Relevant bibliographies by topics / Hemodynamic effects of insulin

Academic literature on the topic 'Hemodynamic effects of insulin'

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Published: 9 March 2023
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Journal articles on the topic "Hemodynamic effects of insulin"

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Schmetterer, L., M. Muller, P. Fasching, C. Diepolder, A. Gallenkamp, G. Zanaschka, O. Findl, et al. "Renal and Ocular Hemodynamic Effects of Insulin." Diabetes 46, no. 11 (November 1, 1997): 1868–74. http://dx.doi.org/10.2337/diab.46.11.1868.

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Schmetterer, L., M. Muller, P. Fasching, C. Diepolder, A. Gallenkamp, G. Zanaschka, O. Findl, et al. "Renal and ocular hemodynamic effects of insulin." Diabetes 46, no. 11 (November 1, 1997): 1868–74. http://dx.doi.org/10.2337/diabetes.46.11.1868.

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Ferrannini, E., D. Santoro, R. Bonadonna, A. Natali, O. Parodi, and P. G. Camici. "Metabolic and hemodynamic effects of insulin on human hearts." American Journal of Physiology-Endocrinology and Metabolism 264, no. 2 (February 1, 1993): E308—E315. http://dx.doi.org/10.1152/ajpendo.1993.264.2.e308.

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Myocardial muscle is considered to be a target tissue for insulin action, but direct measurements of insulin's effects on cardiac hemodynamics and intermediary metabolism in humans are scarce. We combined great cardiac vein (GCV)/arterial catheterization with the euglycemic insulin clamp technique and thermodilution in six healthy middle-aged (53 +/- 2 yr) volunteers. In the fasting state, the myocardium extracted free fatty acid (FFA), lactate, pyruvate, glycerol, and beta-hydroxybutyrate (6.4 +/- 0.8, 6.2 +/- 1.0, 0.58 +/- 0.12, 0.44 +/- 0.15, and 11 +/- 2 mumol/min, respectively) and consumed 0.26 +/- 0.02 mmol/min oxygen. As fasting plasma insulin (73 +/- 6 pmol/l) was raised and clamped at 503 +/- 16 pmol/l for 100 min while maintaining euglycemia (approximately 5 mmol/l), arterial levels of lactate and pyruvate rose (by 121 and 159%, respectively), whereas FFA, glycerol, and beta-hydroxybutyrate fell (by 69, 48, and 85%, respectively, all P < 0.001). Correspondingly, net myocardial uptake of glucose, lactate, and pyruvate increased to 18.9 +/- 3.5, 32.0 +/- 2.3, and 2.7 +/- 0.5 mumol/min, respectively, whereas net extraction of circulating FFA, glycerol, and beta-hydroxybutyrate was abolished (all P < 0.001). The stimulation of lactate and pyruvate uptake was the result of both increased arterial supply and enhanced myocardial extraction ratio (from 19 +/- 3 to 51 +/- 6% for lactate, from 26 +/- 5 to 44 +/- 5% for pyruvate, P < 0.001 for both). This shift from fat to carbohydrate fuel usage occurred in the absence of changes in oxygen consumption, heart rate, GCV blood flow, aortic pressures, coronary vascular resistance, and left ventricular end-diastolic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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Cohen, A. J., D. M. McCarthy, and J. S. Stoff. "Direct hemodynamic effect of insulin in the isolated perfused kidney." American Journal of Physiology-Renal Physiology 257, no. 4 (October 1, 1989): F580—F585. http://dx.doi.org/10.1152/ajprenal.1989.257.4.f580.

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The hemodynamic effect of insulin was examined in isolated perfused kidneys. Experiments were designed to study the effect of the hormone on basal hemodynamics and in the presence of angiotensin II (ANG II). Physiological insulin concentrations caused both renal vasodilation and increased glomerular filtration rate (GFR) during basal perfusion periods and attenuated the vasoconstrictor action of ANG II while limiting the ANG II-induced reduction of GFR. Insulin also increased fractional sodium reabsorption and diminished the natriuretic effect of ANG II. The addition of insulin to perfusions in which ANG II was infused from the start caused renal vasodilation, although supraphysiological concentrations were required. Kidneys perfused with hyperoncotic albumin to prevent filtration similarly demonstrated a vasodilatory effect of insulin that did not require glomerular filtration. Inhibition of prostaglandin (PG) synthesis with indomethacin prevented the vasodilatory effects of insulin. These data support the hypothesis that insulin causes renal vasodilation by a PG-dependent process.
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Stojiljkovic, Milos P., Da Zhang, Heno F. Lopes, Christine G. Lee, Theodore L. Goodfriend, and Brent M. Egan. "Hemodynamic effects of lipids in humans." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, no. 6 (June 1, 2001): R1674—R1679. http://dx.doi.org/10.1152/ajpregu.2001.280.6.r1674.

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Evidence suggests lipid abnormalities may contribute to elevated blood pressure, increased vascular resistance, and reduced arterial compliance among insulin-resistant subjects. In a study of 11 normal volunteers undergoing 4-h-long infusions of Intralipid and heparin to raise plasma nonesterified fatty acids (NEFAs), we observed increases of blood pressure. In contrast, blood pressure did not change in these same volunteers during a 4-h infusion of saline and heparin. To better characterize the hemodynamic responses to Intralipid and heparin, another group of 21 individuals, including both lean and obese volunteers, was studied after 3 wk on a controlled diet with 180 mmol sodium/day. Two and four hours after starting the infusions, plasma NEFAs increased by 134 and 111% in those receiving Intralipid and heparin, P < 0.01, whereas plasma NEFAs did not change in the first group of normal volunteers who received saline and heparin. The hemodynamic changes in lean and obese subjects in the second study were similar, and the results were combined. The infusion of Intralipid and heparin induced a significant increase in systolic (13.5 ± 2.1 mmHg) and diastolic (8.0 ± 1.5 mmHg) blood pressure as well as heart rate (9.4 ± 1.4 beats/min). Small and large artery compliance decreased, and systemic vascular resistance rose. These data raise the possibility that lipid abnormalities associated with insulin resistance contribute to the elevated blood pressure and heart rate as well as the reduced vascular compliance observed in subjects with the cardiovascular risk factor cluster.
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Bradley, Eloise A., Michael G. Clark, and Stephen Rattigan. "Acute effects of wortmannin on insulin's hemodynamic and metabolic actions in vivo." American Journal of Physiology-Endocrinology and Metabolism 292, no. 3 (March 2007): E779—E787. http://dx.doi.org/10.1152/ajpendo.00407.2006.

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Wortmannin, an inhibitor of phosphatidylinositol 3-kinase, was systemically infused during a hyperinsulinemic euglycemic clamp to investigate its effects in vivo. Rats were infused under anesthesia with saline, 10 or 20 mU·min−1·kg−1 insulin, wortmannin (1 μg·min−1·kg−1) + saline, or wortmannin + insulin (10 mU·min−1·kg−1); wortmannin was present for 1 h before and throughout the 2-h clamp. Femoral blood flow (FBF), glucose infusion rate to maintain euglycemia (GIR), glucose appearance (Ra), glucose disappearance (Rd), capillary recruitment by 1-methylxanthine metabolism (MXD), hindleg glucose uptake (HLGU), liver, muscle, and aorta Akt phosphorylation (P-Akt/Akt), and plasma insulin concentrations were determined. Plasma insulin increased from 410 ± 49 to 1,680 ± 430 and 5,060 ± 230 pM with 10 and 20 mU·min−1·kg−1 insulin, respectively. Insulin (10 and 20 mU·min−1·kg−1) increased FBF, MXD, GIR, Rd, and HLGU as well as liver, muscle, and aorta P-Akt/Akt and decreased Ra (all P < 0.05). Wortmannin alone increased plasma insulin to 5,450 ± 770 pM and increased Ra, Rd, HLGU, and muscle P-Akt/Akt without effect on blood glucose, FBF, MXD liver, or aorta P-Akt/Akt. Wortmannin blocked FBF, MXD, and liver P-Akt/Akt increases from 10 mU·min−1·kg−1 insulin. Comparison of wortmannin + 10 mU·min−1·kg−1 insulin and 20 mU·min−1·kg−1 insulin alone (both at ∼5,000 pM PI) showed that wortmannin fully blocked the changes in FBF and Ra and partly those of GIR, Ra, Rd, HLGU, and muscle P-AKT/Akt. In summary, wortmannin in vivo increases plasma insulin and fully inhibits insulin-mediated effects in liver and aorta and partially those of muscle, where the latter may result from inhibition of insulin-mediated increases in blood flow and capillary recruitment.
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Hashimoto, Seiji, Tomochika Maoka, Tetsuya Kawata, Toshio Mochizuki, Takao Koike, and Takashi Shigematsu. "Roles of Insulin Receptor Substrates (IRS) in renal function and renal hemodynamics." PLOS ONE 15, no. 12 (December 3, 2020): e0242332. http://dx.doi.org/10.1371/journal.pone.0242332.

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We have reported previously that renal hemodynamic abnormalities exist in the prediabetic stage of type II diabetic rats. At this prediabetic stage these rats have hyperinsulinemia, insulin resistance and metabolic syndrome. It is well known that insulin resistance is frequently associated with renal abnormalities, but the mechanism underlying this association has remained speculative. Although insulin is known to modify renal hemodynamics, little is known about the roles of insulin receptor substrates (IRS1, IRS2) in the renal actions of insulin. To address this issue, the effects of insulin on renal function and renal hemodynamics were investigated in C57BL/6 (WT: wild type), insulin receptor substrate 1- knockout (IRS1–/–), and IRS2-knockout (IRS2–/–) mice. IRS2–/–mice had elevated glucose level as expected. 24-h urine collections and serum creatinine revealed that creatinine clearance did not significantly differ between these groups. Albuminuria was found in IRS1–/–and IRS2–/–groups. We examined the effects on the IRS during the administration of Losartan, which is widely used for diabetic nephropathy. After the administration of Losartan the IRS displayed improved renal hemodynamics. Moreover, the subjects were also given Pioglitazone, which improves insulin resistance. Losartan significantly reduced albuminuria in both groups. Pioglitazone also showed similar results. We assessed the autoregulatory responses of the total renal blood flow (RBF), the superficial (SBF) and the deep renal cortical blood flow (DBF) with stepwise reductions of renal perfusion pressure (RPP), which was induced by a manual clamp on the abdominal aorta. During the clamp induced reductions of the RPP by 10 to 20mm HG, RBF, SBF and the DBF fell significantly more in the IRS1 and IRS2 than in the WT mice. Furthermore micropuncture studies showded that compared to the WT tubuloglomerular feedback (TGF) responses of the stop flow pressure (Psf) were reduced in both the IRS1 -/- and IRS2 -/-. The results of the IRS1 and IRS2 mice displayed the pressence of hemodynamic abnormalities. Losartan and Pioglitazone have shown the potential to improve these abnormalities. In conclusion the results indicate that IRS plays a major role in the stimulation of renal functions and renal hemodynamics in type type II diabetes.
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Pitre, M., A. Nadeau, and H. Bachelard. "Insulin sensitivity and hemodynamic responses to insulin in Wistar-Kyoto and spontaneously hypertensive rats." American Journal of Physiology-Endocrinology and Metabolism 271, no. 4 (October 1, 1996): E658—E668. http://dx.doi.org/10.1152/ajpendo.1996.271.4.e658.

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The insulin-mediated vasodilator effect has been proposed as an important physiological determinant of insulin action on glucose disposal in normotensive humans. The present study was designed to further examine the acute regional hemodynamic effects of insulin in different vascular beds and to explore the relationships between insulin vascular effects and insulin sensitivity during euglycemic hyperinsulinemic clamps in conscious normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). The rats were instrumented with intravascular catheters and pulsed Doppler flow probes to measure blood pressure, heart rate, and regional blood flows. In WKY rats, the euglycemic infusion of insulin (4 and 16 mU.kg-1.min-1) causes vasodilations in renal and hindquarter vascular beds but no changes in mean blood pressure, heart rate, or superior mesenteric vascular conductance. In contrast, in SHR, the same doses of insulin produce vasoconstrictions in superior mesenteric and hindquarter vascular beds and, at high doses, increase blood pressure. Moreover, at the lower dose of insulin tested, we found a reduction in the insulin sensitivity index in the SHR compared with the WKY rats. The present findings provide further evidence for an association between insulin sensitivity and insulin-mediated hemodynamic responses.
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Sánchez-Lozada, Laura G., Edilia Tapia, Pablo Bautista-García, Virgilia Soto, Carmen Ávila-Casado, Iliana P. Vega-Campos, Takahiko Nakagawa, Lin Zhao, Martha Franco, and Richard J. Johnson. "Effects of febuxostat on metabolic and renal alterations in rats with fructose-induced metabolic syndrome." American Journal of Physiology-Renal Physiology 294, no. 4 (April 2008): F710—F718. http://dx.doi.org/10.1152/ajprenal.00454.2007.

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Increased fructose consumption is associated with hyperuricemia, metabolic syndrome, and renal damage. This study evaluated whether febuxostat (Fx), an investigational nonpurine, and selective xanthine oxidase inhibitor, could alleviate the features of metabolic syndrome as well as the renal hemodynamic alterations and afferent arteriolopathy induced by a high-fructose diet in rats. Two groups of rats were fed a high-fructose diet (60% fructose) for 8 wk, and two groups received a normal diet. For each diet, one group was treated with Fx (5–6 mg·kg−1·day−1 in the drinking water) during the last 4 wk (i.e., after the onset of metabolic syndrome), and the other received no treatment (placebo; P). Body weight was measured daily. Systolic blood pressure and fasting plasma uric acid (UA), insulin, and triglycerides were measured at baseline and at 4 and 8 wk. Renal hemodynamics and histomorphology were evaluated at the end of the study. A high-fructose diet was associated with hyperuricemia, hypertension, as well as increased plasma triglycerides and insulin. Compared with fructose+P, fructose+Fx rats showed significantly lowered blood pressure, UA, triglycerides, and insulin ( P < 0.05 for all comparisons). Moreover, fructose+Fx rats had significantly reduced glomerular pressure, renal vasoconstriction, and afferent arteriolar area relative to fructose+P rats. Fx treatment in rats on a normal diet had no significant effects. In conclusion, normalization of plasma UA with Fx in rats with metabolic syndrome alleviated both metabolic and glomerular hemodynamic and morphological alterations. These results provide further evidence for a pathogenic role of hyperuricemia in fructose-mediated metabolic syndrome.
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Stonestreet, B. S., E. Le, and D. J. Berard. "Circulatory and metabolic effects of beta-adrenergic blockade in the hyperinsulinemic ovine fetus." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 4 (October 1, 1993): H1098—H1106. http://dx.doi.org/10.1152/ajpheart.1993.265.4.h1098.

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Offspring of women with poorly controlled diabetes exhibit hypoxemia, elevated catecholamine concentration at birth, and an increased incidence of fetal death. Experimental fetal hyperinsulinemia results in increased catecholamine concentration and hemodynamic changes including increased combined ventricular output and vasodilation of select fetal organs. We hypothesized that insulin-induced catecholamine-mediated beta-adrenergic stimulation supports some of these hemodynamic changes in the hyperinsulinemic ovine fetus. To study this, 24 chronically instrumented fetal sheep receiving insulin for 24 h were exposed to beta-(propranolol),beta 1-(metoprolol), and beta 2-(ICI 118,551) adrenergic blockade. Insulin infusion resulted in hyperinsulinemic-hypoglycemia, a surge in epinephrine and norepinephrine concentration, and increases in the combined ventricular output and regional blood flow to the heart, adrenal glands, kidney, gastrointestinal tract, liver, fat, muscle, carcass, and placenta. In the hyperinsulinemic state, beta-adrenergic blockade was associated with significant reductions in the combined ventricular output and blood flow to fat, carcass, lungs, and the placenta; beta 1-blockade was associated with reductions in the combined ventricular output and blood flow to the lungs; and beta 2-adrenergic blockade was associated with reductions in blood flow to muscle and lungs. Because beta-adrenergic blockade was associated with reductions in placental blood flow during hyperinsulinemia, oxygen and glucose metabolism were also compromised. We conclude that in the hyperinsulinemic-hypoglycemic normoxemic ovine fetus, insulin-induced catecholamine-mediated hemodynamic changes are modulated in part by beta-adrenergic receptor stimulation.
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Dissertations / Theses on the topic "Hemodynamic effects of insulin"

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OCHOA, MUNERA JUAN EUGENIO. "Effects of insulin resistance on systemic haemodynamics and autonomic cardiovascular regulation in normotensive healthy adults." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/46090.

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Hemodynamic effects of insulin resistance (IR) are thought to be largely dependent on its relationship with body mass index (BMI) and blood pressure (BP) levels. The first part of the present thesis was aimed at exploring whether IR is associated with hemodynamic indices of cardiovascular function in a large sample of non-diabetic individuals from the general population (n=731) and if so, to explore if such relationship is continuous across different categories of BMI (lean, overweight and obese), and BP (normal BP, high-normal BP and hypertension). IR was assessed with the homeostasis model assessment of IR (HOMA-IR). Based on a value of HOMA-IR of 2.09 (75th percentile of distribution curve), subjects were classified as insulin-sensitive (IS, HOMA<2.09) or insulin-resistant (IR, HOMA≥2.09). Synchronized beat-to-beat recordings of stroke volume (impedance cardiography) and R-R interval (ECG), along with repeated BP measurements were performed over 5 minutes. Stroke index (SI), cardiac index (CI), systemic vascular resistance index (SVRI), left cardiac work index (LCWI), pre-ejection period (PEP) and left ventricular ejection time (LVET) were computed and averaged. In analysis of co-variance allowing for confounders, IR subjects showed significantly higher BP levels and SVRI, and reduced R-R interval, SI, CI, LCWI, PEP and LVET. These differences remained significant when analyses were performed within each BMI and BP category. Overall, these results indicate that effects of IR on hemodynamic indices of cardiovascular function are continuous across different BMI and BP categories, reinforcing the importance of IR in the pathogenesis of cardiovascular alterations beyond its association with obesity and hypertension. The finding of a significant association between IR and hemodynamic alterations even in lean and normotensive subjects was the rationale to explore potential mechanisms for these alterations in this selected group of subjects. Specific objectives of this second part of the thesis were: 1) To explore the relationship between insulin resistance and systemic hemodynamics, cardiac baroreflex sensitivity and indices of autonomic CV modulation. 2) To explore the relationship of insulin resistance with 24h heart rate, average blood pressure levels and blood pressure variability over the 24h; and 3) To explore the relationship of insulin resistance with central blood pressure levels and with measures of large artery stiffness and wave reflections. The study population for these analyses was constituted by subjects who were below the 30th percentile of diastolic blood pressure (DBP) distribution curve (DBP ≤72 mmHg) and who had no elevation in systolic BP levels. In addition, subjects were excluded in case of diabetes mellitus (fasting blood glucose ≥126 mg/dL or use of medications for previously diagnosed type 2 diabetes) obesity (BMI≥30) or taking medications with effects on BP. A total of 90 subjects fulfilling inclusion criteria were considered for the present analysis and underwent further assessments. Insulin resistance was assessed with HOMA-index and subjects classified into IR tertiles, based on the distribution of HOMA-index values. 24h Ambulatory BP monitoring was performed. Mean SBP and DBP were averaged for the day, night and 24h, and the respective day-to-night dipping was calculated. BPV was assessed for SBP and DBP as 24h standard deviation (SD), weighted 24h SD (wSD), daytime and night-time SD. Recordings of pulse waveform were obtained by means of a previously validated oscillometric device for ambulatory BP monitoring with in-built transfer-function like method. Aortic pulse wave velocity (PWV, m/s) and other measures derived from pulse wave analysis such as augmentation index (AIx, %), central SBP (cSBP), central DBP (cDBP) and central pulse pressure (cPP) were computed. Peripheral SBP and DBP, and heart rate (HR) were recorded and pulse pressure (PP) calculated as the difference between SBP and DBP. Non-invasive assessment of beat-to-beat BP, R-R interval (ECG) and stroke volume (by means of impedance cardiography) were performed during 10 min in supine position and specific hemodynamic indices associated with their measurement were computed and averaged: RRI (msec), heart rate (HR, bpm), stroke volume index (SI, mL/beat/m2), cardiac index (CI, L/min/m2), SBP (mmHg) and DBP (mmHg), systemic vascular resistance index (SVRI, dyn/sec/cm-5/m2), left cardiac work index (LCWI, Kg/m/m2), pre-ejection period (PEP, msec), left ventricular ejection time (LVET, msec) and PEP/LVET ratio were calculated. Cardiac autonomic modulation was assessed by computer analysis of 10 min beat-to-beat BP and ECG recordings in resting supine position. Cardiac baroreflex sensitivity (BRS) was estimated by sequence method. Total variance, low-frequency (LF) and high-frequency (HF) spectral components of HR variability (HRV) were assessed by autoregressive analysis. LF/HF ratio was calculated. After multiple regression analysis, adjusting for common confounders such as age, sex, HR and BMI, increasing values of HOMA-IR were associated with reduced RRI, SI, CI, and with increased SVRI, SBP and DBP. IR was also associated with reduced BRS (up, down, and total slopes), decreased parasympathetic indices of autonomic CV modulation (SDRRI, HF-power, total power) and a predominance of sympathetic component of HRV (increased LF/HF ratio). Increasing values of HOMA-IR were also associated with increased HR and average SBP levels (during day, night and 24-h period), with augmented BP variability (Day SBP SD, and SBP wSD) and with a reduced dipping of HR. Finally, insulin resistance was shown to be associated with increasing values of aortic PWV, and with higher central and peripheral SBP and DBP levels. Overall, these results support significant associations between insulin resistance and changes in hemodynamic and autonomic indices of cardiovascular function, even after accounting for common confounders. These findings suggest that in normotensive healthy adults, increases in insulin resistance may promote alterations in autonomic cardiovascular modulation, in systemic hemodynamics and in arterial stiffness, all of which are known contributors to the pathogenesis of hypertension.
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Khir, Ashraf William. "The hemodynamic effects of aortic clamping." Thesis, Imperial College London, 2000. http://hdl.handle.net/10044/1/8077.

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Wirtz, Joris Jeroen Johannes Maria. "Hemodynamic and hemostatic effects of erythropoietin therapy." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1993. http://arno.unimaas.nl/show.cgi?fid=5887.

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Ozasa, Neiko. "Relation among left ventricular mass, insulin resistance, and hemodynamic parameters in type 2 diabetes." Kyoto University, 2008. http://hdl.handle.net/2433/135807.

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Rask, Peter. "Aortic stenosis : diagnostic use and hemodynamic effects of dipyridamole." Doctoral thesis, Umeå universitet, Klinisk fysiologi, 1995. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-118692.

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Nievelstein, Hubert Nicolas Maria Willem. "Hemodynamic effects of antihypertensive drugs in conscious spontaneously hypertensive rats." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1987. http://arno.unimaas.nl/show.cgi?fid=5367.

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Rajabi, Jaghargh Ehsan. "Effects of hemodynamic stresses on the remodeling parameters in arteriovenous fistula." University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1427962400.

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Pulcipher, Julie Marie. "The hemodynamic effects of smokeless tobacco during exercise in young men /." The Ohio State University, 1988. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487597424136459.

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Dahlan, Agus Abdurahim. "Effects of insulin on sleep in patients with insulin-dependent diabetes mellitus." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1996. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq23983.pdf.

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Anderson, Richard L. "The effects of cannabinoids on insulin secretion." Thesis, University of Nottingham, 2011. http://eprints.nottingham.ac.uk/11760/.

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Type 2 diabetes mellitus is a chronic condition caused by a deficiency in the secretion of insulin from the islets of Langerhans and/or impaired insulin signalling, resulting in hyperglycaemia. The role of the endocannabinoid system is well-recognised in the CNS and immune system, but its role in glucose homeostasis is poorly understood. The aim of this study was to define the roles of cannabinoids in insulin secretion, to provide insights into their therapeutic potential (or limitation) in the treatment of type 2 diabetes. Isolated islets were used, from Wistar rats, in static incubation studies measuring changes in insulin secretion rates. The endocannabinoid anandamide (AEA) was found to inhibit insulin secretion in a glucose- and concentration-dependent manner, with an IC50 of 1.6μM (95% CI: 227nM to 4.0μM; n= 10). Upon further analysis of the concentration-response data islet sensitivity to AEA appeared to vary, with islets either appearing to be sensative (IC50 220nM; 95% CI: 21.9nM to 2.2μM; n= 5) or less sensative (IC50 12.3μM; 95% CI: 6.8μM to 19.4μM; n= 5) to AEA. Pre-incubation of islets with a fatty acid amide hydrolase inhibitor did not affect islet responsiveness to AEA. AEA-mediated inhibition of insulin secretion was not consistently affected by cannabinoid receptor 1 (CB1) or CB2 antagonism. Surprisingly, the CB1 receptor antagonist AM251 was found to inhibit insulin secretion in a glucose- and concentration-dependent (IC50 1.6μM; 95% CI: 507nM to 3.3μM; n= 6) manner. Results from this study suggest that differences in CB-receptor signalling pathways, rather than endocannabinoid metabolism, could be responsible for the variations in the potency of AEA between islet preparations. Characterisation of cannabinoid signalling in islets was hindered as the CB receptor antagonists used in this study also affected insulin secretion. This study highlights the dynamics of endocannabinoid signalling in islets, which may be linked to their physiological function.
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Books on the topic "Hemodynamic effects of insulin"

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Bailey, David G. Ethanol enhances the hemodynamic effects of felodipine. London: Victoria Hospital, 1987.

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Beaser, Richard S. Outsmarting diabetes: A dynamic approach for reducing the effects of insulin-dependent diabetes. Minneapolis, MN: Chronimed Pub., 1994.

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Duffy, Joan. Effects of insulin sensitising agents on pancreatic beta cell function. [S.l: The Author], 2003.

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Fisher, Simon Jeremy. Use of the matched step tracer infusion procedure to evaluate the effects of different routes of insulin administration and to compare the effects of insulin and insulin-like growth factor I. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1992.

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Lee, Brenda Minfei. Effects of glucose, fructose and sucrose on postprandial glucose and insulin responses. Ottawa]: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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Åkesson, Björn. Islet constitutive nitric oxide synthase and nitric oxide production: Modulatory effects on insulin and glucagon secretion. Lund, Sweden: Dept. of Pharmacology, University of Lund, 1998.

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A, Hawley John, and Zierath Juleen R, eds. Physical activity and type 2 diabetes: Therapeutic effects and mechanisms of action. Champaign, IL: Human Kinetics, 2008.

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Eshraghi, Shervin. Effects of insulin and glucose on reendothelialization of in vitro aortic endothelial wounds. Ottawa: National Library of Canada, 1994.

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patterson, Steven. Homocysteine and the effects of other amino thiols on pancreatic beta cell function and insulin. [S.l: The Author], 2003.

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Segura, Ana-Geny. Short-term metabolic effects of increased meal frequency in non-insulin-dependent diabetes mellitus (NIDDM). Ottawa: National Library of Canada, 1993.

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Book chapters on the topic "Hemodynamic effects of insulin"

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Larner, J. "Effects of Insulin on Glycogen Metabolism." In Insulin, 367–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5_16.

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Strachan, Mark W. J., and Brian M. Frier. "Side-Effects of Insulin." In Insulin Therapy, 43–50. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-4760-2_5.

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Poor, Hooman. "Hemodynamic Effects of Mechanical Ventilation." In Basics of Mechanical Ventilation, 115–27. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-89981-7_10.

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Raineri, A., P. Assennato, B. Candela, G. L. Piraino, G. Mercurio, and M. Traina. "Hemodynamic Effects of Ventricular Pacing." In Assessment of Ventricular Function, 133–46. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-8003-0_11.

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Beatt, K. J., P. W. Serruys, A. Soward, P. J. de Feyter, and P. G. Hugenholtz. "Hemodynamic Effects of Intravenous Nisoldipine." In Nisoldipine 1987, 103–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-73010-8_14.

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Schor, Nestor, Mirian A. Roim, Elvino J. G. Barros, and Oscar F. P. Santos. "Glomerular Hemodynamic Effects of Cyclosporine." In Nephrology, 534–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-662-35158-1_50.

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Casadonte, Lorena, and Maria Siebes. "Hemodynamic Effects of Epicardial Stenoses." In Physiological Assessment of Coronary Stenoses and the Microcirculation, 3–18. London: Springer London, 2017. http://dx.doi.org/10.1007/978-1-4471-5245-3_1.

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Furst, Branko. "Hemodynamic Effects of Aortic Occlusion." In The Heart and Circulation, 181–87. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-5277-4_18.

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Furst, Branko. "Hemodynamic Effects of Aortic Occlusion." In The Heart and Circulation, 211–19. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-25062-1_18.

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McKeigue, Paul M. "Fetal Effects on Insulin Resistance and Glucose Tolerance." In Insulin Resistance, 35–49. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-716-1_3.

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Conference papers on the topic "Hemodynamic effects of insulin"

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Liu, Zhenhao, Jiangli Han, and Xing Chen. "Hemodynamic Analysis of Cardiomems: Adverse Hemodynamic Effects." In 2023 IEEE 36th International Conference on Micro Electro Mechanical Systems (MEMS). IEEE, 2023. http://dx.doi.org/10.1109/mems49605.2023.10052229.

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Cheyne, William Spencer, Jinelle Gelinas, Laura Harp, and Neil D. Eves. "Hemodynamic effects of incremental dynamic hyperinflation." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.oa1963.

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Klenner, Jacob B., Benjamin A. Van Noorden, Jennifer L. Knopp, Lui R. Holder Pearson, Anna R. Hardy, Sarah L. Vergeer, Geoffrey M. Shaw, and J. Chase. "Determining the effects of insulin Detemir on endogenous secretion of insulin." In 2019 41st Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC). IEEE, 2019. http://dx.doi.org/10.1109/embc.2019.8857643.

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Santos, Arnoldo, Jose Milicua, Manuel Perez, NAtividad Arias, Cesar Perez, and Fernando Suarez-Sipmann. "Hemodynamic effects of lung Recruitment In ARDS." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4532.

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Woowon Jeong and Kyehan Rhee. "Computational analysis of hemodynamic effects on aneurysm coil bundle." In 2012 International Conference on Biomedical Engineering (ICoBE). IEEE, 2012. http://dx.doi.org/10.1109/icobe.2012.6179023.

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Guerci, A. D., and R. Beyar. "Intermittent coronary sinus occlusion: hemodynamic and anti-ischemic effects." In Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1988. http://dx.doi.org/10.1109/iembs.1988.94400.

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Hielscher, Andreas H., Joseph M. Lasker, Chris J. Fong, and Edward Dwyer. "Optical Tomographic Imaging of Hemodynamic Effects in Arthritic Joints." In Biomedical Optics. Washington, D.C.: OSA, 2008. http://dx.doi.org/10.1364/biomed.2008.pdpbtuf3.

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Levine, A., N. Helbling, N. Chien, M. Simon, and M. T. Gladwin. "Acute Hemodynamic Effects of Oral Nitrite in PH-HFpEF." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2812.

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Xu, Lin, Xiaoming Wu, and Yanru Zhang. "Near-optimal Waveforms for Improving Hemodynamic Effects during EDCPR." In 2008 International Symposium on Computational Intelligence and Design (ISCID). IEEE, 2008. http://dx.doi.org/10.1109/iscid.2008.71.

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Warnken, M., U. Reitzenstein, M. Fuhrmann, P. Mayer, H. Enzmann, and K. Racke. "Characterization of Proliferative Effects of Insulin and Insulin-Like Growth Factor in Human Airway Epithelial Cells." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4982.

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Reports on the topic "Hemodynamic effects of insulin"

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McCleskey, Anna, Landon McDonald, Tim Moore, Jamie Pitcock, and Dwayne Accardo. Esmolol Compared to Fentanyl on Hemodynamic Effects: A Scoping Review. University of Tennessee Health Science Center, May 2022. http://dx.doi.org/10.21007/con.dnp.2022.0041.

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Craan, Andre-Gerard. Effects of insulin, sodium and D-glucose on amino acid absorption in the intestine of rats. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1448.

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Miao, Chenyun, Qingge Guo, Xiaojie Fang, Yun Chen, Ying Zhao, and Qin Zhang. Effects of Probiotics and Synbiotics Supplementation on Insulin Resistance in Women with Polycystic Ovary Syndrome: A Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2021. http://dx.doi.org/10.37766/inplasy2021.5.0112.

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McGuire, Mark A., Amichai Arieli, Israel Bruckental, and Dale E. Bauman. Increasing Mammary Protein Synthesis through Endocrine and Nutritional Signals. United States Department of Agriculture, January 2001. http://dx.doi.org/10.32747/2001.7574338.bard.

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Objectives To determine endocrine factors that regulate the partitioning of amino acids by the mammary gland. To evaluate dietary flow and supply of energy and amino acids and their effects on milk protein synthesis and endocrine status. To use primary cultures of cow mammary epithelial cells to examine the role of specific factors on the rates and pattern of milk protein synthesis. Milk protein is an increasingly valuable component of milk but little is known regarding the specific hormonal and nutritional factors controlling milk protein synthesis. The research conducted for this project has determined that milk protein synthesis has the potential to be enhanced much greater than previously believed. Increases of over 25% in milk protein percent and yield were detected in studies utilizing abomasal infusion of casein and a hyperinsulinemic-euglycemic clamp. Thus, it appears that insulin, either directly or indirectly, can elicit a substantial increase in milk protein synthesis if additional amino acids are supplied. For additional amino acids, casein provided the best response even though substantial decreases in branched chain amino acids occur when the insulin clamp is utilized. Branched chain amino acids alone are incapable of supporting the enhanced milk protein output. The mammary gland can vary both blood flow and extraction efficiency of amino acids to support protein synthesis. A mammary culture system was used to demonstrate specific endocrine effects on milk protein synthesis. Insulin-like growth factor-I when substituted for insulin was able to enhance casein and a-lactalbumin mRNA. This suggests that insulin is a indirect regulator of milk protein synthesis working through the IGF system to control mammary production of casein and a-lactalbumin. Principal component analysis determined that carbohydrate had the greatest effect on milk protein yield with protein supply only having minor effects. Work in cattle determined that the site of digestion of starch did not affect milk composition alone but the degradability of starch and protein in the rumen can interact to alter milk yield. Cows fed diets with a high degree of rumen undegradability failed to specifically enhance milk protein but produced greater milk yield with similar composition. The mammary gland has an amazing ability to produce protein of great value. Research conducted here has demonstrated the unprecedented potential of the metabolic machinery in the mammary gland. Insulin, probably signaling the mammary gland through the IGF system is a key regulator that must be combined with adequate nutrition in order for maximum response.
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Research, Gratis. Brown Fat Activation: A Future Treatment for Obesity & Diabetes. Gratis Research, November 2020. http://dx.doi.org/10.47496/gr.blog.01.

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Brown fat holds a promising therapeutic approach to prevent obesity and type 2 diabetes by its profound effects on body weight reduction, heat generation, increased insulin sensitivity and glucose metabolism regulation
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Butler, Walter R., Uzi Moallem, Amichai Arieli, Robert O. Gilbert, and David Sklan. Peripartum dietary supplementation to enhance fertility in high yielding dairy cows. United States Department of Agriculture, April 2007. http://dx.doi.org/10.32747/2007.7587723.bard.

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Objectives of the project: To evaluate the effects of a glucogenic supplement during the peripartum transition period on insulin, hepatic triglyceride accumulation, interval to first ovulation, and progesterone profile in dairy cows. To compare benefits of supplemental fats differing in fatty acid composition and fed prepartum on hepatic triglyceride accumulation, interval to first ovulation, progesterone profile, and uterine prostaglandin production in lactating dairy cows. To assess the differential and carry-over effects of glucogenic and fat supplements fed to peripartum dairy cows on steroidogenesis and fatty acids in ovarian follicles. To determine the carry-over effects of peripartum glucogenic or fat supplements on fertility in high producing dairy cows (modified in year 3 to Israel only). Added during year 3 of project: To assess the activity of genes related to hepatic lipid oxidation and gluconeogenesis following dietary supplementation (USA only). Background: High milk yields in dairy cattle are generally associated with poor reproductive performance. Low fertility results from negative energy balance (NEBAL) of early lactation that delays resumption of ovarian cycles and exerts other carryover effects. During NEBAL, ovulation of ovarian follicles is compromised by low availability of insulin and insulin-like growth factor-I (IGF-I), but fatty acid mobilization from body stores is augmented. Liver function during NEBAL is linked to the resumption of ovulation and fertility: 1) Accumulation of fatty acids by the liver and ketone production are associated with delayed first ovulation; 2) The liver is the main source of IGF-I. NEBAL will continue as a consequence of high milk yield, but dietary supplements are currently available to circumvent the effects on liver function. For this project, supplementation was begun prepartum prior to NEBAL in an effort to reduce detrimental effects on liver and ovarian function. Fats either high or low in unsaturated fatty acids were compared for their ability to reduce liver triglyceride accumulation. Secondarily, feeding specific fats during a period of high lipid turnover caused by NEBAL provides a novel approach for manipulating phospholipid pools in tissues including ovary and uterus. Increased insulin from propylene glycol (glucogenic) was anticipated to reduce lipolysis and increase IGF-I. The same supplements were utilized in both the USA and Israel, to compare effects across different diets and environments. Conclusions: High milk production and very good postpartum health was achieved by dietary supplementation. Peripartum PGLY supplementation had no significant effects on reproductive variables. Prepartum fat supplementation either did not improve metabolic profile and ovarian and uterine responses in early lactation (USA) or decreased intake when added to dry cow diets (Israel). Steroid production in ovarian follicles was greater in lactating dairy cows receiving supplemental fat (unsaturated), although in a field trail fertility to insemination was not improved.
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Barash, Itamar, and Robert Rhoads. Translational Mechanisms Governing Milk Protein Levels and Composition. United States Department of Agriculture, 2006. http://dx.doi.org/10.32747/2006.7696526.bard.

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Original objectives: The long-term goal of the research is to achieve higher protein content in the milk of ruminants by modulating the translational apparatus of the mammary gland genetically, nutritionally, or pharmacologically. The short-term objectives are to obtain a better understanding of 1) the role of amino acids (AA) as regulators of translation in bovine and mouse mammary epithelial cells and 2) the mechanism responsible for the synergistic enhancement of milk-protein mRNA polyadenylation by insulin and prolactin. Background of the topic: In many cell types and tissues, individual AA affect a signaling pathway which parallels the insulin pathway to modulate rates and levels of protein synthesis. Diverse nutritional and hormonal conditions are funneled to mTOR, a multidomain serine/threonine kinase that regulates a number of components in the initiation and elongation stages of translation. The mechanism by which AA signal mTOR is largely unknown. During the current grant period, we have studied the effect of essential AA on mechanisms involved in protein synthesis in differentiated mammary epithelial cells cultured under lactogenic conditions. We also studied lactogenic hormone regulation of milk protein synthesis in differentiated mammary epithelial cells. In the first BARD grant (2000-03), we discovered a novel mechanism for mRNA-specific hormone-regulated translation, namely, that the combination of insulin plus prolactin causes cytoplasmic polyadenylation of milk protein mRNAs, which leads to their efficient translation. In the current BARD grant, we have pursued the signaling pathways of this novel hormone action. Major conclusions/solutions/achievements: The positive and negative signaling from AA to the mTOR pathway, combined with modulation of insulin sensitization, mediates the synthesis rates of total and specific milk proteins in mammary epithelial cells. The current in vitro study revealed cryptic negative effects of Lys, His, and Thr on cellular mechanisms regulating translation initiation and protein synthesis in mammary epithelial cells that could not be detected by conventional in vivo analyses. We also showed that a signaling pathway involving Jak2 and Stat5, previously shown to lead from the prolactin receptor to transcription of milk protein genes, is also used for cytoplasmic polyadenylation of milk protein mRNAs, thereby stabilizing these mRNAs and activating them for translation. Implications: In vivo, plasma AA levels are affected by nutritional and hormonal effects as well as by conditions of exercise and stress. The amplitude in plasma AA levels resembles that applied in the current in vitro study. Thus, by changing plasma AA levels in the epithelial cell microenvironment or by sensitizing the mTOR pathway to their presence, it should be possible to modulate the rate of milk protein synthesis. Furthermore, knowledge that phosphorylation of Stat5 is required for enhanced milk protein synthesis in response to lactogenic opens the possibility for pharmacologic approaches to increase the phosphorylation of Stat5 and, thereby, milk protein production.
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Boisclair, Yves R., and Arieh Gertler. Development and Use of Leptin Receptor Antagonists to Increase Appetite and Adaptive Metabolism in Ruminants. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7697120.bard.

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Objectives The original project had 2 major objectives: (1) To determine the effects of centrally administered leptin antagonist on appetite and adaptive metabolism in the sheep; (2) To develop and prepare second-generation leptin antagonists combining high binding affinity and prolonged in vivo half-life. Background Periods of suboptimal nutrition or exaggerated metabolic activity demands lead to a state of chronic energy insufficiency. Ruminants remain productive for a surprisingly long period of time under these circumstances by evoking adaptations sparing available energy and nutrients. The mechanism driving these adaptations in ruminant remains unknown, but could involve a reduction in plasma leptin, a hormone acting predominantly in the brain. In laboratory animals, reduced leptin signaling promotes survival during nutritional insufficiency by triggering energy sparing adaptations such as reduced thyroid hormone production and insulin resistance. Our overall hypothesis is that similar adaptations are triggered by reduced leptin signaling in the brain of ruminants. Testing of this hypothesis in ruminants has not been possible due to inability to block the actions of endogenous leptin and access to ruminant models where leptin antagonistic therapy is feasible and effective. Major achievements and conclusions The Israeli team had previously mutated 3 residues in ovine leptin, with no effect on receptor binding. This mutant was renamed ovine leptin antagonist (OLA) because it cannot activate signaling and therefore antagonizes the ability of wild type leptin to activate its receptor. To transform OLA into an effective in vivo antagonist, the Israeli made 2 important technical advances. First, it incorporated an additional mutation into OLA, increasing its binding affinity and thus transforming it into a super ovine leptin antagonist (SOLA). Second, the Israeli team developed a method whereby polyethylene glycol is covalently attached to SOLA (PEG-SOLA) with the goal of extending its half-life in vivo. The US team used OLA and PEG-SOLA in 2 separate animal models. First, OLA was chronically administered directly into the brain of mature sheep via a cannula implanted into the 3rdcerebroventricule. Unexpectedly, OLA had no effect of voluntary feed intake or various indicators of peripheral insulin action but reduced the plasma concentration of thyroid hormones. Second, the US team tested the effect of peripheral PEG-SOLA administration in an energy sensitive, rapidly growing lamb model. PEG-SOLA was administered for 14 consecutive days after birth or for 5 consecutive days before sacrifice on day 40 of life. Plasma PEG-SOLA had a half-life of over 16 h and circulated in 225- to 288-fold excess over endogenous leptin. PEG-SOLA administration reduced plasma thyroid hormones and resulted in a higher fat content in the carcass at slaughter, but had no effects on feed intake, body weight, plasma glucose or insulin. These results show that the team succeeded in developing a leptin antagonist with a long in vivo half-life. Moreover, in vivo results show that reduced leptin signaling promotes energy sparing in ruminants by repressing thyroid hormone production. Scientific and agricultural implications The physiological role of leptin in ruminants has been difficult to resolve because peripheral administration of wild type leptin causes little effects. Our work with leptin antagonists show for the first time in ruminants that reduced leptin signaling induces energy sparing mechanisms involving thyroid hormone production with little effect on peripheral insulin action. Additional work is needed to develop even more potent leptin antagonists, to establish optimal administration protocols and to narrow down phases of the ruminant life cycle when their use will improve productivity.
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Meidan, Rina, and Robert Milvae. Regulation of Bovine Corpus Luteum Function. United States Department of Agriculture, March 1995. http://dx.doi.org/10.32747/1995.7604935.bard.

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The main goal of this research plan was to elucidate regulatory mechanisms controlling the development, function of the bovine corpus luteum (CL). The CL contains two different sterodigenic cell types and therefore it was necessary to obtain pure cell population. A system was developed in which granulosa and theca interna cells, isolated from a preovulatory follicle, acquired characteristics typical of large (LL) and small (SL) luteal cells, respectively, as judged by several biochemical and morphological criteria. Experiments were conducted to determine the effects of granulosa cells removal on subsequent CL function, the results obtained support the concept that granulosa cells make a substaintial contribution to the output of progesterone by the cyclic CL but may have a limited role in determining the functional lifespan of the CL. This experimental model was also used to better understand the contribution of follicular granulosa cells to subsequent luteal SCC mRNA expression. The mitochondrial cytochrome side-chain cleavage enzyme (SCC), which converts cholesterol to pregnenolone, is the first and rate-limiting enzyme of the steroidogenic pathway. Experiments were conducted to characterize the gene expression of P450scc in bovine CL. Levels of P450scc mRNA were higher during mid-luteal phase than in either the early or late luteal phases. PGF 2a injection decreased luteal P450scc mRNA in a time-dependent manner; levels were significantly reduced by 2h after treatment. CLs obtained from heifers on day 8 of the estrous cycle which had granulosa cells removed had a 45% reduction in the levels of mRNA for SCC enzymes as well as a 78% reduction in the numbers of LL cells. To characterize SCC expression in each steroidogenic cell type we utilized pure cell populations. Upon luteinization, LL expressed 2-3 fold higher amounts of both SCC enzymes mRNAs than SL. Moreover, eight days after stimulant removal, LL retained their P4 production capacity, expressed P450scc mRNA and contained this protein. In our attempts to establish the in vitro luteinization model, we had to select the prevulatory and pre-gonadotropin surge follicles. The ratio of estradiol:P4 which is often used was unreliable since P4 levels are high in atretic follicles and also in preovulatory post-gonadotropin follicles. We have therefore examined whether oxytocin (OT) levels in follicular fluids could enhance our ability to correctly and easily define follicular status. Based on E2 and OT concentrations in follicular fluids we could more accurately identify follicles that are preovulatory and post gonadotropin surge. Next we studied OT biosynthesis in granulosa cells, cells which were incubated with forskolin contained stores of the precursor indicating that forskolin (which mimics gonadotropin action) is an effective stimulator of OT biosynthesis and release. While studying in vitro luteinization, we noticed that IGF-I induced effects were not identical to those induced by insulin despite the fact that megadoses of insulin were used. This was the first indication that the cells may secrete IGF binding protein(s) which regonize IGFs and not insulin. In a detailed study involving several techniques, we characterized the species of IGF binding proteins secreted by luteal cells. The effects of exogenous polyunsaturated fatty acids and arachidonic acid on the production of P4 and prostanoids by dispersed bovine luteal cells was examined. The addition of eicosapentaenoic acid and arachidonic acid resulted in a dose-dependent reduction in basal and LH-stimulated biosynthesis of P4 and PGI2 and an increase in production of PGF 2a and 5-HETE production. Indomethacin, an inhibitor of arachidonic acid metabolism via the production of 5-HETE was unaffected. Results of these experiments suggest that the inhibitory effect of arachidonic acid on the biosynthesis of luteal P4 is due to either a direct action of arachidonic acid, or its conversion to 5-HETE via the lipoxgenase pathway of metabolism. The detailed and important information gained by the two labs elucidated the mode of action of factors crucially important to the function of the bovine CL. The data indicate that follicular granulosa cells make a major contribution to numbers of large luteal cells, OT and basal P4 production, as well as the content of cytochrome P450 scc. Granulosa-derived large luteal cells have distinct features: when luteinized, the cell no longer possesses LH receptors, its cAMP response is diminished yet P4 synthesis is sustained. This may imply that maintenance of P4 (even in the absence of a Luteotropic signal) during critical periods such as pregnancy recognition, is dependent on the proper luteinization and function of the large luteal cell.
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Hansen, Peter J., and Zvi Roth. Use of Oocyte and Embryo Survival Factors to Enhance Fertility of Heat-stressed Dairy Cattle. United States Department of Agriculture, August 2011. http://dx.doi.org/10.32747/2011.7697105.bard.

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The overall goal was to identify survival factors that can improve pregnancy success following insemination or embryo transfer in lactating dairy cows exposed to heat stress. First, we demonstrated that oocytes are actually damaged by elevated temperature in the summer. Then we tested two thermoprotective molecules for their effect on oocyte damage caused by heat shock. One molecule, ceramide was not thermoprptective. Another, insulin-like growth factor-1 (IGF) reduced the effects of heat shock on oocyte apoptosis and oocyte cleavage when added during maturation. We also used lactating cows exposed to heat stress to determine whether bovine somatotropin (bST), which increases IGF1 levels in vivo, would improve fertility in summer. Cows treated with bST received a single injection at 3 days before insemination. Controls received no additional treatment. Treatment with bST did not significantly increase the proportion of inseminated cows diagnosed pregnant although it was numerically greater for the bST group (24.2% vs 17.8%, 124–132 cows per group). There was a tendency (p =0.10) for a smaller percent of control cows to have high plasma progesterone concentrations (≥ 1 ng/ml) at Day 7 after insemination than for bST-treated cows (72.6 vs 81.1%). When only cows that were successfully synchronized were considered, the magnitude of the absolute difference in the percentage of inseminated cows that were diagnosed pregnant between bST and control cows was reduced (24.8 vs 22.4% pregnant for bST and control). Results failed to indicate a beneficial effect of bST treatment on fertility of lactating dairy cows. In another experiment, we found a tendency for addition of IGF1 to embryo culture medium to improve embryonic survival after embryo transfer when the experiment was done during heat stress but not when the experiment was done in the absence of heat stress. Another molecule tested, granulocyte-macrophage colony-stimulating factor (GM-CSF; also called colony-stimulating factor-2), improved embryonic survival in the absence of heat stress. We also examined whether heat shock affects the sperm cell. There was no effect of heat shock on sperm apoptosis (programmed cell death) or on sperm fertilizing ability. Therefore, effects of heat shock on sperm function after ejaculation if minimal. However, there were seasonal changes in sperm characteristics that indicates that some of the decrease in dairy cow fertility during the summer in Israel is due to using semen of inferior quality. Semen was collected from five representative bulls throughout the summer (August and September) and winter (December and January). There were seasonal differences in ion concentration in seminal plasma and in the mRNA for various ion channels known to be involved in acrosome reactions. Furthermore, the proportion of sperm cells with damaged acrosomes was higher in post-thaw semen collected in the summer than in its counterpart collected in winter (54.2 ± 3.5% vs. 51.4 ± 1.9%, respectively; P < 0.08Further examination is required to determine whether such alterations are involved in the low summer fertility of dairy cows.
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