatty acid in the concentration order of PA>SA>OA. EPA content was enriched in PA, SA, and OA species following salmon intake whereas only PA and SA containing DHA species were elevated following intake. Interestingly, PCs containing docosapentaenoic acid (DPA) were not elevated even though the salmon contained DPA. PC species containing n‐6 PUFA demonstrated a similar pattern of PA>SA>OA as the complementary fatty acids. No changes in n‐6 containing PC species occurred following salmon intake. Although linoleic acid (LA) was highly enriched in total PC, LA was not detected as a complementary fatty acid to any n‐3 LCPUFA species and was a minority complementary species for other n‐6 PUFA. In conclusion, our data demonstrate that (1)n‐3 LCPUFA incorporate into selective PC pools some of which increase with dietary n‐3 LCPUFA intake, and (2) there exists a hierarchy of PUFA containing PC species with selectivity for lower carbon length and higher saturation level for the complementary fatty acid. These data allow for a more refined characterization of biomarkers for PUFA intake and understanding of PC biochemistry in humans.

Support or Funding Information

This work was supported by National Institute of Food and Agriculture, U.S. Department of Agriculture, under award number 2014‐67017‐21758 and through USDA‐ARS project 5450‐51000‐048‐00D.
Consumption of the total Western diet (TWD) enhanced and sustained colonic inflammation and promoted colon tumorigenesis in mice, which led to marked changes in the composition of the gut microbiome in mice
Authors: Benninghoff Abby , Hunter Ashli , Monsanto Stephany , Phatak Sumira , Hintze Korry , Ward Robert , Lefevre Michael
Published: June 2021

To improve translation of preclinical rodent nutrition studies to human trials, our research team developed the new Total Western Diet (TWD) for rodents with energy and nutrient profiles that emulate a typical Western diet. A series of pre‐clinical studies was preformed using different models of colon cancer to compare TWD to the AIN93G diet, a standard basal diet designed to promote animal health. Consumption of TWD 1) increased number of aberrant crypt foci in A/J mice initiated with azoxymethane (AOM), 2) significantly enhanced tumorigenesis in C57BL/6J mice initiated with AOM and provided dextran sodium sulfate (DSS) to promote colonic inflammation and 3) enhanced colon tumorigenesis in APCMin/+ mice provided DSS. Using the AOM/DSS model of CAC, we assessed the impact of TWD on the colitis disease activity index, colon tissue histopathology and composition of the gut microbiome by 16S sequencing over the course of disease development (pre‐initiation, colitis, recovery and terminal). We determined that TWD consumption markedly enhanced colitis activity (40‐fold increase) compared to mice fed AIN93G. Moreover, TWD‐fed mice had significantly higher histopathology scores for inflammation and mucosal injury during the period of colitis and, importantly, during the recovery phase of this disease model. Colonic inflammation in TWD‐fed mice persisted to the end of the study (day 105), whereas mucosal injury (save for sites of neoplasia) had resolved. Prior to initiation with AOM/DSS, the gut microbiome compositions of AIN93G‐ and TWD‐fed mice were very similar. As colitis progressed, the populations became more distinct, especially so by the recovery stage (day 45), which was also typified by sustained colonic inflammation and mucosal injury in TWD‐fed mice. By the study end (day 105), separation between the fecal microbiomes for the different diet groups was evident. Finally, examination of the terminal fecal microbiome revealed distinct gut microbiota profiles for TWD‐fed animals initiated with AOM/DSS compared to sham mice, whereas a distinction was not evident for those fed AIN93G. Collectively, these data show that the TWD markedly enhanced colorectal tumorigenesis in repeated experiments and multiple animal models. Moreover, enhanced and sustained inflammation of the colon epithelium is a probable mechanism for promotion of CAC by TWD. Finally, mice with pronounced colitis‐associated colorectal cancer, induced by dietary exposure to TWD, harbored microbiomes distinct from their counterparts fed healthy diets.

Support or Funding Information

Utah Agricultural Experiment Station, Project UTA‐1178; USDA NIFA/AFRI Grant No. 2014‐67017‐21755
Aberrant crypt formation accompanies an increase of opportunistic pathogens/bacteria in the inflammatory gut of C57BL/6 mice fed a high‐fat diet
Authors: Zeng Huawei , Ishaq Suzanne L , Liu Zhenhua , Keehr Kay A , Bukowski Michael R
Published: June 2021

Obesity and high fat diet are risk factors for colon cancer, but the mechanism of this relationship remains to be determined. We tested the hypothesis that a high fat diet promotes the formation of aberrant crypt foci (ACF, preneoplastic lesions) in a manner associated with changes in hindgut bacterial taxa. We examined the susceptibility to azoxymethane (AOM)‐induced colonic ACF and microbiome composition in C57/BL6 mice fed a low fat (LF, 10% energy fat) diet or a high fat (HF, 45% energy fat) diet for 11 weeks. Mice receiving the HF diet exhibited increased plasma leptin, body weight, body fat composition and inflammatory cell infiltration in the ileum compared with those in the LF group. Consistent with a gut inflammatory phenotype, we observed an increase in colonic ACF, plasma interleukin 6 (IL6), tumor necrosis factor α (TNF α), monocyte chemoattractant protein 1 (MCP1), and inducible nitric oxide synthase protein in the ileum of the HF‐AOM group compared with those in the LF‐AOM group. Fecal DNA was extracted and 16S universal eubacterial primers were utilized to determine the microbiome composition using an amplicon pyrosequencing method. Although the HF and LF groups did not differ in bacterial alpha‐diversity, the HF and LF diets resulted in unique bacterial community structures in the hindgut. When treated with AOM, the abundance of certain short chain fatty acid (SCFA) producing bacteria (e.g., Barnesiella) and the amount of fecal SCFA (e.g., acetic acid) were lower in the HF group compared with those in the LF group. Furthermore, we identified a high abundance of Anaeroplasma bacteria (opportunistic pathogens), accompanied with ACF formation in the HF group. Taken together, we demonstrate that HF feeding promotes ACF formation associated with an increase of opportunistic pathogens / bacteria in the hindgut of C57BL/6 mice.

Support or Funding Information

This work was funded by the US Department of Agriculture, Agricultural Research Service, Research Project 3062‐51000‐050‐00D.
Changes in body adiposity and its associated inflammation affect metastasis of Lewis lung carcinoma in mice
Authors: Yan Lin , Sundaram Sneha
Published: June 2021

A hallmark of obesity is the increase in body adiposity and its associated inflammation that contribute to obesity‐related chronic diseases including cancer. Clinical studies show that obesity is related to poor prognosis, early recurrence and metastasis in cancer patients. Recurrence and metastasis are the most devastating aspects of cancer. We studied roles of changes in body adiposity (induced by changes in diet formulation or feeding method) in spontaneous metastasis of Lewis lung carcinoma in mice. Compared to the AIN93G control diet (16% of energy from corn oil), the high‐fat diet (45% of energy from coil oil) significantly increases body fat mass and plasma concentrations of proinflammatory cytokines [e.g. monocyte chemotactic protein‐1 (MCP‐1) and plasminogen activator inhibitor‐1 (PAI‐1)] and significantly increases the extent of metastasis, evidenced by increases in number and size of metastases formed in lungs. A restriction in high‐fat diet intake by 5%, which maintains the body adiposity and plasma MCP‐1 and PAI‐1 levels similar to mice fed the AIN93G diet, significantly reduces lung metastasis compared to unrestricted feeding of the high‐fat diet. Knocking out MCP‐1 or PAI‐1 from mice significantly reduces high‐fat diet‐enhanced metastasis. The metastatic enhancement was not observed in mice fed a 45% high‐sucrose diet, which did not elevate body adiposity and proinflammatory cytokines compared to a 45% high‐fat diet. Furthermore, we found from a feeding study that there are no differences in proinflammatory cytokines (including MCP‐1 and PAI‐1) in mice fed high‐fat diets containing oils with different amounts of n3 and n6 fatty acids. Our results indicate that increases in adiposity and its associated proinflammatory cytokines may contribute to the high‐fat diet‐enhanced metastasis and that sources of dietary energy, rather than the energy itself, may lead to differences in metastatic aggression of Lewis lung carcinoma.

Support or Funding Information

The U.S. Department of Agriculture, ARS, research project 5450‐51000‐045‐00D.
The influence of genetic ablation of tumor necrosis factor‐α on the colonic Wnt pathway cascade under an obese state
Authors: Liu Zhenhua , Li Jinchao , Frederick Armina‐Lyn M. , Jin Yu , Xu Xiaolin , Wood Richard J.
Published: June 2021

Obesity is an established risk factor for colorectal cancer (CRC), but the mechanism(s) responsible for this relationship are still not fully understood. We hypothesize that obesity creates a low‐grade colonic inflammatory microenvironment, which facilitates the development of CRC. Our prior study suggested tumor necrosis factor alpha (TNF‐α) might elevate the Wnt‐signaling, and thereby promote the colonic tumorigenesis. In the present study, we observed that several colonic inflammatory cytokines (TNF‐α, IL‐1β, IFNg) and Wnt pathway specific genes (e.g. Axin2) were upregulated in an obese state (p < 0.05), whereas the genetic ablation of TNF‐α suppressed the elevation of Wnt‐signaling induced by dietary obesity, as indicated by decreased levels of phopho‐GSK3β, and active β‐Catenin (p < 0.05), two key components in Wnt pathway cascade. A Wnt pathway specific gene expression profiling further demonstrated that the genetic abolishment of TNF‐α attenuated aberrations of several genes within the colonic Wnt pathway cascade including the over‐expressed Axin2, a readout of the Wnt pathway (p < 0.05). Colonic epithelial proliferation (Ki‐67), which is partially under the control of Wnt signaling, was also decreased by the blockade of TNF‐in obese mice (p < 0.05). These results indicate that obesity‐driven inflammation plays a role in the regulation of the tumorigenic Wnt‐signaling pathway, which contributes to the development of obesity‐associated CRC.

Support or Funding Information

Supported in part by a USDA/NIFA grant, a USDA/Hatch grant and a HNRCA competitive intramural pilot grant to ZL
Green Tea Extract Protects Against Diethylnitrosamine‐Mediated Liver Injury And Cell Proliferation By Attenuating STAT3 And iNOS Expression In High Fat‐Induced Obese Mice With Nonalcoholic Steatohepatitis
Authors: Kim Joshua B , Li Jinhui , Chitchumroonchokchai Chureeporn , Sasaki Geoffrey Y , Thomas‐Ahner Jennifer M , Clinton Steven K , Bruno Richard S
Published: June 2021

Nonalcoholic steatohepatitis (NASH) increases hepatocellular carcinoma (HCC) risk by increasing inflammation and oncogenesis. Antiinflammatory activities of green tea extract (GTE) protect against dietary high‐fat (HF)‐induced NASH. We hypothesized that the hepatoprotective antiinflammatory activities of GTE during NASH would also prevent diethylnitrosamine (DEN)‐induced progression towards HCC. Male C57BL/6J mice (4 wk old) were fed a HF diet devoid of, or supplemented with, GTE at 2% (w/w) and received once weekly intraperitoneal injections of saline vehicle or DEN (60 mg/kg; wk 5 and 7) until 25 wk old prior to assessing NASH, inflammation, and oncogenic responses. DEN did not (P>0.05) exacerbate liver steatosis, hepatocyte ballooning, or mRNA expression of TNFα and MCP‐1 compared with saline‐treated mice. However, GTE protected against (P<0.05) histologic evidence of NASH and TNFα and MCP‐1 expression to a similar extent in saline‐ and DEN‐injected controls. GTE inhibited DEN‐induced increases in serum alanine aminotransferase (ALT) activity and iNOS mRNA expression, which were not different from the lowered levels observed in saline‐treated mice fed GTE. GTE also similarly inhibited DEN‐induced increases in signal transducer and activator of transcription 3 (STAT3) protein expression to levels not different from those lowered by GTE in saline‐treated mice. GTE attenuated positive staining towards hepatocyte proliferating cell nuclear antigen (PCNA) that was otherwise exacerbated by DEN. Serum ALT was correlated (r = 0.74–0.83; P<0.0001) with iNOS, STAT3, and PCNA. Likewise, iNOS correlated with both PCNA and STAT3 (r = 0.64–0.65; P<0.05), suggesting that iNOS‐induced inflammation centrally regulates liver injury and oncogenic cell proliferation. GTE protects against DEN‐exacerbated STAT3/iNOS‐mediated oncogenic responses that otherwise provoke liver injury and cell proliferation.

Support or Funding Information

Supported by USDA‐NIFA and OSU Comprehensive Cancer Center.
Interactive effects of blueberry supplementation and GPR109A deletion on gut microbiome profiles in mice
Authors: Shankar Kartik , Ying Zhong , Oksana Lazarenko P , Chintapalli Sree V , Chen Jin‐Ran , Wankhade Umesh D
Published: June 2021

Blueberry‐supplemented (BB) diets in rodent models have shown to improve skeletal mass, glucose tolerance and endothelial function. In addition to the bioactive and dietary fibre components of these diets, effects of blueberries may be in part via modulation and action of the gut microbiome. However, few studies have characterized gut microbiome composition following BB supplementation. Since phenolic acids and gut microbiota‐derived short‐chain fatty acids (SCFAs) such as butyrate can bind and activate GPR109A (nicotinic acid receptor) signaling, we examined the interactive roles of GPR109A and BB‐supplementation on microbiome profiles in mice. Male GPR109A global knockouts and WT littermates were fed control or BB‐supplemented diets (5% w/w) for 4 weeks (n=10). All diets were based on the AIN‐93G formulation and contained 19% calories from protein, 17% from fat and 64% from carbohydrates. Body weight, body composition (non‐invasively via Echo MRI) and food intake were measured weekly and did not differ between groups within the study period. At the end of 4 wk serum, liver, adipose tissue depots and cecal contents were collected for further analysis. Microbial community profiling was conducted by sequencing the 16S rRNA (V4 region) followed by analysis using QIIME. BB‐diet fed mice showed greater a‐diversity (OTU richness) in both WT and GPR109A‐KO. Interestingly, GPR109A loss per se was associated with significantly lower a‐diversity relative to WT mice (p<0.05). Principal coordinate analysis of b‐diversity values showed highly significant effects of both genotype and diet (p<0.00001). BB diets affected abundance of 15 genera in WT mice, of which only 5 genera were also affected in GRP109A KO with BB‐treatment (p<0.05, two‐way ANOVA). However, BB diets in GPR109A KO altered 7 genera uniquely suggesting significant genotype‐diet interactions. Two‐way ANOVA analysis showed BB‐diets increased Bacteroidetes and decreased Firmicutes phyla (p<0.001) in both WT and KO mice. OTU abundance of genera including Facklamia, Clostridium, Coprococcus, Dorea, and Ruminoccous was affected by both diet and genotype of mice (p<0.01). LEfSE analysis confirmed enrichment of phyla Bacteroidetes with BB‐diets. Predictive functional metagenomics analysis using PiCRUST identified alterations of pathways involving immune and bacterial response, protein digestion, amino acid metabolism and xenobiotics biodegradation to be affected by genotype and BB‐diet. Associations between alterations in microbial abundance and diet‐associated changes in adipose tissue and liver gene expression will also be presented. Overall, these results suggest changes in microbial community structure with BB‐diets and also reveal novel host genotype dependent alterations in the microbiome. Support USDA CRIS 6206‐51000‐010‐05S

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Support USDA CRIS 6206‐51000‐010‐05S
Extension‐Delivered Diabetes Program for Rural‐residing Latinos Improves Diabetes Self‐management, Self‐efficacy and Knowledge
Authors: Francis Sarah L , Keane Michelle
Published: June 2021

Rural‐residing Latinos are at high diabetes risk due to limited access to healthcare services, high rates of overweight and obesity, and acculturation. Culturally‐sensitive diabetes self‐management education programs are needed to reduce the risk and severity of Type 2 diabetes among rural‐residing Latinos. Improvements in diabetes‐related self‐efficacy and knowledge can lead to improved diabetes self‐management outcomes. Latinos Living Well (LLW) was created using the Social Marketing Theory (SMT) and the Health Belief Model (HBM). SMT ensured the content was audience‐centered and culturally‐relevant. HBM constructs were addressed through facilitative discussion, cooking practicums, and hands‐on activities. LLW is made up of four two‐hour classes with culturally‐relevant food and physical activity examples, were taught in Spanish, and delivered through Cooperative Extension. This study evaluated the impact of LLW on diabetes self‐management practices, diabetes self‐efficacy, and diabetes knowledge. A convenience sample of rural‐residing Latino adults age 18+ in a Midwest state (n=120) were recruited, regardless of diabetes status, through collaborations with established community groups serving Latinos, radio commercials and print media, and word of mouth; 76 completed the program (63.3% completion rate). Participants completed a Spanish questionnaire comprised of validated tools, sociodemographic questions, and questions regarding diabetes status at the start of Class 1 (PRE) and the end of Class 4 (POST). Descriptive statistics analyzed sociodemographic data while paired‐samples t‐tests examined changes in diabetes self‐management, diabetes self‐efficacy and diabetes knowledge from PRE to POST. The majority were females (n=73; 97.3%), between the ages of 30 and 49 years (n=34; 51.6%), who were first generation immigrants (n=63; 87.5%). Two‐thirds (n=49; 65.3%) reported some history of a diabetes diagnosis. Significant increases were detected for diabetes self‐management practices (p<0.006), diabetes self‐efficacy (p<0.0001), and diabetes knowledge (p<0.004). These results suggest LLW is effective in improving diabetes self‐management practices, diabetes self‐efficacy, and diabetes knowledge outcomes among rural‐residing Latinos.

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This research was funded by the United States Department of Agriculture, National Institute of Food and Agriculture Rural Health and Safety Education Grant, #2014‐46100‐22349
Dietary genistein inhibits methylglyoxal‐induced advanced glycation end products formation in high‐fat diet‐fed mice
Authors: Zhao Yantao , Wang Pei , Sang Shengmin
Published: June 2021

The formation and accumulation of advanced glycation end products (AGEs) was considered as a major pathogenic link between hyperglycemia and diabetes‐related complications. Methylglyoxal (MGO), as an important precursor of AGEs, circulates at high concentration in diabetic patients's blood and is linked to the development of diabetes chronic complications. In the present study, we investigated whether long‐term treatment of MGO plus high‐fat diet can cause accumulation of protein glycation in mice and whether dietary genistein can prevent the formation of AGEs and ameliorate high‐fat plus MGO induced metabolic syndrome. Our results indicate that chronic high‐fat plus MGO administration (0.12–0.2% in drinking water for 18 weeks) significantly elevates the levels of MGO and AGEs in mouse plasma, liver and kidney, and cause fatty liver. Dietary genistein treatment (0.067% and 0.2% in high‐fat diet) significantly ameliorates high‐fat plus MGO‐induced fatty liver and metabolic syndrome, such as lowering body weight gain, plasma levels of glucose, cholesterol, aspartate transaminase (AST), alanine transaminase (ALT), and liver triglyceride levels. Moreover, genistein administration also significantly decreases the levels of MGO and AGEs. Further mechanistic studies demonstrate that genistein could trap MGO in mice to form mono‐MGO‐genistein adduct. In addition, genistein could regulate expressions of glyoxalase I and II, and both catalytic and modifier subunits of glutamate‐cystein ligase to promote the detoxification of MGO. Furthermore, genistein down‐regulates the expression of the receptor of AGEs (RAGE) to inhibit the AGEs‐RAGE pathway.

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This work was supported by USDA‐NIFA grants 2012‐38821‐20012.
The nasal salt gland of extant birds: anatomical structure and its relevance for inferring the behavior and habitat preferences of extinct birds
Authors: Caggiano Emily G. , Cerio Donald , Porter Wm. Ruger , Ridgely Ryan C. , Witmer Lawrence M.
Published: June 2021

The kidneys of extant sauropsids (birds, crocodylians, turtles, lepidosaurs) tend to be less efficient at removing excess salt from the blood than are those of mammals, and consequently, sites of extrarenal salt excretion are common in sauropsids. In birds, the nasal gland is involved with concentrating and excreting salt from the blood. In many marine birds (e.g., charadriiforms, procellariiforms), the nasal gland is hypertrophied and occupies a supraorbital position, but other positions are known in birds, such as within the orbit (e.g., suliforms). The basic physiology of avian nasal salt glands has been well‐understood for generations, but the detailed anatomy, particularly with regard to its osteology, is poorly documented. We present the results of our preliminary survey of nasal gland structure in birds to better resolve the osteological correlates of the gland, its ducts, and its vascular supply. The resulting osteological correlates (e.g., bony fossa, supraorbital process of the lacrimal, foramina/grooves for ducts) allow a more rigorous and informed assessment of the presence, position, and size of the nasal gland in extinct birds, potentially allowing rough assessments of salt loads and hence habitat preferences (e.g., marine vs. terrestrial). The extant studies emphasize marine and aquatic birds (e.g., albatrosses, shearwaters, gulls, gannets, cormorants, anseriforms), among others, such as, non‐marine outgroups (e.g., ostrich), drawing on the following anatomical approaches: (1) gross dissection, (2) diceCT (iodine enhanced microCT), and (3) radio‐opaque vascular injection followed by microCT. These studies allow not only detailed information about the relevant soft tissues and their osteological correlates, but also permit quantification of gland volumes and other metrics for comparative analysis. These extant studies shed new light on the interpretation of the nasal glands of extinct birds. Study of original fossil material and microCT scan data provide more refined information on the nasal glands of the Cretaceous marine toothed birds Hesperornis and Ichthyornis. The flightless diver Hesperornis had enormous nasal glands, suggesting that it was forced to consume seawater exclusively, whereas the volant and hence more vagile Ichthyornis had smaller salt glands suggesting that it perhaps also had access to fresh water sources. The Paleogene anseriform bird Presbyornis, typically regarded as inhabiting saline soda lakes, also was sampled and provides new evidence for a modest nasal salt gland.

Support or Funding Information

US National Science Foundation (IOB‐0517257, IOS‐1050154, IOS‐1456503), the Ohio University Honors Tutorial College, and the Ohio University Heritage College of Osteopathic Medicine
Obesity‐Mediated Regulation of the Cardiac Acetylome
Authors: Romanick Samantha S , Hostler Andrew , Schlauch Karen , Quilici David , Feng Yumei , Ferguson Bradley
Published: June 2021

Lysine residues undergo diverse and reversible post‐translational modifications that include acetylation, ubiquitylation and methylation. Lysine acetylation has traditionally been studied in the regulation of gene expression, where acetylation of histone tails alters electrostatic interactions of nucleosomal DNA. However, recent proteomic studies have identified ~4,000 proteins that can be acetylated on ~10,000 lysine residues, suggesting a more complex role for the acetylome in biological function. In the heart, treatment with histone deacetylase (HDAC) inhibitors and thus increases in lysine acetylation have been shown to be cardioprotective. Here we examined the impact of obesity on the regulation of lysine acetylation. In this study, male and female c57BL/6J mice fed a high fat diet (60% kcal from fat) had a significant increase in body weight, heart weight and left ventricle weight compared to mice fed a control diet (10% kcal from fat). Of interest, immunoblot analysis demonstrated that lysine acetylation of the left ventricle was markedly altered in both male and female mice in response to diet‐induced obesity. Moreover, these phenomena appeared to be cardiac tissue specific as no differences in lysine acetylation were observed in skeletal muscle, liver or white adipose tissue in response to obesity. As such, we recently performed isobaric tagging and mass spectral analysis to identify and quantitatively analyze changes in protein abundances as well as lysine acetylation in response to obesity. We postulate that our investigations will demonstrate, with statistical significance, the impact of obesity on regulation of the cardiac acetylome and uncover biological pathways regulated by protein acetylation potentially involved in cardiac pathology.

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The project described was supported by a grant from the National Institute of General Medical Sciences (GM103440). This work is supported by the USDA National Institute of Food and Agriculture (Hatch‐NEV00727).