bluuebunny/crossref_metadata_2025_split huggingface dataset:
Protective Effects of Calcitriol Against Fructose‐induced Hyperglycaemia and Dyslipidaemia in Male Albino Wistar Rats
Authors: Sadau Yakubu , Lai Ibrahim , Gari Fatima Umar Mai 
Published: June 2021

Hyperglycemia and lipidaemia have been found to produce adverse metabolic alterations in glucose and lipid metabolism. The study investigates the preventive role of calcitriol supplementation on fructose‐induced hyperglycaemia and dyslipidaemia in fructose‐drinking Albino Wistar rats. Twenty five male Albino rats were used. The rats were divided into 5 groups of 5 animals each. Group I: Control; received normal rat feed + distilled water, Group II: Received normal rat feed + 125 μg/kg of Calcitriol (CTR), Group III: Received normal rat feed + 10% fructose solution (FDR), Group IV: Received normal rat feed + 10% fructose solution (FDR) + 0.3 mg/kg of glibenclamide (GLIB). Group V: Received normal rat feed + 10% fructose solution (FDR) + 125 μg/kg of Calcitriol (CTR). For the induction of hyperglycaemia and lipidaemia rats were given 10% fructose solution as drinking water for eight weeks. The levels of fasting sugar and HbA1c were measured. Changes in body weights and lipid profile of rats were determined. CTR group exhibited no significant change in plasma glucose levels, HbA1c and body weights when compared to the control. In FDR group fasting sugar levels, glycated haemoglobin (HbA1c) and weights were found to be significantly increased compared group I. Glibenclamide administration in GLIB + FDR group effectively abolished the fructose‐induced hyperglycaemia and glycated haemoglobin in rats when compared to FDR group. In FDR + CTR group calcitriol supplementation successfully blocked and prevented the fructose‐induced increased in fasting sugar, HbA1c levels and weight in rats when compared with FDR group. CTR group exhibited no significant changes in lipid profile parameters compared control. FDR exhibited a significant increase in serum total cholesterol, when compared to control group. Similarly, fructose feeding resulted in a significant elevation in triglycerides levels in comparison to the control rats. FDR group rats had elevated levels of LDL‐C which was significant when compared with the control group. Although, high density lipoprotein cholesterol was increased in FDR group, the increased was not significant and the result was comparable to that of the control. In FDR + CTR group, oral calcitriol supplementation potentially prevented fructose in inducing alterations in serum lipid profiles when compared to FDR group. The result showed that calcitriol supplemention infructose‐drinking rats protects against hyperglycaemia and dyslipidaemia.Support or Funding InformationFunding is through the Tertiary Education Trust Fund, Nigeria. When an acceptance and invitation letter is forwarded to the Fund atleast 3 months before the conference timeThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Effect of Dynamic Eccentric Leg Exercise Training on Functional Fitness and Arterial Stiffness in Older Adults
Authors: Durocher John J. , LewAllen Sarah E. , Maanika Carley B. , Elmer Steven J. , Rajeshkumar Lavanya , Trewartha Kevin M. 
Published: June 2021

Eccentric exercise is shown to offer musculoskeletal benefits in multiple populations, but little is known about the effect of chronic dynamic eccentric exercise training in older adults concerning functional physical fitness and cardiovascular health. Therefore, the purpose of this study was to determine if twelve weeks of dynamic eccentric leg exercise (Eccentron) could improve functional fitness and reduce arterial stiffness. Thirteen older adults (ages 65–79 years; M = 70±1) performed dynamic eccentric leg exercise twice per week at a light to somewhat hard rating of perceived exertion. Exercise duration increased from five minutes per session in the first week to 25 minutes per session during the final week. Timed up and go test significantly improved from pre‐ to post‐training (5.7±0.2 vs. 5.3±0.1 s; p<0.05). Likewise, Berg Balance Score was statistically (p<0.05) improved from pre‐ to post‐training. Participants demonstrated non‐significant increases in single‐leg knee extensor strength (43.0±2.6 vs. 45.2±2.8 kg; p=0.26). Aortic arterial stiffness, assessed via carotid‐femoral pulse wave velocity, did not change from pre‐ to post‐eccentric exercise training (8.6±0.7 vs. 9.2±0.5 m/s; p=0.44). Similarly, leg arterial stiffness, assessed as femoral to dorsalis pedis pulse wave velocity, was unchanged (9.9±0.8 vs. 9.2±0.5 m/s; p=0.31). Our results demonstrate how 12‐weeks of eccentric training can positively influence functional physical fitness measures in older adults without a negative influence on arterial stiffness. Significant improvements in timed up and go and the Berg Balance Score, and non‐significant increases in leg extensor strength, suggests that older adults could improve their agility and balance, and reduce their risk of falling through eccentric leg exercise.Support or Funding InformationSupported by the Portage Health Foundation and Michigan Tech Research Excellence Fund.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Chronic Nicotine Inhalation Promotes the Development of Pulmonary Hypertension
Authors: Yue Xinping , Oakes Joshua M , Xu Jiaxi , Lazartigues Eric , Gardner Jason D 
Published: June 2021

Pulmonary hypertension is a condition of increased blood pressure within the arteries of the lungs, leading to clinical symptoms including shortness of breath, syncope, tiredness, chest pain, swelling of the legs, and a fast heartbeat. The exact cause of pulmonary hypertension is often unknown, but the risk factors include a family history, prior blood clots in the lungs, HIV/AIDS, cocaine use, and smoking. Nicotine is the addictive component of tobacco products including conventional cigarette, cigar, and the increasingly popular electronic cigarette (e‐cigarette). The purpose of this study was to examine the effects of chronic nicotine inhalation in the development of pulmonary hypertension. C57BL/6 mice (male, 8–12 weeks of age) were exposed to air (control) or nicotine vapor (daily, 12 hour on/12 hour off) for 8 weeks. Nicotine exposure was assessed by weekly measurement of serum cotinine levels (a more stable metabolite of nicotine), which showed a weekly average of 599.0 ± 54.28 ng/ml (mean ± SEM) in nicotine exposed mice. As the positive control, a subset of air‐exposed control mice were subjected to Angiotensin‐II (Ang‐II) infusion through subcutaneous osmotic mini‐pumps (450 ng/kg/min) for the last 4 weeks. At the end of the 8 weeks, mice were subjected to right heart catheterization (Millar SPR‐1000 Mikro‐Tip mouse pressure catheter) to measure the right ventricular systolic pressure (RVSP) followed by tissue collection. Nicotine exposed mice exhibited significantly increased RVSP (39.57 ± 4.17 mmHg, n=7) compared to the air‐exposed controls (22.31 ± 1.70 mmHg, n=8, P < 0.01 by unpaired student t‐test). Interestingly, the increase in RVSP by nicotine was as potent as Ang‐II infusion (38.00 ± 2.18 mmHg, n=7, P < 0.001 vs. air controls). Furthermore, our discovery quantitative proteomic analysis identified atrial natriuretic peptide receptor 1 and periostin among the over‐expressed proteins in the lungs from nicotine exposed mice compared to the air controls, both of which have been shown to be involved in the regulation of pulmonary blood pressure. We conclude that chronic nicotine inhalation promotes the development of pulmonary hypertension. In addition, to the immediate relevance to public health, our data suggest that nicotine users, especially young adults with e‐cigarette use, are at elevated risk for the development of pulmonary hypertension. Ongoing experiments are focusing on the mechanisms of nicotine‐induced pulmonary hypertension, including nicotine‐induced pulmonary vascular remodeling.Support or Funding InformationThis work was supported by the National Heart, Lung, and Blood Institute R01 HL135635 and the National Institute of General Medical Sciences P30 GM106392.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Dietary Salt Intake Exaggerates Arterial Blood Pressure during Exercise in healthy Normotensive Adults
Authors: Hammond Stephen , Caldwell Jacob , Banister Heather R , Lovoy Garrett M , Post Hunter K , Sutterfield Shelbi L , Ade Carl J 
Published: June 2021

High dietary salt intake is associated with an increased risk for the development of hypertension, cardiovascular (CVD) and cerebrovascular disease. Additionally, exaggerated blood pressure during dynamic exercise is independently predictive of future CVD beyond resting blood pressure and other conventional risk factors. This is critical given that in animal models, dietary salt negatively augments blood pressure responses during static hind‐limb contractions, suggesting an increased risk of an adverse CVD event during exercise with high dietary salt. However, it currently remains unknown if high salt intake increases arterial blood pressure and impairs vascular function during voluntary dynamic exercise in healthy men and women. Based on previous preclinical reports, we hypothesized that high salt intake would decrease resting vascular endothelial function, increase arterial blood pressure during dynamic exercise and decrease functional sympatholysis. Thirteen healthy men and women underwent a randomized, double‐blind, placebo‐controlled trial for 7 days with either 15g/day sodium chloride supplement or cellulose. Beat‐by‐beat mean (MAP), systolic (SBP) and diastolic (DBP) were recorded throughout the trial on the non‐exercising limb. Forearm blood flow (FBF) was calculated via mean blood velocity derived from ultrasonography on the brachial artery of the exercising limb. All patients performed a flow‐mediated dilation (FMD) protocol followed by (20% maximal voluntary contraction) submaximal hand‐grip exercise for 7 min with lower‐body negative pressure initiated during min 5 – 7. FMD was significantly reduced during the HS condition (HS: 2.2±0.26e−5; Pl: 4.1±0.56e−5; p<0.01). Compared to placebo, the absolute steady‐state exercise MAP and SBP were significantly higher during HS compared to the placebo condition (p<0.05). However, functional sympatholysis was not different between conditions (p=0.07). In summary, the results of this study show the effects of HS intake on arterial blood pressure during handgrip exercise. These findings highlight that the augmented exercise blood pressures may be key mediator for the increased risk for adverse CVD outcomes associated with high dietary salt intake.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Inorganic Nitrate Supplementation Improves Diastolic Function in Cancer Survivors treated with Anthracycline Chemotherapy
Authors: Parr Shannon , Banister Heather R , Caldwell Jacob , Lovoy Garrett M , Post Hunter K , Turpin Vanessa‐Rose G , Ade Carl J 
Published: June 2021

Cancer survivors treated with anthracycline‐based chemotherapy have an increased risk of cardiotoxicity, resulting in the development of cardiac complications up to 10 years after chemotherapy cessation. Thus, cardiovascular events and heart failure are the second leading cause of morbidity and mortality in these women. Notably, the increased generation of reactive oxygen species relative to antioxidant defenses in the cardiomyocyte with anthracyclines results in lipid peroxidation and peroxynitrate formation, at the consequence of a decreased nitric oxide (NO) bioavailability, which over time results in ventricular systolic and diastolic dysfunction. Recently, orally ingested inorganic nitrates (NO3−), which increase NO bioavailability via the nitrate‐nitrite‐nitric oxide pathway and high antioxidant capacity, have shown to improve cardiac function in mice given anthracycline chemotherapy. Therefore, we hypothesized that inorganic NO3− administration would improve of left ventricular (LV) systolic and diastolic function, arterial stiffness, and ventricular‐arterial coupling in human cancer survivors with a history of anthracycline chemotherapy. Ten cancer survivors, 9 with breast cancer and 1 with lymphoma, participated in this randomized, double blind, crossover study comparing a week of daily doses NO3− rich beetroot juice with a nitrate‐depleted placebo. Standard and Tissue Doppler echocardiography were used to assess LV and carotid artery function during systole and diastole. NO3− supplementation significantly improved parameters of LV diastolic function, specifically strain rate in early filling (1.07±0.17 versus 0.80±0.29 1/s; P<0.5), early mitral septal wall annular velocity (0.07±0.02 versus 0.06±0.02 m/s; P=0.02, and mitral A‐wave velocity (0.65±0.23 versus 0.52±0.17 cm/s; P=0.009). There were no differences in LV systolic parameters; ejection fraction (P=0.2) ventricular‐arterial coupling (P =0.10), systolic strain rate (P =0.49). Arterial stiffness (P =0.38) was not different between conditions. These findings suggest that decrease in NO bioavailability may have a mechanistic role in determining LV diastolic function in cancer survivors treated with anthracycline‐based chemotherapy. This is critical information that can be used to developed therapeutic strategies targeting NO‐dependent changes in left ventricular function that occur following anthracycline chemotherapy.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Cutaneous Microvascular Function in Hypertensive Adults is not Altered Following 16‐weeks of Pharmacological Antihypertensive Treatment
Authors: Dillon Gabrielle A , Greaney Jody L , Stanhewicz Anna E , Alexander Lacy M 
Published: June 2021

Hypertension is characterized by pervasive microvascular endothelial dysfunction, resulting in a shift toward a proconstrictor vascular profile and contributing to increased cardiovascular morbidity and mortality. Cross‐sectional data suggest that pharmacologically lowering blood pressure (BP) is associated with improvements in microvascular function via endothelium‐dependent mechanisms. Well controlled longitudinal studies directly assessing mechanisms underlying microvascular dysfunction in hypertensive adults before and after a pharmacological antihypertensive intervention have not been performed. We tested the hypothesis that endothelium‐dependent dilation would be improved and adrenergic‐mediated vasoconstriction would be attenuated following 16‐weeks of pharmacological treatment to lower BP. Microvascular function was assessed before and after 16‐weeks of antihypertensive treatment (diuretic or angiotensin converting enzyme inhibitor) in eleven stage II hypertensive adults (9 men, 54±3 yrs, 29±1 kg/m2, resting BP 143±4/93±3 mmHg). Red blood cell flux (laser Doppler flowmetry) was measured during graded intradermal microdialysis perfusion of the endothelium‐dependent agonist acetylcholine (ACh; 10−10–10−1 M) and the adrenergic receptor agonist norepinephrine (NE, 10−12–10−2 M). Cutaneous vascular conductance (CVC; flux/mmHg) was normalized to and expressed as a percentage of either baseline or maximal conductance (28 mM sodium nitroprusside and heat to 43°C). Resting BP was reduced following treatment (143±4/93±3 pre vs. 105±4/68±2 mmHg post; p=0.003). Neither baseline (0.19±0.03 pre vs. 0.19±0.03 post flux/mmHg; p=0.97) nor maximal CVC (2.16±0.48 pre vs. 1.44±0.24 post flux/mmHg; p=0.24) were different following treatment. There was no difference in ACh‐induced vasodilation following antihypertensive treatment (logEC50: −4.28±0.48 pre vs. −3.15±4.68 post; p=0.83). Further, NE‐induced vasoconstriction was not different after treatment (logEC50: −4.85±1.23 pre vs. −6.28±0.68 post; p=0.65). Contrary to our hypothesis, these preliminary data suggest that a 16‐week pharmacological antihypertensive treatment to reduce BP does not improve cutaneous microvascular function in middle‐aged hypertensive adults.Support or Funding InformationNIH R01HL093238This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Immune Challenge During Reproduction Results in Tissue Specific and Intensity‐Dependent Responses for Mitochondrial Stress
Authors: Parry Hailey A , Josefson Chloe , Taylor Halie A , Andreasen Victoria , Park Noel R , Hood Wendy R , Kavazis Andreas N 
Published: June 2021

Life‐history theory suggests that tradeoffs can occur between self‐maintance and an animal's capacity to allocate resources to reproduction. This effect is thought to be exacerbated when a female is faced with an immune challenge during a reproductive event. Ultimately, such tradeoffs are thought to curtail lifespan, but the bioenergetic underpinnings of this effect are not well understood. We determined the extent of any effects in mitochondrial function and oxidative damage in female mice when exposed to an immune challenge (keyhole limpet haemocyanin) during reproduction. Female ICR mice were paired with a male until just before giving birth and randomly assigned to one of three groups. Female mice in the control group (LC) were injected with saline 2 days after parturition, and then sacrificed 1 week after weaning. In the lactating immune challenge group (LI), females were treated similarly except they were injected with KLH. Finally, in the pregnant‐lactating immune challenge group (PLI), females were treated the same as LI group, except the male was left in the box with the female until 3 days post‐partum, so the female became pregnant again while lactating. The second litter was born within 3 days of weaning, immediately removed, and females were sacrificed 1 week later. Mitochondrial function and reactive oxygen species (ROS) emission were determined in the liver and hindlimb skeletal muscle. Antioxidant protein levels and oxidative damage markers were also analyzed in these tissues. A one‐way ANOVA was performed on all measures, with a Tukey's post hoc test to determine group differences. No significant differences were observed in liver or hindlimb skeletal muscle mitochondrial coupling as measured by the respiratory control ratio (RCR) for both complex I and complex II (p>0.05). Isolated mitochondrial ROS emission in the hindlimb skeletal muscle was significantly lower in LI compared to LC (p=0.041), but no differences were observed in the liver. Additionally, skeletal muscle PGC1‐α was significantly reduced in LI mice compared to LC (p=0.01). In skeletal muscle the antioxidant GPX was significantly increased in the PLI animals compared to LI animals (p=0.022). Lastly, liver SOD1 was significantly higher in LC compared to PLI (p=0.039). The opposite response was observed in HSP70, in which PLI had significantly increased expression compared to LC (p=0.018). In conclusion, females that experienced an immune challenge during reproduction did not appear to experience a decline in mitochondrial respiratory performance but a drop in PGC1‐a in skeletal muscle that could contribute to a reduction in future performance associated with a reduction in mitochondrial density.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
A Physiological Role of Inter‐Organ Network between Gastrointestine and Skeletal Muscle on the Regulation of Skeletal Muscle Volume
Authors: Goto Katsumasa , Aoshima Megumi , Suzuki Takashi , Kanda Yusuke , Inagaki Riko , Akiyama Kensuke , Yokoyama Shingo 
Published: June 2021

Several inter‐organ networks have been proposed. In general, gastrointestinal hormone gastric inhibitory polypeptide (GIP), which is synthesized in and secreted from K cells, regulates nutrient absorption via inhibition of gastric contraction and acid secretion. GIP receptor On the other hand, GIPR expresses in not only a gastrointestinal tract but also β cells in the pancreas. Since GIP also modulates glucose metabolism via insulin synthesis and secretion, GIP is also a member of incretin. Recently, the expression of GIP is also confirmed in skeletal muscle. However, there is no evidence for the inter‐organ network between gastrointestine and skeletal muscle. In the present study, we investigated a physiological role of the inter‐organ network between gastrointestine and skeletal muscle via GIP. GIP stimulates myogenic differentiation of C2C12 cells. Expression of GIPR was observed in C2C12 myoblasts and myotubes. Knockdown of GIPR induced the down‐regulation of Pax7 in C2C12 myoblasts. In addition, GIPR‐knockdown‐associated depression of myotube formation of C2C12 cells were observed. On the other hand, GIPR‐knockdown stimulated proliferation of C2C12 myoblasts. Therefore, GIP‐GIPR intracellular signal(s) might play a role in the regulation of skeletal muscle volume via the mediation of myogenic differentiative potential.Support or Funding InformationThis study was supported, in part, by Grants‐in‐Aid for Challenging Exploratory Research (16K13022), and Grants‐in‐Aid for Scientific Research (17K01762, 18H03160) from the Japan Society for the Promotion of Science, the Descente Sports Foundation, the All Japan Coffee Association, the Science Research Promotion Fund from Promotion and Mutual Aid Corporation for Private Schools of Japan, and the research grants from Graduate School of Health Sciences, Toyohashi SOZO University.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.