bluuebunny/crossref_metadata_2025_split huggingface dataset:
Calculation of Retention Factors for Flavonoids in Cooked Broccoli
Authors: Wu Xianli , Zhao Yang , Bhagwat Seema , Haytowitz David B , Harnly James M , Pehrsson Pamela R , Chen Pei 
Published: June 2021

Thermal processes such as cooking have a large influence on flavonoids in foods, which further impact the accuracy of developing food flavonoid database and the estimation of their dietary intake. The objective of this study was to determine how common cooking methods alter complex flavonoids in broccoli, and to compare the effects of different cooking and calculating methods for estimating retention factors. Fresh broccoli samples were purchased from local grocery chains and were cooked by three common ways (boiling, steaming and microwaving). Flavonoids were analyzed by HPLC‐MS/MS. Eight major kaempferol (Km) tri‐ or tetra‐glycosides and one quercetin tri‐glycoside were identified and quantified in raw and cooked broccoli. Retention factors were calculated on individual flavonoids based on the dry weight; they ranged widely from 33.9% to 237.2%, depending on the chemical structure and cooking method. Contents of certain Km glycosides elevated after cooking, probably due to the increased release from cells or from binding with other components. In addition, different calculation methods to generate an overall retention factor for multiple flavonoids with the same aglycone were compared. Among the three methods, namely “retention factor by aglycone”, “retention factor by weight” and “retention factor by average”, the “retention factor by aglycone” was shown to be an appropriate method. The retention factors by aglycone for Km glycosides in broccoli was calculated as 83.9% for boiling, 131.6% for steaming and 136.1% for microwaving.Support or Funding InformationNIH Agreement 58‐1235‐3‐126 and USDA
Vasopressin‐Altered Glycemic Control May Lead to Metabolic Disorders of Severe Hemorrhagic Shock
Authors: Uyehara Catherine F T , Wetstein Paul J , Murata Lee‐Ann M , Ichimura Wayne M , Hernandez Claudia A , Richards Carly R , McMurray Robert C , Kajiura Lauren N , Wong Sara A 
Published: June 2021

Metabolic disorders associated with trauma and hemorrhage typically follow an early hyperglycemic reflex aimed at increasing brain blood glucose in the face of oxygen debt. The hyperglycemic reflex is believed to be initiated by hypoxia‐induced carotidbody stimulation via a vasopressin (VP) V1a receptor mechanism. We hypothesized that elevated circulating VP levels released in response to severe shock contribute not only to restoring blood pressure, but may also prolong altered glycemic control. Thus, we examined VP influence on glucose regulation after severe oxygen debt from hemorrhagic shock using Yorkshire cross pigs (n=29, body weight 31.1+0.3 kg). Rapid hemorrhage (30 ml/kg bloodshed over 20 minutes) was induced to cause a 50% drop in mean arterial pressure and an oxygen debt of 68+5 ml/kg. Blood glucose levels rose from 124+10 mg/dl at baseline to 174+10mg/dl after hemorrhage (p<0.01), with accompanying increases in VP, epinephrine, glucagon, and insulin. Relationships between blood glucose, VP, epinephrine, glucagon, insulin, pancreatic blood flow and liver blood flow were examined. Multiple regression analysis of glycemic control from baseline through the end of hemorrhage indicated that glucose levels were strongly associated with VP and epinephrine, and inversely related to glucagon which correlated with VP (p<0.01). VP and pancreatic blood flow remained negatively correlated in all phases of baseline, hemorrhage and resuscitation with exogenous VP (30 ng/kg/min i.v., n=7). Thus pancreatic blood flow was significantly lower (p<0.01) with VP‐treated pigs (0.14+0.02 ml/kg/min) than in pigs that were resuscitated with normal saline where pancreatic blood flow (0.36+0.04ml/kg/min, n=10) did not further decrease. Exogenous VP during resuscitation also stimulated liver blood flow, and seemed to keep glucagon from decreasing despite the decreased pancreatic blood flow. VP did not affect insulin levels. Results suggest that VP mediates a hyperglycemic response in severe hemorrhagic shock via influence on glucagon secretion. If hyperglycemia continues beyond this acute response to hemorrhage, long‐term metabolic disorders could develop which would lead to tissue oxidative damage and contribute to trauma‐induced multisystem organ failure. Strategies for critical care management of hemorrhagic shock need to incorporate understanding of VP‐induced metabolic alterations of glycemic control.Support or Funding InformationThis project was supported by U.S. Army Medical Research and Materiel Command Congressionally Directed Medical Research Program grant #DAMD17‐03‐1‐0072. The views expressed in this abstract are those of the authors and do not reflect the official policy or position of the Department of the Army, Department of Defense, or the U.S. Government.
Ontogeny of breathing pattern and ventilatory chemosensitivity in altricial red‐winged blackbird (Agelaius phoenixes) nestlings
Authors: Dzialowski Edward M , Sirsat Tushar S. , Sirsat Sarah K.G. , Price Edwin 
Published: June 2021

Altricial bird species, like the red‐winged blackbird, hatch at an immature level of functional maturity with very limited aerobic capacity. Over the next 9 days, red‐winged blackbirds develop increased metabolic capacity and fledge. Metabolic capacity is limited in the early neonate and the ontogeny of the ventilator chemosensitivity is unknown. Here we examined developmental changes in chemosensitivity of tidal volume (VT), breathing frequency (f), minute ventilation (VE), and whole‐animal oxygen consumption (Vo2) from hatching to fledging in the red‐winged blackbird on days 3, 5, 7, and 9 days post hatching (dph) in response to hypercapnia (2 and 4% CO2) and hypoxia (15 and 10% O2). The barometric technique was used to estimate VT. Under control conditions, there was a developmental increase in VE with age that was due in part to increased VT with age. All ages exhibited a hypercapnic and hypoxic chemosensitivity. In response to hypercapnia, the 3 dph neonates increased VE by increasing both f and VT. From 5 dph on, the hypercapnic increase in VE was accounted for by increases in VT and not f. In response to hypoxia, all ages exhibited an increase in f at 10% O2, while VT decreased in older animals. This resulted in an increased VE at 3 dph with no change in VE at the later ages. Chemosensitivity in response to O2 and CO2 appear to mature early in the neonatal red‐winged blackbird, well before they are able to increase Vo2 in response to cooling.Support or Funding InformationNational Science Foundation IOS‐1146758
Postnatal Muscle Growth Is Dependent on Satellite Cell Proliferation Which Demonstrates A Specific Requirement for Dietary Protein
Authors: Fiorotto Marta L. , Columbus Daniel A. , Steinhoff‐Wagner Julia , Suryawan Agus , Nguyen Hanh V. , Davis Teresa A. 
Published: June 2021

Extrauterine growth faltering is a serious problem for premature neonates due in large part to insufficient nutrient intake secondary to physiological immaturity and feeding intolerance. Growth of lean mass is especially compromised in these patients due to poor muscle growth. In neonates, short‐term supplementation with leucine of a reduced protein, but energy adequate, feed promoted muscle protein synthesis by stimulating mTORC1 activity similar to feeding a high protein feed. Whether sustained long‐term leucine supplementation of a protein limiting diet can enhance muscle growth is unknown. Five‐d‐old pigs (n = 8–11/diet) were fed by gastric catheter a milk replacement diet with either a high protein (HP) or restricted protein (RP) content or RP supplemented with leucine to the same level as in the HP diet (RPL); all feeds were isocaloric. Pigs were fed every 4 h for 21 d. BrdU (25 mg/(kg.d)) was given as an i.v. bolus every 12 hrs over 3 d from day 6. After 21 d, longissimus dorsi muscle was collected and muscle mass, BrdU+ myonuclei and sublaminal Pax7+ nuclear frequency in muscle cross‐sections were quantified (>1000 fibers/pig). Average fiber cross‐sectional area (CSA) was correlated (r=0.83, P=0.001) with muscle weight and was lower in RP compared to HP pigs (P=0.01), with no improvement in muscle mass with leucine supplementation. Total myonuclear number/fiber also was lower in RP and RPL compared to HP (P=0.01) and was correlated to CSA (r=0.77; P=0.001), with no difference in nuclear domain size (fiber CSA/myonucleus) among groups. There were 40% fewer Pax7+ nuclei in RP and RPL than HP muscles (P=0.001) and their frequency was predictive of myonuclear number/fiber (r=0.79, P=0.001). RP and RPL muscle on average had 30% fewer BrdU+ myonuclei than HP (P=0.003) muscle; the average number of myonuclei per fiber was correlated to the number of BrdU+ nuclei (r=0.76; P=0.001) and the average ratio was similar among groups. The results demonstrate that in the immature muscle fiber hypertrophy is dependent on sustained satellite cell proliferation and myonuclear accretion. This process is highly sensitive to protein intake even when concurrent energy and leucine intakes are optimized for growth.Support or Funding InformationStudies were funded by NIH grants: HD072891, AR 46308, AR44474; USDA NIFA 2013‐67015‐20438; USDA/ARS/CSREES 6250‐51000‐55
Maternal Choline Supplementation Modulates Maternal and Fetal Choline Metabolism and Downregulates Inflammatory Gene Expression in a Mouse Model of Placental Insufficiency
Authors: King Julia H , Kwan Sze Ting (Cecilia) , Yan Jian , Jiang Xinyin , Fomin Vladislav G , Roberson Mark S , Caudill Marie A 
Published: June 2021

A properly functioning placenta allows efficient transfer of nutrients from mother to fetus and promotes fetal growth. Decreased placental efficiency is commonly associated with intrauterine growth restriction, preeclampsia, and miscarriage. Choline is an essential nutrient that is a precursor for several molecules with crucial roles in fetal development: betaine, an osmolyte and methyl donor; acetylcholine, a neurotransmitter and signaling molecule; and phosphatidylcholine (PC), the most prevalent membrane phospholipid. We previously showed that maternal choline supplementation (MCS) in the Dlx3+/− mouse, a model of placental insufficiency, increases fetal growth in early gestation and lowers expression of pro‐angiogenic genes implicated in preeclampsia. To explore the mechanisms contributing to these effects, we measured choline metabolites in the maternal liver and placentas of Dlx3+/− female mice consuming 1X (control), 2X or 4X the recommended intake levels of choline during gestation. Additionally, we measured expression of inflammatory genes that are elevated in preeclampsia and indicative of placental dysfunction. Dams were sacrificed at embryonic days E10.5, E12.5, E15.5, and E18.5. Data were analyzed using linear mixed models with dam as a random factor. MCS increased betaine concentrations in the maternal liver at all four time points (p<.01) and prevented a decline in maternal hepatic betaine stores in late pregnancy. 4X choline also increased phosphocholine, a precursor of PC, at E15.5 (p=.014), and decreased glycerophosphocholine, a product of PC breakdown, at E12.5 (p=.025). In the placenta, MCS increased betaine concentrations at E10.5 and 12.5 (p=.005 and .041, respectively). These data suggest that effects of MCS may be primarily driven by betaine, potentially through increased supply of methyl groups for one‐carbon reactions including DNA methylation. This is supported by data demonstrating widespread effects of choline on gene expression. In Dlx3+/− placentas, choline decreased (p<0.05) expression of pro‐inflammatory genes Il1b (at E12.5, 15.5 and 18.5), Tnf‐α (at E12.5) and NfκB (at E15.5). Further studies are ongoing to identify downstream effects of increased betaine on placental DNA methylation and growth factor signaling pathways.Support or Funding InformationFunding provided by USDA‐NIFA 2012‐67017‐30176
Dietary Tomato Powder Inhibits Hepatic Steatosis, Inflammation and Tumorigenesis in Beta‐carotene‐15, 15′‐oxygenase (BCO1) and Beta‐carotene‐9, 10′‐oxygenase (BCO2) Double Knockout Mice
Authors: Li Cheng‐Chung , Liu Chun , Hu Kangquan , Smith Donald E. , von Lintig Johannes , Wang Xiang‐Dong 
Published: June 2021

Consumption of tomatoes and tomato products which are rich in lycopene, is associated with a decreased risk of chronic disease. Lycopene can be cleaved by beta‐carotene‐15, 15′‐oxygenase (BCO1) and beta‐carotene‐9′, 10′‐oxygenase (BCO2) to produce biological active apolycopenoids. We have recently shown that lycopene and apolycopenoid have different mechanisms of protection against high fat diet (HFD)‐induced hepatic steatosis and hepatocellular carcinoma (HCC) development in BCO2 knockout (KO) mice (Ip, 2014, 2015). Since apolycopenoids also exist in tomato and tomato products (Kopec, 2010), the present investigation examined whether or not the whole tomato (tomato powder, TP) can inhibit HFD‐induced hepatic steatosis, inflammation and HCC in the absence of both BCO1/BCO2 in mice.BCO1/BCO2 double KO mice were injected with a carcinogen (diethylnitrosamine, i.p. 25 mg/kg body weight) at 2 weeks of age. At the age of 6 weeks, the mice were randomly assigned to either the HFD (n=9, 60% of energy as fat) feeding alone group or the HFD feeding with TP supplementation (n=9, HFD+TP, 41.8 g TP/kg diet, equivalent to 36 mg lycopene/day in human, which is 3–4 times higher than the average intake of lycopene) for 24 weeks. BCO1/BCO2 double KO mice (n=9) of the same age were fed with a chow diet as the control group.Results showed that TP supplementation significantly decreased hepatic steatosis and HCC development (67% reduction in incidence, 83% reduction in multiplicity, and 95% reduction in tumor volume) in BCO1/BCO2 double KO mice, as compared with the mice fed with HFD alone. The protective effects of TP supplementation were associated with 1) decreased hepatic inflammatory foci (89% reduction) and mRNA expressions of pro‐inflammatory biomarkers [interleukin (IL)‐6, IL‐12a, monocyte chemoattractant protein‐1, and inducible NO synthase]; 2) increased mRNA expressions of deacetylase sirtuin 1, sirtuin 3, and nicotinamide phosphoribosyltransferase involving NAD+ production; and 3) restored HFD‐reduced circadian clock gene expressions (circadian locomotor output cycles kaput, period 2, and cryptochrome‐2) to the normal levels of the control group. Taken together, the present study demonstrates that dietary TP can effectively inhibit HFD‐promoted steatosis, inflammation and tumorigenesis in the absence of BCO1/BCO2. The protective effects of TP against HFD‐induced liver injury may involve the regulations of sirtuin deacetylation and its related molecular clock function.Support or Funding InformationSupported by USDA/NIFA (2015‐67017) and USDA/ARS (58‐1950‐0014)
The Effect of Dietary Protein on Bone during Weight Loss: A Meta‐Analysis and Systematic Review
Authors: Wright Christian S , Li Jia , Campbell Wayne W 
Published: June 2021

The pervasiveness of obesity and excess adiposity is an ever prevalent reality amongst US adults, decreasing quality of life and predisposing individuals to metabolic dysfunction. Weight loss is an effective and widely used strategy for decreasing adiposity and improving overall metabolic health. In particular, higher protein weight loss diets (≥25% of energy from protein or ≥1.0 g/kg/day; HP) are shown to retain lean mass and decrease fat mass more than normal protein weight loss diets (<25% of energy from protein or <1.0 g/kg/day; NP). However, weight loss is also shown to significantly decrease bone quantity and the impact of a HP weight loss diet on bone is both unclear and controversial. With individual studies reporting conflicting results, either an exacerbation or an attenuation of weight‐loss induced bone loss with higher protein intakes, a recommendation for total protein intake during weight loss for the preservation of bone health is uncertain. Currently, no comprehensive analyses of randomized controlled trials have investigated the effects of HP weight‐loss diets on bone outcomes. The purpose of this systematic review and meta‐analysis was to assess the effects of HP versus NP weight loss diets (≥12 weeks) on bone mineral density (BMD) and bone mineral content (BMC) in healthy adults (≥19 years old). Two independent researchers collected and assessed a total of 1799 citations spanning the years 1969 to 2015 from multiple literary databases (Pubmed, Cochrane, CINAHL, Scopus, and Web of Science). Out of 1310 abstracts, 108 full articles were acquired for further inspection and 29 met the inclusion criteria for the systematic review. Data from 10 of the 29 studies displaying differences in total protein intake were extracted and a random‐effects model meta‐analysis was conducted (STATA/SE 12 software; StataCorp LP., College Station, TX). Collectively, this systematic review included 1,940 individuals (79.2% women, ~46 years old) actively engaged in a weight loss intervention lasting on average 6.2 ± 4.2 months. Average total protein intake during HP weight‐loss diets was 99.5 ± 13.5g (1.24 ± 0.16 g/kg BW; 26.2 ± 4.4 % of energy from protein), which was largely achieved through the consumption of mixed protein‐rich whole food sources (59% of studies). Though the majority of studies concluded a significant decrease in bone quantity following active weight loss (62%), the current meta‐analysis revealed neither an exacerbation nor an attenuation of bone loss while utilizing a HP weight loss diet (total BMD, p=0.11; total BMC p=0.42). An apparent positive effect was noted for lumbar spine with HP weight loss diets (Lumbar BMD, p=0.053, weighted mean difference: 0.007 g/cm2, 95% CI: −0.001, 0.016). In conclusion, a higher protein weight loss diet is known to favorably influence soft tissue compartments; however it does not appear to influence weight loss induced bone loss.Support or Funding InformationUSDA‐NIFA #2011‐38420‐20038 (WWC)
High‐Calorie Diet Induced Chronic Colonic inflammation: A Human‐Relevant Porcine Model to Assess Whole Food Approach to Reduce Colon Cancer Risk
Authors: Vanamala Jairam , Sido Abigail , Eriksson Elisabeth , Kim Sung Woo , Bhat Vadiraja , Radhakrishnan Sridhar , Reddivari Lavanya 
Published: June 2021

Recent studies have shown a critical link between high‐calorie diet (HCD)‐induced chronic inflammation and colon cancer. A recent prospective study revealed a positive association between interleukin‐6 (IL‐6), a pro‐inflammatory cytokine, and colon cancer risk. Recently, we developed a human‐relevant pig model for diet‐induced chronic inflammation where clinical markers of inflammation, calprotectin and LCN‐2, were elevated in colonic digesta and mucosa. In the current study, we hypothesized that HCD will elevate the IL‐6 signaling pathway proteins and these proteins levels will correlate with colon cancer risk (Ki‐67 proliferative index and zone) markers. We further hypothesized that anthocyanin rich purple‐fleshed potatoes suppress IL‐6 pathway proteins and colon cancer risk factors. We observed elevated colonic mucosal IL‐6 expression in HCD‐consuming pigs (3 weeks post‐weaning consumed diets for 13 weeks, n = 8 / group) compared to standard diet (SD, qPCR, P = 0.04) and IL‐6 expression levels strongly correlated with Ki‐67 proliferative index and zone (r = 0.604, 0.743; P = 0.017, 0.002; respectively). LC/MS‐MS‐based proteomic analysis and Ingenuity Pathway Analysis showed that HCD consumption alters IL‐6 signaling pathway proteins (PI3KR4, IL‐1α, Mapk10, Akt3, PIK3CG, PIK3R5, Map2k2). Furthermore, these proteins strongly correlated (r = 0.811, P = 0.001) with Ki‐67 proliferative index/zone. We observed that supplementation of HCD with anthocyanin containing purple‐fleshed potatoes (10% w/w), even after baking, tended to suppress HCD‐elevated IL‐6 expression (P ≤ 0.1) and IL‐6 linked proteins, IL‐1α and Map2k1 (P ≤ 0.1). Our results highlight the importance of IL‐6 signaling in diet‐linked induction/prevention of chronic colonic inflammation/cancer and demonstrate the potential of whole foods as a dietary intervention to counteract chronic inflammation and carcinogenesis using a human‐relevant pig model.Support or Funding InformationNational Research Initiative Grant 2009‐55200‐05197 from the USDA National Institute for Food and Agriculture (2009–2012)
Impact of cranberry on gut microbiota in a colon carcinogenesis mouse model
Authors: Cai Xiaokun , Sun Jin , Qi Ce , Gu Min , Goulette Timothy , Wu Xian , Song Mingyue , You Xiaomeng , Sela David , Neto Catherine , Xiao Hang 
Published: June 2021

Accumulating evidence showed that microbiota play important roles in colonic inflammation and inflammation‐associated colon carcinogenesis. Fruits and vegetable are know to have protective effects against colon carcinogenesis. In this study, we studied the protective effects of whole cranberry powder against inflammation‐associated colon carcinogenesis in mice treated with azoxymethane (AOM) and dextran sulfate sodium (DSS), and its impact on gut microbiota. Whole cranberry powder was administered to mice through diet at 1.5% w/w for 20 week. Our results demonstrated that treatment with cranberry powder significantly reduced the incidence and multiplicity of colon tumors. These protective effects were associated with decreased inflammation and increased apoptosis in the colonic tumors. Using Miseq sequencing and qPCR, we analyzed the composition of fecal microbiota of the mice. Compared to that of the negative control group, fecal microbiota of AOM/DSS‐treated mice showed relative abundance shifts, alterations in the abundance of Clostridiales and Bacteroidales, and an increase of the low abundant Enterobacteriales and Deferribacterales. Dietary treatment with whole cranberry powder reversed aforementioned alterations in the fecal microbiota of AOM/DSS‐treated mice. Moreover, whole cranberry powder also increased the number of Bifidobacteriales and Lactobacillus in the fecal microbiota. These composition alterations induced by whole cranberry powder were associated with suppressed colonic inflammation and carcinogenesis. In conclusion, our results demonstrated that whole cranberry powder modulated the composition of gut microbiota in AOM/DSS‐treated mice, which may contribute to its anti‐inflammatory and anti‐carcinogenic effects in the colon.Support or Funding InformationThis study was partially supported by fund from USDA