Home About us Contact
|
Home About us Contact | ||
|
|
||
Increased Metabolism (increased + metabolism)
Selected AbstractsCardiac natriuretic peptides and continuously monitored atrial pressures during chronic rapid pacing in pigsACTA PHYSIOLOGICA, Issue 2 2000Changes in atrial natriuretic peptide (ANP), N-terminal proatrial natriuretic peptide and brain natriuretic peptide (BNP) were evaluated in relation to continuously monitored atrial pressures in a pacing model of heart failure. Pigs were subjected to rapid atrial pacing (225 beats min,1) for 3 weeks with adjustments of pacing frequencies if the pigs showed overt signs of cardiac decompensation. Atrial pressures were monitored by a telemetry system with the animals unsedated and freely moving. Left atrial pressure responded stronger and more rapidly to the initiation of pacing and to alterations in the rate of pacing than right atrial pressure. Plasma natriuretic peptide levels were measured by radioimmunoassay and all increased during pacing with BNP exhibiting the largest relative increase (2.9-fold increase relative to sham pigs). Multiple regression analysis with dummy variables was used to evaluate the relative changes in natriuretic peptides and atrial pressures and the strongest correlation was found between BNP and left atrial pressure with R,2=0.81. Termination of pacing resulted in rapid normalization of ANP values in spite of persistent elevations in atrial pressures. This may reflect an increased metabolism or an attenuated secretory response of ANP to atrial stretch with established heart failure. In conclusion, 3 weeks of rapid pacing induced significant increases in atrial pressures and natriuretic peptide levels. All the natriuretic peptides correlated with atrial pressures with BNP appearing as a more sensitive marker of cardiac filling pressures than ANP and N-terminal proatrial natriuretic peptide. [source] The mechanisms that underlie glucose sensing during hypoglycaemia in diabetesDIABETIC MEDICINE, Issue 5 2008R. McCrimmon Abstract Hypoglycaemia is a frequent and greatly feared side-effect of insulin therapy, and a major obstacle to achieving near-normal glucose control. This review will focus on the more recent developments in our understanding of the mechanisms that underlie the sensing of hypoglycaemia in both non-diabetic and diabetic individuals, and how this mechanism becomes impaired over time. The research focus of my own laboratory and many others is directed by three principal questions. Where does the body sense a falling glucose? How does the body detect a falling glucose? And why does this mechanism fail in Type 1 diabetes? Hypoglycaemia is sensed by specialized neurons found in the brain and periphery, and of these the ventromedial hypothalamus appears to play a major role. Neurons that react to fluctuations in glucose use mechanisms very similar to those that operate in pancreatic B- and A-cells, in particular in their use of glucokinase and the KATP channel as key steps through which the metabolic signal is translated into altered neuronal firing rates. During hypoglycaemia, glucose-inhibited (GI) neurons may be regulated by the activity of AMP-activated protein kinase. This sensing mechanism is disturbed by recurrent hypoglycaemia, such that counter-regulatory defence responses are triggered at a lower glucose level. Why this should occur is not yet known, but it may involve increased metabolism or fuel delivery to glucose-sensing neurons or alterations in the mechanisms that regulate the stress response. [source] Contemporary egg size divergence among sympatric grayling demes with common ancestorsECOLOGY OF FRESHWATER FISH, Issue 1 2008F. Gregersen Abstract, This study documents divergence in egg size that has occurred over less than 25 generations among sympatric demes of European grayling (Thymallus thymallus) from Lake Lesjaskogsvatnet in Norway. A cluster analysis identified two clusters of tributaries: one of small, warm tributaries (SW) and the other of large, cold tributaries (LC). Spawning occurs more regularly and up to 4 weeks earlier in SW tributaries compared with that in LC ones. We explored numerous mixed models predicting egg size from year (random effect), basin and tributary (fixed effects), and female length. The most supported model estimated length-adjusted egg size to be larger in SW tributaries compared with that in LC tributaries. Combinations of density-dependent (competition for food/space) and density-independent (temperature) factors along with phenotypic plasticity and maternal effects are discussed as potential differentiation sources. We suggest high temperatures (increased metabolism) to reinforce the selective advantage of large eggs under conditions with highly density-dependent fry interactions. [source] LKB1 is essential for the proliferation of T-cell progenitors and mature peripheral T cellsEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 1 2010Peter Tamás Abstract The serine/threonine kinase LKB1 has a conserved role in Drosophila and nematodes to co-ordinate cell metabolism. During T lymphocyte development in the thymus, progenitors need to synchronize increased metabolism with the onset of proliferation and differentiation to ensure that they can meet the energy requirements for development. The present study explores the role of LKB1 in this process and shows that loss of LKB1 prevents thymocyte differentiation and the production of peripheral T lymphocytes. We find that LKB1 is required for several key metabolic processes in T-cell progenitors. For example, LKB1 controls expression of CD98, a key subunit of the L -system aa transporter and is also required for the pre-TCR to induce and sustain the regulated phosphorylation of the ribosomal S6 subunit, a key regulator of protein synthesis. In the absence of LKB1 TCR-,-selected thymocytes failed to proliferate and did not survive. LBK1 was also required for survival and proliferation of peripheral T cells. These data thus reveal a conserved and essential role for LKB1 in the proliferative responses of both thymocytes and mature T cells. [source] Regulation of Muscle Blood Flow in ObesityMICROCIRCULATION, Issue 4-5 2007Benjamin L. Hodnett ABSTRACT Obesity has been shown to impair muscle blood flow in humans. Vasodilatory control mechanisms such as metabolic control, myogenic mechanisms, conducted vasodilation, and release of endothelium-derived factors may be impaired in obesity due to insulin resistance, hyperglycemia, dyslipidemia, inflammation, oxidative stress, and endothelial dysfunction. The physiological importance of these blood flow control mechanisms has predominately been determined during the increase in blood flow (functional hyperemia) that occurs in response to the increased metabolism associated with exercise. This review examines the mechanisms by which functional hyperemia may be impaired in obesity and indicates areas where further studies are needed. The most extensively studied area of obesity-induced changes in muscle blood flow has been the role of endothelium-derived mediators during resting blood flow and exercise-induced hyperemia. Elevations in oxidative stress alter endothelium-derived factors, resulting in impaired vasodilatory responses. Alterations in metabolic and conducted vasodilatory regulation of blood flow have not been extensively studied in obesity, providing a potential area of research. [source] Review of select transplant subpopulations at high risk of failure from standard immunosuppressive therapyCLINICAL TRANSPLANTATION, Issue 5 2000Mark H Deierhoi Despite improvements in short-term graft and patient survival rates for solid organ transplants, certain subgroups of transplant recipients experience poorer clinical outcome compared to the general population. Groups including pediatrics, African-Americans, diabetics, cystic fibrosis patients, and pregnant women require special considerations when designing immunosuppressive regimens that optimize transplant outcomes. Problems specific to pediatric transplant recipients include altered pharmacokinetics of immunosuppressive drugs, such as cyclosporine (CsA) and tacrolimus (poor absorption, increased metabolism, rapid clearance), the need to restore growth post-transplantation, and a high incidence of drug-related adverse effects. African-Americans have decreased drug absorption and bioavailability, high immunologic responsiveness, and a high incidence of post-transplant diabetes mellitus. Diabetics and cystic fibrosis patients exhibit poor absorption of immunosuppressive agents, which may lead to underimmunosuppression and subsequent graft rejection. Pregnant women undergo physiologic changes that can alter the pharmacokinetics of immunosuppressives, thus requiring careful clinical management to minimize the risks of either under- or overimmunosuppression to mother and child. To achieve an optimal post-transplant outcome in these high-risk patients, the problems specific to each group must be addressed, and immunosuppressive therapy individualized accordingly. Drug formulation greatly impacts upon pharmacokinetics and the resultant level of immunosuppression. Thus, a formulation with improved absorption (e.g., CsA for microemulsion), higher bioavailability, and less pharmacokinetic variability may facilitate patient management and lead to more favorable outcomes, especially in groups demonstrating low and variable bioavailability. Other strategies aimed at improving transplant outcome include the use of higher immunosuppressive doses, different combinations of immunosuppressive agents, more frequent monitoring, and management of concurrent disease states. [source] | |||||||||||||